MundaHoshiarpuriya
Maavan Thandiyan Shavaan
Atelectasis
Author: Tarun Madappa, MD, MPH, Attending, Department of Pulmonary and Critical Care Medicine, Elkhart General Hospital, Elkhart, Indiana
Coauthor(s): Sat Sharma, MD, FRCPC, Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital
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.
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.
Clinical
History
Atelectasis may occur postoperatively following thoracic or upper abdominal procedures.
The physical examination findings show dullness to percussion over the involved area and diminished or absent breath sounds. Chest excursion in the area is reduced or absent. The trachea and the heart are deviated toward the affected side.
Causes
Disclaimer: Courtesy of Medscape
Author: Tarun Madappa, MD, MPH, Attending, Department of Pulmonary and Critical Care Medicine, Elkhart General Hospital, Elkhart, Indiana
Coauthor(s): Sat Sharma, MD, FRCPC, Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital
Introduction
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.
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.
Clinical
History
Atelectasis may occur postoperatively following thoracic or upper abdominal procedures.
- Most symptoms and signs are determined by the rapidity with which the bronchial occlusion occurs, the size of the lung area affected, and the presence or absence of complicating infection.
- Rapid bronchial occlusion with a large area of lung collapse causes pain on the affected side, sudden onset of dyspnea, and cyanosis. Hypotension, tachycardia, fever, and shock may also occur.
- Slowly developing atelectasis may be asymptomatic or may cause only minor symptoms. Middle lobe syndrome often is asymptomatic, although irritation in the right middle and right lower lobe bronchi may cause a severe, hacking, nonproductive cough.
The physical examination findings show dullness to percussion over the involved area and diminished or absent breath sounds. Chest excursion in the area is reduced or absent. The trachea and the heart are deviated toward the affected side.
Causes
- 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
- 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:
- Hyaline membrane disease
- Acute respiratory distress syndrome
- Smoke inhalation
- Cardiac bypass surgery
- Uremia
- Prolonged shallow breathing
- Cicatrization atelectasis is caused by the following:
- Idiopathic pulmonary fibrosis
- Chronic tuberculosis
- Fungal infections
- Radiation fibrosis
- 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 airway is long and thin and has the poorest drainage or clearance of all the lobes of the lung, resulting in trapped mucus. 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 by asbestos pleural plaques.
Disclaimer: Courtesy of Medscape
