Background
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 radiology findings. Recognizing an abnormality due to atelectasis on chest x-ray films 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 without 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 function differently, eg, the middle and lower lobes collapse more than the upper lobe in the presence of pleural effusion, while the upper lobe may be affected more by pneumothorax.
Compression atelectasis occurs from any space-occupying lesion of the thorax compressing the lung and forcing 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.
Right middle lobe syndrome
Right 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.[1] Timely medical intervention in patients (especially children) with middle lung syndrome, including fiberoptic bronchoscopy with bronchoalveolar lavage, prevents bronchiectasis that may be responsible for recurrent infections and an ultimately unfavorable outcome of chronic atelectasis.[2]
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.[3]
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.
Pathophysiology
The mechanism of obstructive and nonobstructive atelectasis is quite different and is determined by several factors.
Obstructive atelectasis
Following obstruction of a bronchus, the circulating blood absorbs the gas in the peripheral alveoli, leading to retraction of the lung and an airless state within a few hours. In the early stages, blood perfuses the airless lung; this results in ventilation-perfusion mismatch and arterial hypoxemia. A 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 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 develops and the lung becomes bronchiectatic.
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 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.[4]
Epidemiology
Frequency
United States
Postoperative atelectasis is extremely common. Lobar atelectasis is also common. The incidence and prevalence of this disorder are not well documented.
Mortality/Morbidity
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.
Race
Atelectasis has no racial predilection.
Sex
Atelectasis has no sexual predilection.
Age
The mean age at presentation for rounded atelectasis is 60 years.
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