The term atelectasis is derived from the Greek words ateles and ektasis, which mean incomplete expansion. Atelectasis is defined as diminished volume affecting all or part of a lung. 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 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 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.  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. 
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. 
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.
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.
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.
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.
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.
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.
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
- A large emphysematous bulla
Compression atelectasis is caused by the following:
- Chest wall, pleural, or intraparenchymal masses
- Loculated collections of pleural fluid
Atelectasis of a significant size can result in hypoxemia as measured on arterial blood gas determinations. Arterial blood gas evaluation may demonstrate that despite a low PaO2. The PaCO2 level is usually normal but may be low as a result of the increased minute ventilation.
Atelectasis in the mechanically ventilated patient can result in the reduction of both dynamic and static compliance, and increased shunt physiology.  Complete left- or right-lung atelectasis in a mechanically ventilated patient can result in decreased lung compliance manifested by a decline in static compliance. Therefore, when monitoring peak and end-inspiratory plateau pressures, one should observe for a rise in both pressures.
Chest radiographs and CT scans may demonstrate direct and indirect signs of lobar collapse.  Direct signs include displacement of fissures and opacification of the collapsed lobe.
Indirect signs include 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 lobes, and silhouetting of the diaphragm or the heart border.
Complete atelectasis of an entire lung (see images below) is when (1) complete collapse of a lung leads to opacification of the entire hemithorax and an ipsilateral shift of the mediastinum and (2) the mediastinal shift separates atelectasis from massive pleural effusion.
Lobar atelectasis is a common problem caused by a variety of mechanisms including resorption atelectasis due to airway obstruction, passive atelectasis from hypoventilation, compressive atelectasis from abdominal distension, and adhesive atelectasis due to increased surface tension. Evidence-based studies on the management of lobar atelectasis are lacking. Assessment of air bronchograms on a chest radiograph may be helpful to determine whether the airway obstruction is proximal or distal. Chest physiotherapy, nebulized dornase alfa (DNase), and, possibly, fiberoptic bronchoscopy might be helpful in patients with mucous plugging of the airways. In passive and adhesive atelectasis, positive end-expiratory pressure might be a useful adjunct to treatment.
Fiberoptic bronchoscopy may have a role management. In one study, bronchoscopy allowed diagnosing the degree of tracheobronchial tree obstruction and its causes in all cases. Single suction fiberoptic bronchoscopy led to normalization and encouraged positive dynamics in 76% of all cases (57 patients). Repeated endoscopic sanitation in the first two days was necessary for 25 patients (25.3%) with unresolved or reoccurring atelectasis. The effectiveness of second research was to 84%. Most patients with unresolved or recurring atelectasis had serious chest injury. In these cases, blood was mainly seen through the tracheobronchial tree lumen. Thus, when a mechanically obstructed bronchus is suggested and coughing or suctioning is not successful, bronchoscopy should be performed. 
Nonpharmacologic therapies for improving cough and clearance of secretions from the airways include chest physiotherapy, including postural drainage, chest wall percussion and vibration, and a forced expiration technique (called huffing). Increased airway clearance as assessed by sputum characteristics (ie, volume, weight, viscosity) and clearance of the radioaerosol from the lung show that the long-term efficacy of these techniques compared with unassisted cough alone is unknown. 
The treatment of atelectasis depends on the underlying etiology. Treatment of acute atelectasis, including postoperative lung collapse, requires removal of the underlying cause.
For postoperative atelectasis, prevention is the best approach. Anesthetic agents associated with postanesthesia narcosis should be avoided. Narcotics should be used sparingly because they depress the cough reflex. Early ambulation and use of incentive spirometry are important. Encourage the patient to cough and to breathe deeply. Nebulized bronchodilators and humidity may help liquefy secretions and promote their easy removal. In the case of lobar atelectasis, vigorous chest physiotherapy frequently helps re-expand the collapsed lung. When these efforts are not successful within 24 hours, flexible fiberoptic bronchoscopy could be performed.
Prevention of further atelectasis involves (1) placing the patient in such a position that the uninvolved side is dependent to promote increased drainage of the affected area, (2) giving vigorous chest physiotherapy, and (3) encouraging the patient to cough and to breathe deeply.
Patients may require nasotracheal suctioning if atelectasis recurs. This is particularly true in patients with neuromuscular disease and poor cough.
Therapy with a broad-spectrum antibiotic is started and modified appropriately if a specific pathogen is isolated from sputum samples or bronchial secretions.
Postoperative atelectasis is treated with adequate oxygenation and re-expansion of the lung segments. Supplemental oxygen should be titrated to achieve an arterial oxygen saturation of greater than 90%.
Severe hypoxemia associated with severe respiratory distress should lead to intubation and mechanical support. Intubation not only provides oxygenation and ventilatory support, but also provides access for suctioning of the airways and facilitates performing bronchoscopy, if needed. The positive pressure ventilation and larger tidal volumes may help to re-expand collapsed lung segments.
Continuous positive airway pressure delivered via a nasal cannula or facemask may also be effective in improving oxygenation and re-expanding the collapsed lung.
Broad-spectrum antibiotics should be prescribed if evidence of infection is present, such as fever, night sweats, or leukocytosis, because secondary atelectasis usually becomes infected regardless of the cause of obstruction. Obstruction of a major bronchus may cause severe hacking or coughing. Antitussive therapy reduces the cough reflex and may produce further obstruction. Thus, it should be avoided.
Fiberoptic bronchoscopy is commonly required for diagnosis, particularly if an endobronchial lesion is suggested. This procedure has a limited role in the management of postoperative atelectasis. Fiberoptic bronchoscopy is not more effective than standard chest physiotherapy, deep breathing, coughing, and suctioning of patients who are intubated. Therefore, simple and standard respiratory therapy techniques should be administered to patients who spontaneously ventilate or patients on mechanical ventilation. Fiberoptic bronchoscopy should be reserved for those situations in which chest physiotherapy is contraindicated (eg, chest trauma, immobilized patient), poorly tolerated, or unsuccessful.
Judicious use of perioperative analgesia is an essential adjunct, permitting patients to breathe deeply, cough forcefully, and participate in chest physiotherapy maneuvers. In patients with underlying pulmonary disease, use of epidural analgesia is a very effective pain control measure, thereby aiding aggressive chest physiotherapy.
N -acetylcysteine aerosols commonly are administered in an effort to promote clearance of tenacious secretions. However, their efficacy has not been documented. In addition, N -acetylcysteine may cause acute bronchoconstriction. Some clinicians recommend its use be limited to direct instillation at the time of fiberoptic bronchoscopy.
In a study of noncystic fibrosis in children who had atelectasis of infectious origin, treatment with DNase led to rapid clinical improvement observed within two hours and radiologic improvement documented within 24 hours. DNase may be an effective treatment for infectious atelectasis in pediatric patients with noncystic fibrosis. Such data does not exist for adult patients, but DNase could be used as a trial of therapy in adults as well. 
Prophylactic maneuvers for reducing the incidence and magnitude of postoperative atelectasis in high-risk patients should be encouraged. These techniques are deep-breathing exercises, coughing exercises, and incentive spirometry. For maximal benefit, prophylactic measures should be taught and instituted before surgery and used regularly, on an hourly basis, after surgery. Early ambulation of patients after surgery is as effective as physical therapy.
Kato et al reported on the use of the RTX respirator for extensive atelectasis in elderly patients. Patients were placed in the lateral decubitus position. The RTX respirator was reported to be a useful tool to clear retained sputum in elderly patients.