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Kuliah Respirologi Anak: Divisi Respirologi Departemen Ilmu Kesehatan Anak FK Undip / Rsup DR Kariadi Semarang

This document summarizes a lecture on pediatric respiratory diseases. It discusses acute bronchitis, pneumonia, bronchiolitis, asthma, and bronchiectasis. For acute bronchitis, pneumonia, and bronchiolitis, it covers definitions, etiology, pathogenesis, clinical presentation, diagnosis, and treatment recommendations. It provides treatment guidelines for pneumonia based on age, including antibiotic recommendations. The document aims to educate medical students and residents on key respiratory illnesses commonly seen in children.

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Lailatuz Zakiyah
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0% found this document useful (0 votes)
40 views

Kuliah Respirologi Anak: Divisi Respirologi Departemen Ilmu Kesehatan Anak FK Undip / Rsup DR Kariadi Semarang

This document summarizes a lecture on pediatric respiratory diseases. It discusses acute bronchitis, pneumonia, bronchiolitis, asthma, and bronchiectasis. For acute bronchitis, pneumonia, and bronchiolitis, it covers definitions, etiology, pathogenesis, clinical presentation, diagnosis, and treatment recommendations. It provides treatment guidelines for pneumonia based on age, including antibiotic recommendations. The document aims to educate medical students and residents on key respiratory illnesses commonly seen in children.

Uploaded by

Lailatuz Zakiyah
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPT, PDF, TXT or read online on Scribd
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KULIAH RESPIROLOGI ANAK

DIVISI RESPIROLOGI
DEPARTEMEN ILMU KESEHATAN ANAK
FK UNDIP / RSUP DR KARIADI SEMARANG
POKOK BAHASAN
• Bronchitis Akut
• Pneumonia
• Bronkhiolitis
• Asma Bronkhial
• Bronkiektasis
ACUTE BRONCHITIS
DEFINITION
Inflammation of the mucous membrane within the Bronchial Tube

Bronchus  conducting
respiratory tract zone
from trachea to
bronchiolus
ACUTE
Less than 6 weeks

CHRONIC
Reoccuring frequently for more
than 2 years
ETIOLOGY
• Usually caused by VIRAL  often caused by the same
viruses that cause the flu and the common cold
• < 1 year  RSV, parainfluenza, and corona
• 1 – 10 years  parainfluenza, enterovirus, RSV, rhinovirus
• > 10 years  influenza virus, RSV, adenovirus

Risks factors for acute bronchitis include:


o Dust or other air pollution
o Fumes or vapors
o Tobacco smoke, including second hand smoke
o Comorbid lung disease
o Elderly, children and infants
Etiology……….
PATHOGENESIS &
PATHOPHYSIOLOGY

Inflammation  edema, mucous secretion, partial


obstruction, damaged cillia cell
• Inflammation
– Low grade fever
– Malaise

• Obstruction
– Stimulate cough receptor 
cough
– Respiratory sign : tachypnea,
prolonged expiration,
wheezing, abnormal
bronchovesicular sound,
DIAGNOSIS
• Sign & Symptoms
– Cough, Sputum production, Wheezing, Dyspnea,
Chest pain, Fever, Hoarseness, Malaise
• Physical Examination & Diagnostic Studies
– Fever, tachypnea, wheezing, rhonki, and
prolonged expiration
– NO Consolidation on chest x-ray
TREATMENT
• Protussives and antitussives
– Protussives (hypertonic saline, guaifenesin)
– Antitussives (hydrocodon, codein,
dextrometorphan, carbetapentane, benzonatate)
• Bronchodilators
– Beta agonis
• Antibiotics
– Wide spectrum antibiotics
PNEUMONIA
Terminologi 
Pneumonia,
Bronchopneumonia,
Acute Respiratory Tract Infection (Ispa)
Lung Infection
etc
DEFINITION
Inflamasi parenkim paru

Penyebab

Infeksi
Non Infeksi

Inflamasi parenkim paru yang disebabkan oleh


aspirasi benda asing disebut PNEUMONIA
ASPIRASI
ETIOLOGY
• INFEKSI
– BAKTERI : >> SERING
– VIRUS : segera diikuti infeksi sekunder bakteri
– JAMUR : Aspergilus, Candida
– PARASIT : jarang (Loeffler Disease)
• NON INFEKSI
– INHALAN  Pneumokoniosis
– ASPIRASI BENDA ASING  isi lambung, zat luar
– POSITIONING  Orthostatik Pneumonia
ETIOLOGI……………………………….
CLASSIFICATION
• Community Acquired Pneumonia
Pneumonia yang terjadi di komunitas
Kuman paling sering Streptococcus
pneumonia, Haemopylus Influenza
• Hospital Acquired Pneumonia
Pneumonia yang terjadi setelah minimal 2 hari
perawatan di RS
Kuman tergantung dari pola kuman RS
setempat
Other Classification…………..
• Anatomical
– Lobar Pneumonia
• BRONCHOPNEUMONIA (Lobaris Duplex)
– Lobularis/Segmental Pneumonia
– Interstitial Pneumonia
• Etyological
– Viral, Bacterial, Fungal, Paracytic
• Causes
– Infection and Non Infection
LOBARIS PNEUMONIA

Affect one lobus of the lung

BRONCHOPNEUMONIA

Affect more than one lobus of


the lung, usually duplex
PATHOGENESIS &
PATHOPHYSIOLOGY
INFECTION DETERMINED BY

1.integrity of pulmonary host defenses


2.microbial pathogenicity and
3.external environmental exposures
PULMONARY DEFENSE IN UPPER AND LOWER RESPIRATORY TRACT
PATHOGENESIS
Bacterial entry into the host
Pulmonary pathogens may reach the lung
parenchyma by the following routes:
MOST
•Direct inhalation of bacterial-laden aerosols COMMON
•Aspiration of oropharyngeal or gastric ROUTE

contents
•Direct spread of infection from the upper
respiratory system to the lower parts along
mucosal surfaces
•Haematogenous spread to the lungs from an
adjacent infected organ
Microbial virulence factors
IMMUNE DEFENSES AND INFLAMMATORY
RESPONSE

In bacterial pneumonia, injury to the lung parenchyma usually


results from activation of the immune system in response to
bacterial infection
MORPHOPATHOLOGICAL FINDINGS
4 STAGES
1. CONGESTION
2. RED HEPATIZATION
3. GREY HEPATIZATION
4. RESOLUTION
STAGES OF PNEUMONIA
CONGESTION
• vascular congestion
• intra-alveolar proteinaceous fluid
• small numbers of scattered
neutrophils, and
• numerous bacteria within the alveoli.
• the infected lobes are grossly heavy,
hyperaemic, dark-red and boggy
RED HEPATIZATION

• Few days later


• Eritrocyte in alveolar
• Neutrofil , and
• Fibrin
• Cause by persisting vascular congestion with red cell
extravasation
• Lung appearance like liver, solid and consolidated
GREY HEPATIZATION

• One or two days


• Eritrocyte lysis
• Fibrinosuppurative exudate
• Large Mononuclear cell
• Lung still looks consolidated but is paler, gray, dry, firm
and non crepitant
RESOLUTION

• Uncomplicated cases
• Alveolar exudate
enzymatically digested
producing a semifluid granular
debris that is resorbed, cleared by macrophages, expectorated
or undergoes organization
• Alveolar epithelium soon regenerates and is becomes normal
again within 8-14 days
• Macroscopically, the consolidated lung softens and liquefies
and returns to its normal red colour
PATHOPHYSIOLOGY
Inflammatory Response

Fever
Inadequate Gas Exchange

Respiratory syptoms; cough,


tachypnea, dyspnea, retraction,
hypoxia, sianosis; Obstruction
symptoms; abnormal physical
finding (ronkhi)
0 – 2 BULAN
2 BULAN – 5 TAHUN
GEJALA KLINIS
• Demam  tinggi • Desaturasi
• Sesak napas • Retraksi (suprasternal,
• Batuk intercostal, subcostal)
• Napas cepat • Suara napas menurun
• Sianosis • Rhonki basah halus
• Malas minum/makan
• Penurunan kesadaran
Simple Clinical Signs of Pneumonia (WHO)
Fast breathing (tachypnea)

Respiratory thresholds
Age Breaths/minute
< 2 months 60
2 - 12 months 50
1 - 5 years 40

Chest Indrawing
(subcostal retraction)
DIAGNOSIS PNEUMONIA
Radiographic patterns
1. Diffuse alveolar and interstitial pneumonia
(perivascular and interalveolar changes)
2.  Bronchopneumonia
(inflammation of airways and parenchyma)
3.  Lobar pneumonia
(consolidation in a whole lobe)
4.  Nodular, cavity or abscess lesions
(esp.in immunocompromised patients)
Complications
• Pleural effusion (empyema)
• Piopneumothorax
• Pneumothorax
• Pneumomediastinum
Management
Severe Pneumonia
• Hospitalization
• Antibiotic administration
– Amoxycilline
– Ampicilline + Gentamicyne
– Ceftriaxone
• Intra Venous Fluid Drip
• Oxygen
• Detection and management of complications
ANTIBIOTIC
ANTIBIOTIC
• Community setting
– Amoxycilline  ORAL
• 25 – 50 mg/kg/day  3x
• 80 mg/kg/day  2x (high dose)
• Hospital
– Injectable antibiotic
– Combination
• Ampicilline (50-100 mg/kg/day 3-4x) + Gentamycine
• Ceftriaxone
NO DIAGNOSIS KUMAN REKOMENDASI
PENYEBAB ANTIBIOTIK DOSIS FREK LAMA CARA
2 Pneumonia ß-Streptokokus atau Lini pertama
usia < 2 bulan kombinasi kuman gram Ampicilin 50-100 mg/kg/hari 3-4 x 7-10 hari i.v
positif dan gram DAN (+)
negative Gentamicin 7,5 mg/kg/hari 1-2 x 7-10 hari i.v
Lini kedua
Ceftriakson 50-100 mg/kg/hari 1-2 x 7-10 hari i.v
Pneumonia Streptococcus Lini pertama
usia 2 bln - 5 thn pneumonia, Ampicilin 50-100 mg/kg/hari 3-4 x 7-10 hari i.v
Hemophylius influenza, DAN (+)
staphylococcus Gentamicin 7,5 mg/kg/hari 1–2 x 7-10 hari i.v
aureus Lini kedua
Ceftriakson 50-100 mg/kg/hari 1-2 x 7-10 hari i.v
Pneumonia Streptokokus Lini pertama
Usia > 5 Tahun pneumonia dan Ampicilin 50-100 mg/kg/hari 3-4 x 7-10 hari i.v
ß-Streptokokus, DAN (+)
Mycoplasma, Gentamicin 7,5 mg/kg/hari 1-2 x 7-10 hari i.v
pneumonia, Lini kedua
chlamidia Ceftriakson 50-100 mg/kg/hari 1-2 x 7-10 hari i.v
Eritromisin 50 mg/kg/hari 3-4 x 7-10 hari p.o/i.v
BRONCHIOLITIS

LEVEL
KOMPETENSI

3B
ETIOLOGY
• Typically caused by VIRAL
• The MOST common 
Respiratory Syncytial Virus (RSV)
• Others viruses : influenza,
parainfluenza, adenovirus,
coronavirus, rhinovirus
• Myc. Pneumonia  very rare 
thought isolated not recognized as
etiologic agent
DEFINITION
Inflammation of the BRONCHIOLUS

Bronchiolus  the end


of conducting respiratory
tract zone
PATHOGENESIS &
PATHOPHYSIOLOGY
Obstructed Bronchiolus cause respiratory
symptoms  difficult breathing, tachypnea,
dyspnea, sianosis, hypoxemia, nasal flaring, etc.
Inflammation cause low grade fever, rhinorrea,
cough, etc
Physical finding; tachypnea,
low grade fever, retraction of
the chest wall, raised work of
breathing, sianosis,
Lung auscultation wheezing,
abnormal bronchovesicular
sound, late experium

Obstruction of the bronchiolus  hyperinfaltion lung,


air trapped, emphysematous
Hyperinfaltion
Lung Air Trapped

emphysematous
Differentiation with pneumonia
• Affect young infant (2 month – 24 month, usually 11 month)
 penumonia under 5 years
• Etiology Virus  pneumonia (mostly bacterial)
• Located in bronchiolus (pneumonia  reached alveolus)
• Low grade fever (pneumonia  high grade)
• Pathological dominancy  obstruction of the airway
• Lung auscultation wheezing  pneumonia rhonki
• Chest X-Ray hyperinflation, air trapped, emphysematous
 pneumonia consolidation, infiltrate, etc
Clinical Manifestation
• History
o early rhinorrhea, cough, low-grade fever
o later tachypnea, wheezing, retractions, fussiness, poor
feeding, lethargy, apnea
• Physical Examination
o tachypnea, retractions, fever, tachycardia
o fever may suggest more severe infection, longer hospital
stay and worse lung disease
o Skin: sianosis concurrent conjunctivitis, otitis media or
pharyngitis, auscultation wheezing, prolonged expiratory
phase
DIAGNOSIS
• Based on history and physical exam, and should
not routinely order laboratory and radiologic
studies for diagnosis
• Typical bronchiolitis presents as seasonal
respiratory illness in children < 2 years old with
– fever
– tachypnea
– wheezing
– increased respiratory effort (grunting, nasal flaring,
and intercostal and/or subcostal retractions)
TREATMENT
 Assess hydration and ability to take fluids orally
(SR)
 Temperature regulation (SR)
 Oxygen
o Insufficient evidence to determine when to use
oxygen therapy in children with lower respiratory
tract infections
o American Academy of Pediatrics recommendations
o if oxyhemoglobin saturation (SpO2) persistently below 90%,
adequate supplemental oxygen should be used to maintain
SpO2 ≥ 90% (AAP Option D)
o oxygen may be discontinued if SpO2 ≥ 90% and infant is
feeding well and has minimal respiratory distress (
AAP Option D)
LEVEL
KOMPETENSI
ASMA BRONKHIAL
4A
Asma adalah penyakit saluran respiratori dengan dasar
inflamasi kronik yang mengakibatkan obstruksi dan
hiperreaktivitas saluran respiratori dengan derajat bervariasi

UKK RESPIROLOGI IDAI


Pedoman Nasional
Asma Anak
PATHOPHYSIOLOGY

• AIRWAY INFLAMMATION
• AIRWAY REMODELING
NO ATTACK
• AIRWAY OBSTRUCTION
– BRONCHOCONSTRICTION
• BRONCHIAL HIPERREACTIVITY
• MUCOUS HIPERSECRETION

ATTACK
Patofisiologi serangan asma
INSULT
Genetika
Lingkungan
Infeksi virus

PATOFISIOLOGI SIMPTOM
Bronkhokonstriksi, Obsturuksi Saluran napas
hiperreaktivitas bronkhus,  batuk kronik, sesak
hipersekresi mukus, napas, nyeri dada, dada
edema mukosa tertekan, mengi
Gejala asma adalah batuk, mengi, sesak napas,
dada tertekan yang timbul secara kronik dan atau
berulang, reversibel, cenderung memberat pada
malam atau dinihari, dan biasanya timbul jika ada
pencetus.
Diagnosis

• Anamnesis
• Pemeriksaan Fisis
• Pemeriksaan Penunjang

Dasar utama diagnosis adalah anamnesis untuk


menggali manifestasi klinis dengan karakteristik
yang khas mengarah ke asma
Anamnesis (1)

Karakteristik yang mengarah ke asma adalah1:


• Episodisitas : gejala timbul episodik/berulang
• Faktor pencetus
– Iritan: asap rokok, asap bakaran sampah, asap obat
nyamuk, suhu dingin, udara kering, makanan minuman
dingin, penyedap rasa, pengawet makanan, pewarna
makanan
– Alergen: debu, tungau debu rumah, rontokan hewan,
serbuk sari
– Infeksi respiratori akut karena virus
– Aktivitas fisis: berlarian, berteriak, menangis, atau tertawa
berlebihan

1. Papadopoulus NG, Arakawa H, Carlsen KH, Custovic A, Gern J, Lemanske R et al. International consensus on (ICON) pediatric asthma. Allergy 2012.
Anamnesis (2)

• Riwayat alergi pada pasien atau riwayat asma


dalam keluarga
• Variabilitas: intensitas gejala bervariasi dari
waktu ke waktu, bahkan dalam 24 jam.
Biasanya malam hari lebih berat (nokturnal)
• Reversibilitas: gejala dapat membaik secara
spontan atau pemberian obat pereda asma
Pemeriksaan Fisik

• Gejala asma:
– Tanpa gejala
– Ada gejala: batuk, sesak,
wheezing, ekspirasi Allergic shiner

memanjang
• Tanda alergi:
– Dermatitis atopik, rinitis alergi
– Allergic shiners, geographic
tongue
Geographic tongue
Pemeriksaan Penunjang (1)

• Uji fungsi paru


– Spirometri
– Peak flow meter
• Uji cukit kulit (skin prick test),
eosinofil total darah,
pemeriksaan IgE spesifik Spirometri

• Uji inflamasi respiratori: FeNO


(fractional exhaled nitric oxide),
eosinofil sputum
• Uji provokasi bronkus dengan
exercise, metakolin, hipertonik
salin Peak flow meter
Pemeriksaan Penunjang (2)

• Uji defisiensi imun


• CT-scan toraks
• Endoskopi
respiratori
(rinoskopi,
laringoskopi,
bronkoskopi)
Kriteria Diagnosis Asma 2

Gejala Karakteristik
Wheezing , batuk ,  Biasanya lebih dari 1 gejala respiratori
sesak napas, dada  Gejala berfluktuasi intensitasnya seiring
tertekan, produksi waktu
sputum  Gejala memberat pada malam atau
dinihari
 Gejala timbul bila ada pencetus
Konfirmasi adanya limitasi aliran udara ekspirasi
Gambaran obstruksi FEV1 rendah (<80% nilai prediksi)
saluran respiratori FEV1 / FVC ≤ 90%
Uji reversibilitas
(pasca-bronkodilator) Peningkatan FEV1 >12%
Variabilitas Perbedaan PEFR harian >13% 
Uji provokasi Penurunan FEV1 >20%, atau PEFR >15%
2. The Global Initiative for Asthma (GINA). Global strategy for asthma management and prevention 2014. Available from: www.ginasthma.org
Alur Diagnosis Asma (1)

• Outline :
Alur Diagnosis Asma (2)
Alur Diagnosis Asma (3)
Diagnosis Banding (1)
Gejala klinis tidak sesuai dengan karakteristik asma sehingga
perlu dipertimbangkan kemungkinan diagnosis banding 1,2 :

Inflamasi: infeksi, alergi Obstruksi mekanis


• Rinitis, rinosinusitis • Laringomalasia,
• Chronic upper airway trakeomalasia
cough syndrom • Hipertrofi timus
• Infeksi respiratori • Pembesaran KGB
berulang • Aspirasi benda asing
• Bronkiolitis • Vascular ring, laryngeal web
• Aspirasi berulang • Disfungsi pita suara
• Defisiensi imun • Malforasi kongenital saluran
• Tuberkulosis respiratori
1. Papadopoulus NG, Arakawa H, Carlsen KH, Custovic A, Gern J, Lemanske R et al. International consensus on (ICON) pediatric asthma. Allergy 2012.
2. The Global Initiative for Asthma (GINA). Global strategy for asthma management and prevention 2014. Available from: www.ginasthma.org
Diagnosis Banding (2)

Patologi bronkus Kelainan sistem organ


• Bronkopulmonari lain
displasia • Penyakit refluks gastro-
• Bronkiektasis esofagus (GERD)
• Diskinesia silia primer • Penyakit jantung
• Fibrosis kistik bawaan
• Gangguan
neuromuskular
• Batuk psikogen

1. Papadopoulus NG, Arakawa H, Carlsen KH, Custovic A, Gern J, Lemanske R et al. International consensus on (ICON) pediatric asthma. Allergy 2012.
2. The Global Initiative for Asthma (GINA). Global strategy for asthma management and prevention 2014. Available from: www.ginasthma.org
KLASIFIKASI ASMA PADA ANAK
BERDASARKAN KLASIFIKASI
USIA Asma bayi – baduta (bawah dua tahun), Asma balita, Asma usia
sekolah (5-11 tahun), Asma remaja (12-17 tahun)
KEKERAPAN GEJALA Asma intermiten, Asma persisten ringan, Asma persisten sedang,
Asma persisten berat
FENOTIP Asma tercetus infeksi virus, Asma tercetus aktivitas (exercise
induced asthma), Asma tercetus alergen, Asma terkait obesitas,
Asma dengan banyak pencetus (multiple triggered asthma)
DERAJAT BERATNYA Asma serangan ringan-sedang, Asma serangan berat, Serangan
SERANGAN asma dengan ancaman henti napas
DERAJAT KENDALI Asma terkendali penuh (well controlled), Asma terkendali sebagian
(partly controlled), Asma tidak terkendali (uncontrolled)

KEADAAN SAAT INI Tanpa gejala, Ada gejala, Serangan ringan-sedang, Serangan
berat, Ancaman gagal napas
Kekerapan Gejala

Kekerapan Uraian kekerapan gejala asma


Intermiten <6x/tahun atau jarak antar gejala ≥6 minggu
Persisten
>1x/bulan, <1x/minggu
ringan
Persisten
>1x/minggu, namun tidak setiap hari
sedang
Persisten
Gejala asma terjadi hampir tiap hari
berat
Kesetaraan klasifikasi PNAA 2004 dengan PNAA
2015 adalah:

PNAA 2004 PNAA 2015


Episodik Jarang Intermiten
Episodik Sering Persisten Ringan
Persisten Sedang
Persisten
Persisten Berat
Klasifikasi

Berdasarkan derajat beratnya serangan2,4


• Asma serangan ringan-sedang
• Asma serangan berat
• Serangan asma dengan ancaman henti napas
Dalam pedoman ini klasifikasi derajat serangan
digunakan sebagai dasar penentuan tatalaksana.

2. The Global Initiative for Asthma (GINA). Global strategy for asthma management and prevention 2014. Available from: www.ginasthma.org
4. Hamasaki Y, Kohno Y, Ebisawa M, Kondo N, Nishima S, Nishimuta T et al. Japanese Guideline for Childhood Asthma 2014. Allergol Inter 2014; 63:335-56.
 
Penilaian derajat serangan asma
Asma serangan Serangan asma dengan
Asma serangan berat
ringan-sedang ancaman henti napas
• Bicara dalam kalimat • Bicara dalam kata • Mengantuk
• Lebih senang duduk • Duduk bertopang • Letargi
daripada berbaring lengan • Suara napas tak
• Tidak gelisah • Gelisah terdengar
• Frekuensi napas • Frekuensi napas
meningkat meningkat
• Frekuensi nadi • Frekuensi nadi
meningkat meningkat
• Retraksi minimal • Retraksi jelas
• SpO2 (udara kamar): 90 • SpO2 (udara kamar) <
– 95% 90%
• PEF > 50% prediksi atau • PEF < 50% prediksi
terbaik atau terbaik
Klasifikasi
Berdasarkan derajat kendali 1,2,4
• Asma terkendali penuh (well controlled)
– Tanpa obat pengendali : pada asma intermiten
– Dengan obat pengendali : pada asma persisten (ringan/sedang/berat)
• Asma terkendali sebagian (partly controlled)
• Asma tidak terkendali (uncontrolled)

Dalam pedoman ini, klasifikasi derajat kendali dipakai untuk menilai


keberhasilan tatalaksana yang tengah dijalankan dan untuk penentuan
naik jenjang (step-up), pemeliharaan (maintenance) atau
turun jenjang (step-down) tatalaksana yang akan diberikan.
1. Papadopoulus NG, Arakawa H, Carlsen KH, Custovic A, Gern J, Lemanske R et al. International consensus on (ICON) pediatric asthma. Allergy 2012.
2.The Global Initiative for Asthma (GINA). Global strategy for asthma management and prevention 2014. Available from: www.ginasthma.org
4. Hamasaki Y, Kohno Y, Ebisawa M, Kondo N, Nishima S, Nishimuta T et al. Japanese Guideline for Childhood Asthma 2014. Allergol Inter 2014; 63:335-56.
LEVEL OF CONTROL
Penilaian pengendalian klinis (dalam 4 minggu terakhir)

Karakteristik Terkontrol Terkontrol Tidak terkontrol


sebagian
Gejala harian Tidak ada Lebih dari Tiga atau lebih
(<2x/minggu) 2x/minggu gambaran dari
Keterbatasan aktivitas Tidak ada Ada tingkat terkontrol
Gejala malam Tidak ada Ada sebagian
hari/terbangun saat
tidur
Butuh obat Tidak ada Lebih dari
pereda/terapi (<2x/minggu) 2x/minggu
Fungsi paru (PEF atau Normal <80% predicted
FEV1) atau terbaik (jika
diketahui)
Klasifikasi
Berdasarkan keadaan saat ini:
• Tanpa gejala
• Ada gejala
• Serangan ringan-sedang
• Serangan berat
• Ancaman gagal napas
Serangan asma adalah episode perburukan yang progresif akut
dari gejala-gejala batuk, sesak nafas, mengi, rasa dada
tertekan, atau berbagai kombinasi dari gejala-gejala tersebut.
Tahapan Penegakan Diagnosis Asma

1. Diagnosis kerja : Asma


– Dibuat sesuai alur diagnosis asma anak
– Tatalaksana umum : penghindaran pencetus, pereda,
dan tatalaksana penyakit penyulit
2. Diagnosis klasifikasi kekerapan
– Dibuat dalam waktu 6 minggu, dapat kurang dari 6
minggu bila informasi klinis sudah kuat
3. Diagnosis derajat kendali
– Dibuat setelah 6 minggu menjalani tatalaksana
jangka panjang awal sesuai klasifikasi kekerapan
TATALAKSANA ASMA
Tata laksana serangan asma di fasyankes (1)
Tata laksana serangan asma di fasyankes (2)

Bila tidak tersedia obat-obatan lain, ADRENALIN untuk asma yang berhubungan dengan anafilaksis
dan angioedema, dosis 10 ug/kg (0,01 ml/kg adrenalin 1:1.000), maksimal 500 ug (0,5 ml)
Tata laksana serangan asma di fasyankes & RS/UGD (1)
Tata laksana serangan asma di fasyankes & RS/UGD (2)
**Pilihan steroid untuk serangan asma

Nama Generik Sediaan Dosis

tablet 4 mg 0,5−1 mg/kgBB/hari


Metilprednisolon
tablet 8 mg tiap 6 jam

Prednison tablet 5 mg 0,5−1 mg/kgBB/ hari - tiap 6 jam

Metilprednisolon vial 125 mg 30 mg dalam 30 menit (dosis tinggi)


suksinat injeksi vial 500 mg tiap 6 jam
Hidrokortison- vial 100 mg
4 mg/kgBB/kali - tiap 6 jam
suksinat injeksi  
Deksametason 0,5−1 mg/kgBB – bolus, dilanjutkan 1
ampul
injeksi mg/kgBB/hari diberikan tiap 6−8 jam
Betametason injeksi ampul 0,05−0,1 mg/kg BB - tiap 6 jam
TATALAKSANA ASMA JANGKA
PANJANG

• Keterangan gambar: ICS (inhaled corticosteroids, steroid inhalasi); LTRA


(Leukotriene Receptor Antagonist); SABA (short acting beta agonist, β2-agonis
kerja pendek); LABA (long acting beta agonist, β2-agonis kerja panjang)
BRONCHIECTASI
S
DEFINITION
• 1819  Rene-Theophile-Hyacinthe Laennec
• Abnormal irreversibly dilated and often thick walled bronchi , resulting
from a variety of pathological process that cause destruction of the
bronchial wall and its surrounding supporting tissues
TREATMENT
GENERAL GOALS
1. To limit the cycle of infection and inflammation
2. To limit the progression of the airway damage
3. To reduce the symptoms
4. To reduce the number of exacerbations, AND
5. To improve the quality of life
1. General Supportive Therapy
• Good nutrition
• Avoid smoking and exposure
• Regular exercise
• Exposure to fresh air
• Multi team health care professionals
– Physicians
– Physiotherapist
– Nurses
– Occupational therapist
– Phsycologist
2. Treatment of the Underlying Causative
Conditions
3. Prevention of Secondary Infection
with Vaccination
• Influenza vaccine
• Pneumococcal vaccine
4. Mobilization of Airway Secretions

Chest physiotherapy
• Postural drainage
• Active Cycles of Breathing Technique (ABCT)
• Positive Expiratory Pressure (PEP)
• Oscillatory PEP device
• High frequency chest wall percussion
• Exercise
• Inspiratory muscle training
4. Mobilization of Airway Secretions……… cont

Mucolytic and inhaled hiperosmolar agent s


• Bromhexine (combination with antibiotics)
• Erdostein
• Recombinant human DNA-ase (harm for non CFB)
• Inhaled mannitol
• Inhaled hypertonic saline (NaCl  3-5-7 %)
5. Bronchodilator Therapy

• Short acting beta agonist


• Long acting beta agonist
• Anti cholinergic
• Methylxanthine
• Leucotrien antagonist
6. Antibiotics Therapy

• Acute infective exacerbation


– Broad spectrum antibiotics (P aurug, Staph Aureus,
Haemophyl Inf)
– Treating pneumonia
• Maintenance
– Macrolide longterm treatment
7. Antiinflammatory agents

• Corticosteroids
– High dose inhaled
CS
– Oral CS (no study)
• Macrolide
THANK YOU

02/22/22 114

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