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ATELEKTASIS

Dr. Abdul Rohman,

BACKGROUND
Greek : ateles - imperfect or incomplete,

ektasis - expansion = incomplete expansion = diminished vol. affecting all or part of

lung Several types etiology

a characteristic radiographic pattern and

EPIDEMIOLOGY
Frequency US postoperative atelectasis : extremely common lobar atelectasis : also common Mortality/Morbidity depends on the underliyng cause atelectasis Age mean age of presentation rounded atelectasis : 60 ys Race and Sex : No racial and sexual predilection exists

CLASIFICATION
Primary lung fails to expand at birth Secondary caused by obstructive and nonobstructive Nonobstructive : relaxation, compressive, adhessive, cicatrization, replacement, and rounded

PATHOPHYSOLOGY
Obstructive atelectasis : Obstruction absorbsion retraction Nonobstructive atelect : Loss of contact between the visceral and parietal pleura Platelike atelectasis : obstruction of small bronchus Postoperative atelect : diaphragmatic dysfunction and diminished surfactant activity

Atelectasis ( Collapse )
= Loss of volume of lung, lobe, or segment for any cause The most important mechanism is obstruction of a major bronchus by tumor, foreign body, or bronchial plug Sign of labor collapse - Decreased lung volyme - Displacement of pulmonary fissure - Compensatory hyperinflation of remaining part of the ipsilateral lung - Elevation of hemidiaphram of ipsilateral side - Mediastinal and hilar displacement. Trachea pulled to

CLINICAL
A. History

Postoperative : thoracic or upper abdomen


Symptoms & signs rapidity, size, and infection :

- Rapid bronchial obstruction :

pain on the affected side, dyspnea, cyanosis, hypotension, tachycardia, fever, and shock
- Slowly asymptomatic

- Middle lobe syndr (asymptomatic irritation) : severe,hacking, non-

productive cough

B. Physical
involved area - dullness on percussion - diminished or absent breath sound

Comparison of acute and chronic obstruction Acute Chronic Inhalation and Tumors impaction of foreign bodies Mucus plugging of Lymphadenopathy bronchi (e. g. after anesthesia) After tracheostomy Aneurysm Lung infection

C. Causes
1. Bronchial obstruction : foreign bodies, endobronchial tumor, etc 2. External pulm compression : pleural effusion, pneumothorax 3. Abnormalities of surfactant : oxygen toxicity, ARDS 4. Resorptive atelectasis : bronchogenic Ca, mucous plug 5. Relaxation atelectasis : pleural effusion, a large emphysematous bulla 6. Adhesive atelectasis : ARDS, smoke inhalation,prolonged shallow breathing 7. Cicatrization atelectasis : IPF, chronic TB, radiation fibrosis, fungal infection 8. Replacement atelectasis : alveoli filled by

DIFFERENTIAL DIAGNOSIS
Asthma Asbestosis Blunt chest trauma Diaphragmatic paralysis Lung abscess Lung cancer Obesity Pneumonia Pneumothorax Pulmonary embolus Pulmonary fibrosis, idiopathic

WORKUP
Lab studies
ABG : - hypoxemia atelectasis of a significant size - PaCO : usually normal or low hyperventilation ( pH = pK log {[HCO]/[CO]} )

Procedures
FOB : - evaluate the cause of bronchial obstruction - clear mucus plug - limitations visualized only the subsegmental

Histologic finding FOB washing, brushing and biopsy specimens : 1. Obstructing mass : malignancy 2. Mucous plugging : aspergillus

Imaging studies (Chest R & CT scan)


Direct signs : - displacement of fissure - opacification of the collapsed lobe Indirect signs :

displacement of the hilum mediastinal shift toward the side of collapse loss of volume on ipsilateral hemithorax elevation of ipsilateral diaphragm crowding of the ribs compensatory hyperlucency of the remaining lobe

TREATMENT
1. Nonpharmacologic :
improving cough & clearance secretions

Chest physiotherapy : postural drainage, chest wall percussion Nebulised Dnase Fiberoptic bronchoscopy mucous plugging PEEP Passive and adhessive

2. Medication Suplemental O

SaO > 90 % Bronchodilators sputum expectoration & increasing ventilation Antibiotics : infection (fever, night sweat, or leukocytosis) Analgesia perioperative : breathe deeply, cough forcefully

Dnase cystic fibrosis in children + infection N-acetylcystein ? acute bronchoconstriction 3. Surgical care chronic atelectasis

COMPLICATIONS

Acute pneumonia Bronchiectasis Hypoxemia and respiratory failure Postobstructive drowning of the lung

Patient with ATELECTASIS


History A Physical examination

B CT
C

Chest x-ray examination

Identify: Postoperative atelectasis

Evaluaate degree, chronicity of atelectasis, and associated problems

D Acute
Platelike atelectasis Evaluate for:
Asthma Rib fracture Pulmonary embolus Neuromuscular disease

Chronic

E Lobar

atelectasis

Lobar atelectasis

Platelike atelectasis

Evaluate sputum

F CT

G PFT

Normal PFT Positive cytologist Rule out:

Restrictive
Obesity Interstitial lung disease Neuromuscular disease Pulmonary embolus Asthma

Negative cytologist

Rule out :
Infection

Bronchoscopy

Therapy

Lesion seen

No lesion seen

Follow

Rule out :
Neoplasm

Therapy

Therapy

Follow

Collapse
Atelectasis (collapse) is loss of volume of a lung, lobe, or segment for any cause. The most important mechanism is obstruction of a major bronchus by tumor, foreign body, or bronchial plug PA and lateral radiographs are required. Compare with old films where available. The lateral borders of the mediastinum are silhoutted against the air-filled lung that lies underneath. This silhoutte is lost if there is consolidation in the underlying lung.

Signs of labor collapse


Decreased lung volume Displacement of pulmonary fissures Compensatory hyperinflation of remaining part of the ipsilateral lung Elevation of hemidiaphragm on ipsilateral side Mediastinal and hilar displacement. Trachea pulled to side of collapse Radiopacity (white lung) Absence of air bronchogram

In upper lobe collapse of the right lung, a PA film is most valuable in making diagnose; the collapsed lobe lied adjacent to mediastinum In the left lung, a lateral film is most valuable in making diagnoses; the lobe collapses superiomedially and arteriorly

Lower lobe collapse causes rotation and visualization of the oblique fissure on PA film
A lateral film is most valuable in diagnosing middle lobe collapse. Thin, wedge-shaped opacity between horizontal and oblique fissures is seen.

Consolidation
Is seen as an area of white lung and represents fluid or cellular matter where there would normally be air There are many causes of consolidation including : - Pneumonia - Pulmonary edema

In contrast to collapse: The shadowing is typically heterogeneous (i.e. not uniform) The border is ill-defined Fissures retain their normal position There are two pattern of distribution: Segmental or lobar distribution Bats-wing distribution

Peripheral lung fields may be spared (e.g., in pulmonary edema). Air bronchograms may be seen; these are air-filled bronchi delineated by surrounding consolidated lung.

Atelectasis (from the Greek ateles, meaning imperfect, and ektasis, meaning expansion) Primary lung fails to expand at birth Secondary caused by obstruction or compression

Obstructive atelectasis
Obstruction is the most common cause of atelectasis; this also known as resorptive atelectasis. (Fig. 1) - Follows an acute and complete obstruction of a large bronchus. Air in the collapsed area of the lung is absorbed and secretions distal to the obstruction accumulate; subsequently these bronchial secretions become infected and suppurate. Distal to the blockage, the bronchi mechanically distend. - If the collapse has been present for some time, irreversible pulmonary fibrosis occurs. Pulmonary artery branches may have narrowed lumens.

Compressive atelectasis
In compressive atelectasis, bronchial obstruction does not occur; therefore, bronchial secretions are free to drain up the bronchial tree. As such, the collapsed lung does not become seriously infected. Compressive atelectasis results from external compression of the lung. Causes of compression include pleural effusion, hemothorax, empymema, pneumothorax, space-occupying intrathoracic lession, and abdominal distension. Hemodynamic and vascular changes occur. High inflation pressures on inspiration are required to overcome retractive forces. Reexpansion of the lung usually occurs after compression is resolved.

Patchy atelectasis
Depending on the cause, atelectasis may occur in a patchy or diffuse distribution

- Follows an acute and complete obstruction of a large bronchus. Air in the collapsed area of the lung is absorbed and secretions distal to the obstruction accumulate; subsequently these bronchial secretions become infected and suppurate. Distal to the blockage, the bronchi mechanically distend. Obstructive atelectasis - If the collapse has been present for some time, irreversible pulmonary fibrosis occurs. Pulmonary artery branches may have narrowed lumens. Compressive atelectasis Obstruction is the most common cause of atelectasis; this also known as resorptive atelectasis. (Fig. 1) In compressive atelectasis, bronchial obstruction does not occur; therefore, bronchial secretions are free to drain up the bronchial tree. As such, the collapsed lung does not become seriously infected. Compressive atelectasis results from external compression of the lung. Causes of compression include pleural effusion, hemothorax, empymema, pneumothorax, space-occupying intrathoracic lession, and abdominal distension. Hemodynamic and vascular changes occur. High inflation pressures on inspiration are required to overcome retractive forces. Re-expansion of the lung usually occurs after compression is resolved. Patchy atelectasis Depending on the cause, atelectasis may occur in a patchy or diffuse distribution

Radiologic distribution of alveolar processes Bat-wing pattern


Segmental pattern pneumonia Acute Chronic pulmonary edema atypical pneumonia

pulmonary infarct

pneumonia

lymphoma
sarcoidosis pulmonary alveolar proteinosis alveolar cell

pulmonary collapse pulmonary hemorrhage alveolar cell carcinoma

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