BROCHIECTASIS & ATELECTASIS

ERWIN ARIEF

DEPARTMENT OF INTERNAL MEDICINE

HASANUDDIN UNIVERSITY
MAKASSAR
I. INTRODUCTION
The term
bronchiectasis
is derived from
the Greek

bronkia
(bronchial,
tubes), ek (out),
and tasis
(stretching)
Bronchiectasis
literally mean
the
outstretching of
the bronchi
 Bronchiectasis is an uncommon disease
with irreversible abnormal dilatation of the
bronchi due to the destruction of elastic
and muscular components of the bronchial
wall.
PREVALENCE

The true
prevalence of
United States 
bronchiectasis is
52 cases per
unknown for
100,000 adults
most regions of
the world.
PREVALENCE

Very high prevalences in certain natives, such as

Alaskan natives, New Zealand Maoris, and
Australian Aborigines.
One recent study in the United States 1993 to
2006 16.5 hospitalizations per 100.000
population  increased significantly  2.4% in
men and 3.0% in women
The highest rate of hospitalizations was in women
and persons over 60 years.

In Indonesia there has been no definitive report, in

fact, the disease is often found at clinics and
suffered in men and women.
 The most common cause in developing countries are post
infection.

The economic burden associated with bronchiectasis

Various causes of bronchiectasis has been reported in adults,

more than half the cases of unknown cause.

In Europe, the most commonly bronchiectasis in patients with

cystic fibrosis.
 II. Anatomy of
Tracheobronchial
Tree

• Trachea
• Right and left bronchi
• Lobar bronchi
• Segmentalis bronchi.
• Terminal bronchioles,
• Acini comprising:
respiratory bronchioles,
alveolar ducts and alveolar
sakkus terminalis
 III. CLASSIFICATION OF
BRONCHIECTASIS

Saccular or
cystic
bronchiectasis
Classification
Varicose
of
bronchiectasis
bronchiectasis

Cylindrical
bronchiectasis
 IV. Etiology

Etiology of bronchiectasis is still unclear, it can

be classified as idiopathic, post infection or due
to anatomical disorder or systemic disease.

Bronchiectasis could be expected to occur in

congenital or acquired. There are many medical
conditions that can lead to the development of
bronchiectasis.
 Etiologi
• Post Infection
• Chronic obstructive Pulmonary
Disease
• Bronchial obstruction
• Allergic bronchopneumonia
aspergillosis
• Aspiration
• Deficiency of alpha 1-antitrypsin
• Systemic disease
• Congenital abnormalities
• Dysfunction of immune system
• Exposure to toxic gases
PATHOGENESIS BRONCHIECTASIS
Mucus
hypersecretion

Impaired ciliary
function
Inflamatory
INFECTION response

Loss of
Tissue
Acumulation of ciliated cell
damage
mucus

Impaired mucus clearance

mechanism
VI. DIAGNOSIS

• Chronic cough
• Dyspnea
• Hemoptysis
History and • Whezing
physical • Pleuritic chest pain
examination
• Fever
• Weight loss
 • Thorax photo
• Bronchography
DIAGNOSI • CT-Scan thorax
S
Thorax photo
Bronchography
CT-Scan of thorax

Figure A Figure B

Figure C Figure D

Figure A shows a normal bronchial, Figure B shows cylindrical

bronchiectasis, Figure C shows varicose bronchiectasis, Figure D shows
cystic bronchiectasis
DIAGNOSIS

• Analysis of sputum
• Quantitative
immunoglobulin
Examination levels
to identify the • Serum alpha-1 anti-
underlying trypsin
disease • Total serum IgG
level
• Autoimmune
screening tests
VII. MANAGEMENT
• The goal of therapy in patients with
bronchiectasis is to improve symptoms,
reduce complications, control of
exacerbations and reduce morbidity and
mortality and improve quality of life.
MANAGEMENT
• Early recognition of the underlying causes of
bronchiectasis was necessary to treatment
 • The use of drugs and chest
physiotherapy have been done to
mobilize secretions.
• Chest physiotherapy in the form of
postural drainage, active breathing
techniques, therapies lid positive
Improve drainage expiratory pressure, positive expiratory
of bronchial pressure with high frequency chest
secretions wall vibration.
• Mucolytics to reduce the viscosity of
secretions and inhalation of hypertonic
saline or mannitol inhalation to reduce
the osmolarity of secretions is also an
adjunct therapy to improve mucus
clearance
 Antibiotics

• Antibiotics are given to patients who are accompanied by acute

exacerbation of infection .
• Antibiotics should be given based on the results of bacterial culture
of isolated airway secretions .
• Broad spectrum oral antibiotics may be given if there is no culture
results , antibiotics can be given for 7-14 days until the bacteria
causing the infection eradicated or until a conversion of the original
sputum color is yellow / green to mucoid ( white and clear ) .
• The addition of other oral antibiotics or the use of parenteral
antibiotics can be given if there is a failure of treatment .
• Macrolide class has an added advantage because it suppreses
inflammatory mediators without suppressing the immune system.
Anti- inflammatory therapy

• Rationally, anti inflammatory

therapy reduces airway
inflammation in patients with
bronchiectasis .
• Two classes of drugs that can be
used as anti inflammatory drugs
are inhaled corticosteroids and
macrolides .
 Bronchodilators therapy

Bronchodilators include beta - agonists and

anticholinergics can help reduce shortness of
breath in some patients with bronchiectasis
when accompanied by airway obstruction
VIII. COMPLICATIONS

Bronchiectasis can result in massive hemoptysis,

pneumonia, cor pulmonale, heart failure and
respiratory failure.
Which heart failure and respiratory failure is a
common cause of death in patients with
bronkiektasis.
 IX. PROGNOSIS
Before the introduction of adequate antibiotic treatment, prevention and
operations, bronchiectasis prognosis is still poor.

After adequate antibiotic treatment, prevention by vaccination,

physiotherapy, good nutrition and surgery in certain conditions in people
with bronchiectasis, the life expectancy for the better.

Early recognition and adequate treatment can help control and reduce
the symptoms of bronchiectasis.

Awareness of the need for life long treatment can allow people with
bronchiectasis to minimize complications and maximize the life
expectancy.

The cause of congenital bronchiectasis, such as cystic fibrosis, is likely

to have a poorer prognosis than acquired bronchiectasis.
 ARDS
(Acute Respiratory Distress
Syndrome)
ARDS :
Gangguan fungsi paru akibat
kerusakan alveoli yg difus yg
menyebabkan edema alveoli yang
disertai dgn hipoksemia
 Kriteria diagnosis menurut
AECC (1994):

 Onset : akut
 Indeks oksigenasi (PaO2/FiO2) < 200
mmHg
 Foto toraks : infiltrat alveolar bilateral
 PAWP < 18 mmHg atau tidak ada bukti
klinis HT atrium kiri
PENYEBAB ARDS
I . LANGSUNG
II. TIDAK LANGSUNG
 Langsung
 Aspirasi
 Tenggelam
 Inhalasiasap atau bahan
kimia toksik
 Kontusio paru
 Keracunan oksigen
 Pneumonia
 Tidak langsung :
 Syok berat
 Sepsis

 Pankreatitis
 Emboli lemak

 Transfusi berlebihan

 Pasca transplantasi paru

PATOGENESIS
Belum diketahui dengan
pasti  diduga kelainannya
terletak pada membran
alveolar-kapiler
 Berbagai sebab ARDS

membran alveolo-kapiler

permeabilitas

aliran cairan dari intra ke

ekstra vaskuler

edema
Patogenesis ARDS secara
umum:

1. Edema paru
2. Shunting dalam darah paru

3. Fibrosis pada jar. paru

Gambaran Klinis
 Dispnea , takipnea
 Hipoksemia dgn sianosis yang
menetap
 Krepitasi yg luas pada kedua paru
Laboratorium
Analisa gas darah 
hipoksemia  PaO 2 < 50
mmHg
Radiologi :
Infiltrat paru difus  edema
bilateral
( snow storm appearance )
 PENATALAKSANAAN

Terapi sangat kompleks

1. Terapi suportif
2. Terapi penyakit dasarnya
 Terapi Suportif
a. Ventilasi mekanik  meningkatkan
oksigenasi yang adekuat
b. Perubahan posisi  mengeluarkan
sekret & fisioterapi
c. Nitrat oksida  memperbaiki
oksigenasi arteri paru dan
menurunkan resistensi vaskuler
paru
d. Surfaktan
e. Kortikosteroid
 PROGNOSIS
Prognosis buruk oleh karena :
 Gegala dini sulit dikenali
 Mekanisme tidak diketahui
 Patofisiologinya kompleks
 Gejala klinis yang bervariasi
 Proses progresif
 Korelasi antara th/ & hasilnya tidak
memuaskan
ATELECTASIS
• Classification:
– Primary atelectasis: failure of lung to
expand (newborn)
– Secondary atelectasis: obstructive or
compression process
• Atelectasis:
– ateles  “uncompletely”
– ectasis  “expansion”
–  uncompletely expansion.
• Atelektasis obstruksif
– Most common
– Other name: resorption atelectasis
– Usually there is pe existing
obstruction process (acute &
complete) at the bronchus.
– Infection can be occur if secret was
accumulated at distal part
• Compression atelectasis
– No obstruction
– Due to extenal compression (pleural
effusion, pneumothorax, lung tumor,
distended abdomen)
– Infection rarely occur
• Adhesive atelectasis
(mikroatelectasis)-deficiency of
surfactant
– NRDS (neonatal respiratory distress
syndrome)
– ARDS (adult respiratory distress
syndrome)
Signs and symptoms
– symptoms  according to causes,
shortness of breath >>>, cough,
fever
– Diminish of movement of the affected
side,
– dullness
– Diminished or abscen of breath sound
– Vocal fremitus diminished
– Mediastinal shift to the affected area
Diagnosis
– Clinical manifestation
– Radiology
– CXR  diagnosis confirmtaion,
location & distribution
– CT scan  location of obstructive
– Signs of atelektasis: mediastinum
shift, narrowing ICS, elevated
hemidiafragma, hilar shift.
Atelektasis
Atelektasis
Management:
– causatives (obstruksi,
kompresi,adhesive)
– Secret  drainage (suction, chest
fisioterapi/postural drainage,
bronchoscopy)
– Obstruction due to tumor 
operation/surgery.
– Expectorantia ; less benefit
– Antibiotic
– Surfactant def  mechanical
ventilation, surfactant therapy.
 Pleural effusion: Introduction

• Collection of excess quantity of fluid in pleural space

• Cause:
- Inflammatory
- Non inflammatory
• Normal condition:
 Fluid in pleural space (0,3 ml/kgBW)
 Maintain by the balance of pleural fluid production and
absorption
 Dinding Rongga Paru
toraks pleura

Kapiler Kapiler
sistemik pulmonal
Efusi
Tek koloid Pleura Tek koloid
osmotik osmotik
(cm H2O) (cm H2O)
Tek negatif
intrapleura

Tek
Tek
hidrostatik
hidrostatik
(cm H2O)
(cm H2O)

Pleura Pleura
parietalis viseralis
CXR
 Arah cairan dalam
kavitas pleura
Fluid direction,
posteroinferior
posteroinferior
CT-Scan
 Pleural effusion: Classification

• Transudates: due to diseases that affect the

filtration of pleural fluid: CHF & hypoproteinemia

• Exudates: inflammation or injury increases pleural

membrane permeability to proteins and various
types of cells
Pleural effusion: Other Classification

• Purulent → Empyema
• Blood → Hemothorax
• Milky → Chylothorax
 Pleural Effusion fluid
Tests Transudate Exudates Exudates
(tubercular) (Empyema)
Physical appearance Clear Straw coloured Cloudy /
Turbid
Microscopy <1000 >1000 >5000 PMNs
Lympho/M Lymphocytes Pus cells

Pleural fluid protein < 3 gm/dl >3 gm/dl >3 gm/dl

Pleural fluid Protein / <0.5 >0.5 >0.5
Serum protein
Pleural fluid LDH / <0.6 >0.6 >0.6
Serum LDH
Pleural fluid pH >7.3 <7.3 <7.2
Pleural fluid glucose >40 mg/dl <40 mg/dl <40 mg/dl
 Pleural effusion: Causes

• Bacterial pneumonias - Most common

• TB, CCF, Hypoproteinemia
• Obstruction to lymphatic drainage
• Collagen vascular disease
• Malignancies, Rheumatoid arthritis
• Aspiration pneumonia, traumatic
• Pulmonary embolism, chylothorax
 Pleural effusion: 3 Types

1. Dry or plastic pleurisy

2. Serofibrinous or serosanguineous pleurisy
3. Purulent pleurisy or empyema
 1. Dry pleurisy or plastic pleurisy

Associated with
• Acute bacterial infections
• Tuberculosis
• Connective tissue disorders- rheumatic fever
 Dry pleurisy: Pathology

• Involvement of visceral pleura with small amount of

yellow serous fluid
• Adhesion between pleural surfaces
• Pleural thickening
• Fibrothorax due to fibrin deposition and severe
adhesions
 Dry pleurisy: Clinical manifestations

• Signs & symptoms of primary disease

• Dull pleural pain, exaggerated by deep
inspiration,cough, straining, referred to shoulder and
back
• Increased dullness on percussion and decreased breath
sounds
• Leathery, rough inspiratory and expiratory friction rub
early in the disease
• X-ray- haziness at the pleural surface or a dense, sharply
demarcated shadow
 Dry pleurisy: Treatment

• Treat underlying condition

• If pneumonia is not present- strapping of chest to
restrict expansion and analgesics
• Strapping and cough suppressants not given if
pneumonia is present
 2. Serofibrinous pleurisy

• Infections of lungs
• Inflammatory conditions of mediastinum
• Less commonly with- SLE, RF, neoplasms
 Serofibrinous pleurisy: Clinical features

• Initially signs and symptoms of dry pleurisy

• Asymptomatic if effusion is small
• Large effusion: cough, dyspnoea, retractions,
orthopnoea, cyanosis
• Shift of mediastinum away from affected side,
fullness of intercostal space, diminished tactile vocal
fremitus
• Dullness to flatness on percussion
• Decreased or absent breath sounds
Serofibrinous pleurisy: Clinical features...

• In infants- bronchial breath sounds instead of absent

breath sounds
• Friction rub in the early stages
• X-ray: homogenous opacity obliterating the normal
pulmonary marking, obliteration of costophrenic
angles and widening of interlobar fissure
X-ray chest: Pleural Effusion
 Serofibrinous pleurisy: Treatment

• Treat underlying cause

• Thoracocentesis, up to 1 Liter of fluid
• Tube thoracostomy in older child with
parapneumonic effusion if pleural fluid pH<7.2 or
glucose <50mg/dl
 3. Purulent pleurisy / Empyema

• Pus or microorganism in pleural fluid

• Microorganism- by smear or culture
In the absence of these:
• pH of pleural fluid < 7.2
• Lactic dehydrogenase (LDH) >1000IU/L
• Glucose <than 40mg/dl
• Lactate > 45mg/ml
Thank You