Atelectasis

Background
 Greek words ateles and ektasis meaning
incomplete expansion
 One of the most commonly encountered
abnormalities in chest radiology
 Divided physiologically into
 Obstructive causes
 Non obstructive causes
 What is atelectasis?
 2 schools of thought
 Alveolar collapse (volume loss)
 Fluid accumulation
 Types
 Obstructive
 Compression atelectasis
 Right middle lobe syndrome
 Non-obstructive
 Relaxation/passive atelectasis
 Adhesive atelectasis
 Cicatrization atelectasis
 Rounded atelectasis
 Obstructive Atelectasis
 Most common
 Causes: foreign body, tumor and mucus
plugging
 Rate of development and extent depend
on:
 Extent of collateral ventilation
 Composition of inspired gas
 Pathophysiology
 Obstructive atelectasis

Obstruction of a bronchus

Circulating blood absorbs gas in the peripheral

alveoli

Retraction of the affected lung

 Pathophysiology
Uninvolved surrounding lung tissue distends

Displacing the surrounding structures and

mediastinal shift toward the atelectatic area

Diaphragm is elevated and chest wall flattens

Obstructive atelectasis
 Pathophysiology
 Non obstructive atelectasis
 Loss of contact between the visceral and
parietal pleura
 Adhesive atelectasis
 Due to lack of surfactant
 Replacement atelectasis
 Due to filling by a tumor
 Cicatrization atelectasis
 Due to scarring of the lung parenchyma
 Pathophysiology
 Platelike atelectasis
 Also called discoid or subsegmental atelectasis
 Most commonly seen in CXR
 Probably occur because of obstruction of a
small bronchus
 In hypoventilation, pulmonary embolism or
LRTI
 Pathophysiology
 Post operative atelectasis
 Due to diaphragmatic dysfunction and
diminished surfactant activity
 Typically basilar and segmental
 History
 Signs and symptoms are determined by the
rapidity with which the occlusion occurs
 Rapid bronchial occlusion – sudden onset of
dyspnea and cyanosis
 Slowly developing atelectasis – maybe
asymptomatic or with only minor symptoms
 Middle lobe syndrome is often asymptomatic
 Irritation in the middle and right lower lobe bronchi
may cause a severe hacking, non productive cough
 Physical Examination
 Dullness on the affected area
 Diminished or absent breath sounds
 In atelectasis of the upper lobes – bronchial
breath sounds
 Chest excursion is reduced or absent
 Trachea and heart are deviated on the
affected side
 Causes
 Primary cause: bronchial obstruction
 Plugs of tenacious sputum
 Foreign bodies
 Endobronchial tumors
 Tumors, lymph node or an aneurysm
 External pulmonary compression
 By pleural fluid or air
 Causes
 Abnormalities of surfactant production
 In ARDS
 Causes
 Resorptive atelectasis
 Bronchogenic carcinoma
 Obstruction from metastatic neoplasm
 Inflammatory etiology (TB, fungal infection)
 Aspirated foreign body
 Mucous plug
 Malpositioned endotracheal tube
 Extrinsic compression of an airway
 Neoplasm, lymphadenopathy, aortic aneurysm or cardiac
enlargement
 Causes
 Relaxation atelectasis
 Pleural effusion
 Pneumothorax
 Large emphysematous bullae
 Causes
 Compression atelectasis
 Chest wall, pleural, or intraparenchymal
masses
 Loculated collections of pleural fluid
 Causes
 Adhesive atelectasis
 Hyaline membrane disease
 ARDS
 Smoke inhalation
 Cardiac bypass surgery
 Prolonged shallow breathing
 Causes
 Cicatrization atelectasis
 Idiopathic pulmonary fibrosis
 Chronic tuberculosis
 Fungal infections
 Replacement atelectasis
 Alveoli filling of fluid or tumor
 Rounded atelectasis
 Asbestos pleural plaques
 Consequences
 Impaired gas exchange
 Impaired lung mechanics
 Increased pulmonary vascular resistance
 Worsening lung injury
 Consequences
 Impaired gas exchange
 Most obvious effect
 Basis: absence of ventilation with persistent
perfusion (VQ mismatch)
 Consequences
 Impaired lung mechanics
 Worsened compliance
 Larger transpulmonary pressure are required
to generate a given tidal volume
 Work of breathing is increased
 In mechanically ventilated children, increased

ventilatory pressured are required

 Consequences
 Increased pulmonary vascular resistance
 Due to regional alveolar hypoxia with reduced
alveolar and mixed oxygen venous oxygen
tension

 Local hypoxic pulmonary vasoconstriction

 Consequences
 Worsening of lung injury
 Potentiation of lung injury
 Ventilator induced lung injury
 Imaging Studies
 Direct signs
 Displacement of fissures
 Opacification of the collapsed lobe
 Indirect signs
 Displacement of the hilum
 Mediastinal shift towards the side of the collapse
 Loss of volume on ipsilateral hemithorax
 Elevation of ipsilateral diaphragm, rib crowding
 Compensatory hyperlucency of the remaining lobes
 Silhouetting of the diaphragm or the heart border
 Imaging Studies
 Complete atelectasis of an entire lung
 Opacification of entire hemithorax
 Ipsilateral shift of the mediastinum
 Imaging Studies
 RUL collapse
 RUL shifts medially and superiorly, resulting in
elevation of the right hilum and minor fissure
 Tenting of the diaphragmatic pleura
juxtaphrenic peak
 Imaging Studies
 RML collapse
 Obscures the right heart border on PA
 Occasionally, a triangular opacity may be seen
because the major fissure shifts upward and
minor fissure shifts downward
 Imaging Studies
 RLL collapse
 RLL shifts posteriorly and inferiorly
 Triangular opacity obscuring the RLL
 Imaging Studies
 LUL collapse
 Shifts anteriorly and superiorly
 On lat views – major fissure displaced
anteriorly and the hyperexpanded RUL may
herniate across the midline…
 Imaging Studies
 LLL collapse
 Increased retrocardiac opacity silhouettes the
LLL pulmonary artery and L hemidiaphragm
 Flat waist sign
 Superior mediastinum may shift and
obliterate…
 Procedures
 Flexible fiberoptic bronchoscopy
 Help evaluate the cause of the obstruction
 Helps clear mucous plugs

 Limitations: distal endobronchial lesions are not

accessible
 Treatment
 Medical care
 Non-pharmacologic
 Pharmacologic
 Surgical care
 Treatment
 Non-pharmacologic
 Chest physiotherapy
 Postural drainage, chest wall percussion and
vibration
 Positive end-expiratory pressure
 Non-pharmacologic treatment
 Post operative atelectasis
 Prevention
 Avoid anesthetic agents associated with
postanesthesia narcosis
 Early ambulation
 Incentive spirometry
 If lobar atelectasis, vigorous chest
physiotherapy
 Non-pharmacologic treatment
 Post operative atelectasis
 Adequate oxygenation
 Supplemental oxygen
 If with severe hypoxemia – mechanical
ventilation
 Positive pressure and larger tidal volumes help to
re-expand collapsed lung segments
 Continuous positive airway pressure
 Fiberoptic bronchoscopy
 Pharmacologic treatment
 Bronchodilators
 Mucolytics
 N-acetylcysteine
 Inhaled recombinant human dNase
 Antibiotics
 Antitussives
 Pharmacologic treatment
 Bronchodilators
 Encourage sputum expectoration
 Of underlying airflow is present, may also
improve ventilation
 Pharmacologic treatment
 Mucolytics
 May promote sputum removal of thick mucous
plugs
 N-acetylcysteine – only recommended for
direst installation via fiberoptic bronchoscopy
or in an intubated patient.
 Inhaled recombinant human dNase
 Decreases viscoelasticity and surface tension of
purulent sputum
 Pharmacologic treatment
 Antibiotics
 To treat underlying bronchitis or post
obstructive infection
 Because secondary atelectasis usually
becomes infected regardless of the cause of
obstruction
 Pharmacologic treatment
 Antitussives
 Reduces the cough reflex
 Obstruction of a major bronchus may cause
severe hacking or coughing
 Surgical Care
 Segmental resection or lobectomy – for
chronic atelectasis
 Complications
 Acute pneumonia
 Bronchiectasis
 Hypoxemia and respiratory failure
 Postobstructive drowning of the lung
 Sepsis
 Pleural effusion and empyema