Updated: Oct 22, 2020
  • Author: Tarun Madappa, MD, MPH; Chief Editor: Nader Kamangar, MD, FACP, FCCP, FCCM  more...
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Practice Essentials

Atelectasis is a partial or complete collapse of the entire lung or a specific area, or lobe, of the lung, leading to impaired exchange of carbon dioxide and oxygen. [1] Atelectasis occurs when the alveoli (small air sacs) within the lung become deflated or fill with alveolar fluid.

Sign and symptoms of atelectasis

Signs and symptoms of atelectasis include the following:

  • Pain on the affected side
  • Sudden onset of dyspnea
  • Cyanosis (bluish skin discoloration)
  • Dullness to percussion over the involved area
  • Diminished or absent breath sounds
  • Reduced or absent chest excursion of the involved hemithorax
  • Deviation of trachea and heart toward the affected side

Diagnosis of atelectasis

Diagnosis of atelectasis involves the following:

  • Arterial blood gas evaluation
  • Chest radiographs and CT scans - May demonstrate direct and indirect signs of lobar collapse (collapsed lung)
  • Flexible fiberoptic bronchoscopy - Useful diagnostically and therapeutically

Treatment of atelectasis

Treatment of atelectasis can involve the following:

  • Flexible fiberoptic bronchoscopy
  • Chest physiotherapy - Postural drainage, chest wall percussion and vibration, a forced expiration technique (called huffing)
  • Adequate oxygenation and re-expansion of lung segments
  • Continuous positive airway pressure delivered via a nasal cannula or facemask
  • Bronchodilators - To encourage sputum expectoration
  • Surgical - Segmental resection or lobectomy (chronic atelectasis)


Atelectasis is defined as diminished volume affecting all or part of a lung. It is a partial or complete collapse of the entire lung or a specific area, or lobe, of the lung (collapsed lung). [1] Atelectasis occurs when the alveoli (small air sacs) within the lung become deflated or fill with alveolar fluid. The primary cause of acute or chronic atelectasis is bronchial obstruction by plugs of tenacious sputum; foreign bodies; endobronchial tumors; or tumors, a lymph node, or an aneurysm compressing the bronchi and bronchial distortion. It is one of the most common postoperative respiratory complications.

Pulmonary atelectasis is one of the most commonly encountered abnormalities in chest radiographs. Recognizing an abnormality due to atelectasis on chest radiographs can be crucial to understanding the underlying pathology. Several types of atelectasis exist; each has a characteristic radiographic pattern and etiology. Atelectasis is divided physiologically into obstructive and nonobstructive causes.

Obstructive atelectasis

Obstructive atelectasis is the most common type and results from reabsorption of gas from the alveoli when communication between the alveoli and the trachea is obstructed. The obstruction can occur at the level of the larger or smaller bronchus. Causes of obstructive atelectasis include foreign body, tumor, and mucous plugging. The rate at which atelectasis develops and the extent of atelectasis depend on several factors, including the extent of collateral ventilation that is present and the composition of inspired gas. Obstruction of a lobar bronchus is likely to produce lobar atelectasis; obstruction of a segmental bronchus is likely to produce segmental atelectasis. Because of the collateral ventilation within a lobe or between segments, the pattern of atelectasis often depends on collateral ventilation, which is provided by the pores of Kohn and the canals of Lambert.

Nonobstructive atelectasis

Nonobstructive atelectasis can be caused by loss of contact between the parietal and visceral pleurae, compression, loss of surfactant, and replacement of parenchymal tissue by scarring or infiltrative disease. Examples of nonobstructive atelectasis are described below.

Relaxation or passive atelectasis results when a pleural effusion or a pneumothorax eliminates contact between the parietal and visceral pleurae. Generally, the uniform elasticity of a normal lung leads to preservation of shape even when volume is decreased. The different lobes also respond differently, eg, the middle and lower lobes collapse more than the upper lobe in the presence of pleural effusion, while the upper lobe is typically affected more by pneumothorax.

Compression atelectasis occurs from any space-occupying lesion of the thorax compresses the lung and forces air out of the alveoli. The mechanism is similar to relaxation atelectasis.

Adhesive atelectasis results from surfactant deficiency. Surfactant normally reduces the surface tension of the alveoli, thereby decreasing the tendency of these structures to collapse. Decreased production or inactivation of surfactant leads to alveolar instability and collapse. This is observed particularly in acute respiratory distress syndrome (ARDS) and similar disorders.

Cicatrization atelectasis results from diminution of volume as a sequela of severe parenchymal scarring and is usually caused by granulomatous disease or necrotizing pneumonia. Replacement atelectasis occurs when the alveoli of an entire lobe are filled by tumor (eg, bronchioalveolar cell carcinoma), resulting in loss of volume.

Middle lobe syndrome

Middle lobe syndrome is a disorder of recurrent or fixed atelectasis involving the right middle lobe and/or lingula. It can result from either extraluminal (bronchial compression by surrounding lymph nodes) or by intraluminal bronchial obstruction. It may develop in the presence of a patent lobar bronchus without identifiable obstruction. Inflammatory processes and defects in the bronchial anatomy and collateral ventilation have been designated as the nonobstructive causes of middle lobe syndrome. [2] Timely medical intervention with fiberoptic bronchoscopy with bronchoalveolar lavage in patients, particularly children, with middle lung syndrome may prevent the long-term consequence of bronchiectasis. Bronchiectasis in turn may be responsible for recurrent infections and, ultimately, the unfavorable outcome of chronic atelectasis. [3]

Middle lobe syndrome has been reported as a pulmonary manifestation of primary Sjögren syndrome. Transbronchial biopsies performed in such patients revealed lymphocytic bronchiolitis in the atelectatic lobes. Atelectasis responds well to glucocorticoid treatment, suggesting that the peribronchiolar lymphocytic infiltrates may play an important role in the development of middle lobe syndrome in these patients. [4]

Rounded atelectasis

Rounded atelectasis represents folded atelectatic lung tissue with fibrous bands and adhesions to the visceral pleura. Incidence is high in asbestos workers (65-70% of cases), most likely due to a high degree of pleural disease. Affected patients typically are asymptomatic, and the mean age at presentation is 60 years. Rounded atelectasis may mimic a neoplastic tumor. The comet tail sign or talon sign is its distinguishing radiographic characteristic.



The mechanism of obstructive and nonobstructive atelectasis is quite different and is determined by several factors.

Obstructive atelectasis

Following obstruction of a bronchus, the blood circulating in the alveolar-capillary membrane absorbs the gas from alveoli. This process can lead to retraction of the lung and an airless state within those alveoli in a few hours. In the early stages, blood then perfuses the unventilated lung. This results in a shunt and, potentially, arterial hypoxemia. Subsequent to obstruction of a bronchus, filling of the alveolar spaces with secretions and cells may occur, thereby preventing complete collapse of the atelectatic lung. The uninvolved surrounding lung tissue distends, displacing the surrounding structures. The heart and mediastinum shift toward the atelectatic area, the diaphragm is elevated, and the chest wall flattens.

If the obstruction to the bronchus is removed, any complicating postobstructive infection subsides and the lung returns to its normal state. If the obstruction is persistent and infection continues to be present, fibrosis and/or bronchiectasis may develop.

Nonobstructive atelectasis

The loss of contact between the visceral and parietal pleurae is the primary cause of nonobstructive atelectasis. A pleural effusion or pneumothorax causes relaxation or passive atelectasis. Pleural effusions affect the lower lobes more commonly than pneumothorax, which affects the upper lobes. A large pleural-based lung mass may cause compression atelectasis by decreasing lung volumes.

Adhesive atelectasis is caused by a lack of surfactant. The surfactant has phospholipid dipalmitoyl phosphatidylcholine, which prevents lung collapse by reducing the surface tension of the alveoli. Lack of production or inactivation of surfactant, which may occur in acute respiratory distress syndrome (ARDS), radiation pneumonitis, and blunt trauma to the lung, cause alveolar instability and collapse.

Middle lobe syndrome (recurrent atelectasis and/or bronchiectasis involving the right middle lobe and/or lingula) has recently been reported as the pulmonary manifestation of primary Sjögren syndrome.

Scarring of the lung parenchyma leads to cicatrization atelectasis.

Replacement atelectasis is caused by filling of the entire lobe by a tumor such as bronchoalveolar carcinoma.

Platelike atelectasis

Also called discoid or subsegmental atelectasis, this type is seen most commonly on chest radiographs. Platelike atelectasis probably occurs because of obstruction of a small bronchus and is observed in states of hypoventilation, pulmonary embolism, or lower respiratory tract infection. Small areas of atelectasis occur because of inadequate regional ventilation and abnormalities in surfactant formation from hypoxia, ischemia, hyperoxia, and exposure to various toxins. A mild-to-severe gas exchange abnormality may occur because of ventilation-perfusion mismatch and intrapulmonary shunt.

Postoperative atelectasis

Atelectasis is a common pulmonary complication in patients following thoracic and upper abdominal procedures. General anesthesia and surgical manipulation lead to atelectasis by causing diaphragmatic dysfunction and diminished surfactant activity. The atelectasis is typically basilar and segmental in distribution. After induction of anesthesia, atelectasis increases from 1 to 11% of total lung volume. End-expiratory lung volume is also found to be decreased.

In 2009 study, a recruitment maneuver plus positive end-expiratory pressure (PEEP) reduced atelectasis to 3 ±4%, increased end-expiratory lung volume, and increased the PaO2/FiO2 ratio from 266 ±70 mm Hg to 412 ±99 mm Hg. It was found that the PEEP alone did not reduce the amount of atelectasis or improve oxygenation, but a recruitment maneuver followed by PEEP reduced atelectasis and improved oxygenation. [5]



The primary cause of acute or chronic atelectasis is bronchial obstruction by the following:

  • Plugs of tenacious sputum

  • Foreign bodies

  • Endobronchial tumors

  • Tumors, a lymph node, or an aneurysm compressing the bronchi and bronchial distortion

External pulmonary compression by pleural fluid or air (ie, pleural effusion, pneumothorax) may also cause atelectasis.

Abnormalities of surfactant production contribute to alveolar instability and may result in atelectasis. These abnormalities commonly occur with oxygen toxicity and ARDS.

Conditions that may increase the risk of developing atelectasis include smoking, obesity, sleep apnea, or lung diseases such as asthma, chronic obstructive pulmonary disease, or cystic fibrosis.

Resorptive atelectasis is caused by the following:

  • Bronchogenic carcinoma

  • Bronchial obstruction from metastatic neoplasm (eg, adenocarcinoma of breast or thyroid, hypernephroma, melanoma)

  • Inflammatory etiology (eg, tuberculosis, fungal infection)

  • Aspirated foreign body

  • Mucous plug

  • Malpositioned endotracheal tube

  • Extrinsic compression of an airway by neoplasm, lymphadenopathy, aortic aneurysm, or cardiac enlargement

Relaxation atelectasis is caused by the following:

  • Pleural effusion

  • Pneumothorax

  • A large emphysematous bulla

Compression atelectasis is caused by the following:

  • Chest wall, pleural, or intraparenchymal masses

  • Loculated collections of pleural fluid

Adhesive atelectasis is caused by the following:

Cicatrization atelectasis is caused by the following:

Replacement atelectasis is caused by alveoli filled by tumor or fluid.

Right middle lobe syndrome (also known as Brock syndrome) refers to recurrent right middle lobe collapse secondary to airway disease, infection, or a combination of the two. The right middle lobe bronchus is long and thin, has the poorest drainage or clearance of all the lobes of the lung, which can result in retained mucus, and is more prone to extrinsic compression by the lymphatic system. Individuals with middle lobe syndrome are often asymptomatic, although some present with recurrent productive cough and history of right-sided pneumonias.

Rounded atelectasis is caused primarily by asbestos-related pleural disease and uremic pleuritis.



US frequency

Postoperative atelectasis is extremely common. Lobar atelectasis is also common. The incidence and prevalence of this disorder are not well documented.


Atelectasis has no racial predilection.


Atelectasis has no sexual predilection.


The mean age at presentation for rounded atelectasis is 60 years.



Patient mortality depends on the underlying cause of atelectasis. In postoperative atelectasis, the condition generally improves. The prognosis of lobar atelectasis secondary to endobronchial obstruction depends on treatment of the underlying malignancy.


Patient Education

Patients should know that difficulty breathing is an immediate reason to seek medical care. Atelectasis also is one of the most common complications after surgery. Deep-breathing exercises can help reduce atelectasis risk and can improve lung function.

For patient education information, see the Lung Disease and Respiratory Health Center, as well as Collapsed Lung and Bronchoscopy.