You are in: eMedicine Specialties > Radiology > CHEST Atelectasis, LobarArticle Last Updated: Mar 6, 2008AUTHOR AND EDITOR INFORMATIONSection 1 of 11
  Author: 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 Sat Sharma is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and World Medical Association Coauthor(s): Bruce Maycher, MD, Director of Pulmonary Radiology, St Boniface General Hospital; Associate Professor, Department of Radiology, University of Manitoba Editors: Kitt Shaffer, MD, PhD, Director of Undergraduate Medical Education, Associate Professor, Department of Radiology, Cambridge Health Alliance; Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand; W Richard Webb, MD, Chief of Thoracic Imaging, Professor, Department of Radiology, University of California at San Francisco; Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute; Eugene C Lin, MD, Consulting Staff, Department of Radiology, Virginia Mason Medical Center Author and Editor Disclosure Synonyms and related keywords: obstructive atelectasis, nonobstructive atelectasis, platelike atelectasis, discoid atelectasis, subsegmental atelectasis postoperative atelectasis, cicatrization atelectasis, rounded atelectasis, folded-lung syndrome, Blesovsky syndrome, Blesovsky's syndrome, replacement atelectasis, incomplete expansion, diminished lung volume, pulmonary volume deficiency, lung foreign body, lung tumor, mucus plugging, pleural effusion, right middle lobe syndrome, atelectatic lung tissue, bronchial obstruction, pneumothorax lobar collapse, pneumothorax, airless lung INTRODUCTIONSection 2 of 11
  BackgroundThe term atelectasis, which is defined as diminished lung volume, is derived from the Greek words ateles and ektasis, which mean incomplete expansion (see Image 1). Atelectasis may affect all or part of a lung, and it is one of the most common radiographic abnormalities. Recognizing atelectasis on a chest radiograph is important because a sinister underlying pathology may be present.1, 2, 3, 4, 5 Several types of atelectasis have been described; each has a unique radiographic pattern. Atelectasis can be categorized as obstructive or nonobstructive. Obstructive atelectasis An obstruction between the alveoli and trachea causes reabsorption of alveolar gas, leading to an obstructive atelectasis. The obstruction can occur at the level of the larger or smaller bronchus, and it may be secondary to a foreign body, benign or malignant tumor, mucus plug, and blood clot, as well as bronchial transection, fibrotic stenosis from granulomas or inflammation, polychondritis, post brachytherapy or radiotherapy stenosis, and other obstructive lesions. The development of atelectasis depends on several factors, including the extent of collateral ventilation and the composition of inspired gas. Obstruction of a larger bronchus is likely to produce lobar atelectasis, whereas the obstruction of a smaller bronchus causes segmental atelectasis. The pattern of atelectasis often depends on collateral ventilation, which is provided by the pores of Kohn and the canals of Lambert. Right middle lobe (RML) syndrome, a form of chronic atelectasis, usually results from bronchial compression and obstruction by surrounding lymph nodes or bronchial scarring. Partial bronchial obstruction and recurrent infection may also lead to chronic atelectasis and acute or chronic pneumonitis. Nonobstructive atelectasis Loss of contact between the parietal and visceral pleurae causes nonobstructive atelectasis. The etiologies may be lung compression, the loss of surfactant, and scarring or infiltrative disease of the lung. Several types of nonobstructive atelectasis are known to occur from a variety of causes. A pleural effusion or a pneumothorax eliminates contact between the parietal and visceral pleurae, and relaxation or passive atelectasis results. The uniform elasticity of a normal lung preserves the shape, even after atelectasis is present. The middle and lower lobes collapse more than the upper lobes in the presence of a pleural effusion, whereas the upper lobes are more affected by a pneumothorax. Compression atelectasis occurs when 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 lowers the surface tension of the alveoli and therefore plays an important role in preventing the alveoli from collapsing. Decreased production or inactivation of surfactant, as observed in acute respiratory distress syndrome (ARDS) and similar disorders, leads to alveolar instability and atelectasis. Cicatrization atelectasis results as a sequela of severe parenchymal scarring and is usually caused by granulomatous disease or necrotizing pneumonia. The lobar collapse from cicatrization may be either obstructive if the bronchi are involved or nonobstructive because of the fibrotic process in the lung parenchyma. Replacement atelectasis occurs when the alveoli of an entire lobe are filled by tumor (eg, bronchioalveolar cell carcinoma), resulting in a loss of volume. Rounded atelectasis, also called folded-lung syndrome or Blesovsky syndrome, occurs as the lung collapses and folds secondary to fibrous bands and adhesions to the visceral pleura.6 The incidence is high in asbestos workers (65-70% of cases). Patients are typically asymptomatic, and the mean age at presentation is 60 years. Rounded atelectasis is a benign disorder. For excellent patient education resources, visit eMedicine's Lung and Airway Center and Cancer and Tumors Center. Also, see eMedicine's patient education articles Collapsed Lung and Lung Cancer. PathophysiologyThe mechanisms of obstructive, nonobstructive, platelike, and postoperative atelectasis are different and determined by several factors. Obstructive atelectasis After the obstruction of a bronchus, the absorption of gas in the peripheral alveoli leads to retraction of the lung and an airless state within a few hours. 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 becomes distended and displaces the surrounding structures, shifting the heart and mediastinum toward the atelectatic area, elevating the diaphragm, and flattening the chest wall. If the obstruction is removed, any complicating postobstructive infection subsides, and the lung returns to its normal state. 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 do pneumothoraces, which affect the upper lobes. A large pleural-based lung mass may cause compression atelectasis by decreasing lung volumes. Surfactant has phospholipid dipalmitoyl phosphatidylcholine, which prevents lung collapse by reducing the surface tension of the alveoli. The lack of production or the inactivation of surfactant may occur in ARDS, radiation pneumonitis, and blunt trauma to the lung; this change causes adhesive atelectasis. Scarring of the lung parenchyma leads to cicatrization atelectasis. Filling of the entire lobe by a tumor such as bronchoalveolar carcinoma causes replacement atelectasis. Platelike atelectasis Also called discoid or subsegmental atelectasis, platelike atelectasis probably occurs because of obstruction of a small bronchus.7 It is observed in states of hypoventilation, pulmonary embolism, or lower respiratory tract infections. Small areas of atelectasis occur because of inadequate regional ventilation and abnormalities in surfactant formation from hypoxia, ischemia, hyperoxia, and exposure to various toxins. Postoperative atelectasis Postoperative atelectasis is commonly observed after thoracic and upper abdominal procedures. Diaphragmatic dysfunction and reduced surfactant are consequences of general anesthesia and surgical manipulation that can lead to atelectasis. The atelectasis is typically basilar and segmental in distribution. Postoperative atelectasis is extremely common. Lobar atelectasis is also common. FrequencyUnited StatesThe incidence or prevalence of this disorder has not been well documented. InternationalData on the international prevalence of this disorder are not available. Mortality/Morbidity
RaceNo data are available regarding the racial predilection of lobar atelectasis; the disorder affects people of all racial origins. SexNo sex preference has been documented. AgeAge as such does not appear to be a risk factor or contributor to atelectasis. AnatomyIn children and young adults, the trachea passes downward and backward, close to the midline. In older individuals, a slight deviation to the right occurs because of the left-sided aortic arch. The trachea divides into the 2 mainstem bronchi at the level of carina, which is generally at the level of the fifth thoracic vertebra. The right lung has 3 lobes, and each has its individual bronchus. The right upper lobe (RUL) bronchus takes off from the right mainstem bronchus, close to the carina. The RUL has 3 segments: the apical segment, the posterior segment, and the anterior segment. The right mainstem bronchus continues downward as the bronchus intermedius before dividing into the RML bronchus and right lower lobe (RLL) bronchus. The RML bronchus has a medial segment and a lateral segment. The RLL bronchus has 5 segments: the superior segment, the anterior basal segment, the lateral basal segment, the posterior basal segment, and the medial basal segment. The left main bronchus is approximately 50 mm long. It divides into the left upper division and the left lower lobe (LLL) bronchus. The right main bronchus is approximately 25 mm in length and has a steeper angle than the left. The left upper division further divides into the left upper lobe (LUL) bronchus, which terminates into 2 segmental bronchi, the left anterior and the apical posterior. The left apical posterior segment bronchus further divides into apical and posterior segments. Clinical DetailsAtelectasis commonly occurs after thoracic or upper abdominal procedures. Signs and symptoms 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 of a complicating infection. Rapid lung collapse causes pain on the affected side, a sudden onset of dyspnea, and cyanosis. Hypotension, tachycardia, fever, and shock may also occur. Slowly developing atelectasis may be asymptomatic or cause only minor symptoms. Patients with middle-lobe syndrome are often asymptomatic, although they may have a severe, hacking, nonproductive cough. Physical examination reveals 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 caused by the following: plugs of tenacious sputum; foreign bodies; endobronchial tumors; or compression of the bronchi and bronchial distortion due to a tumor, lymph node, or aneurysm. External pulmonary compression caused by pleural fluid or air (eg, 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 due to a metastatic neoplasm (eg, adenocarcinoma of the breast or thyroid, hypernephroma, melanoma); an inflammatory etiology (eg, tuberculosis, fungal infection); an aspirated foreign body; a mucus plug; a malpositioned endotracheal tube; or extrinsic compression of an airway by a neoplasm, lymphadenopathy, aortic aneurysm, or cardiac enlargement. Relaxation atelectasis is caused by the following: a pleural effusion, pneumothorax, or large emphysematous bulla. Compression atelectasis is caused by the following: chest wall, pleural, or intraparenchymal masses or loculated collections of pleural fluid. Adhesive atelectasis is caused by the following: hyaline membrane disease, ARDS, smoke inhalation, cardiac bypass surgery, uremia, or prolonged shallow breathing. Cicatrization atelectasis is caused by the following: idiopathic pulmonary fibrosis, chronic tuberculosis, fungal infections, or radiation fibrosis. Replacement atelectasis is caused by alveoli filled by tumor or fluid. Rounded atelectasis is caused by asbestos pleural plaques. Related eMedicine topics:Airway Foreign Body Effusion, Pleural Hyaline Membrane Disease Lung, Postprimary Tuberculosis Preferred ExaminationChest radiographs are generally sufficient to diagnose lobar atelectasis and to identify the collapsed lobe. Chest radiographs are also useful in diagnosing platelike atelectasis, postoperative atelectasis, and rounded atelectasis, as well as for following the course of the atelectasis. For example, chest radiographs can be used to determine whether an intervention, such as chest physiotherapy, has resulted in improvement. However, in some situations, chest radiographic findings may not be diagnostic. This generally occurs when a concomitant pleural fluid or large pulmonary masses are present. In such cases, computed tomography (CT) scanning is a useful next imaging study. CT scanning should be used to assess obstructive atelectasis; this modality is also helpful in evaluating the mediastinum, chest wall, hilum, pleura, and adjacent lung.8, 9, 10, 11, 12 Magnetic resonance imaging (MRI) has no particular value in the diagnosis of lobar atelectasis, except for distinguishing obstructive from nonobstructive atelectasis.13 Limitations of TechniquesA concomitant pleural effusion, pleural mass, or large lung mass may limit the usefulness of chest radiography in the diagnosis of atelectasis. When a basal opacity, an opacity of the hemithorax, and other signs of atelectasis are not obvious, determining whether the opacity is a pleural effusion or a lobar collapse may be difficult. In those situations, a CT scan can be of immense help. Intravenous contrast enhancement is often required for appropriate imaging and for differentiating among various causes of atelectasis. The limitation of CT scanning may be in differentiating between obstructive and nonobstructive causes of atelectasis. Furthermore, a CT scan may not be useful in determining whether the obstructing lesion is a tumor, mucus plug, nonopaque foreign body, or blood clot. DIFFERENTIALSSection 3 of 11
Other Problems to Be ConsideredBronchogenic carcinoma, which may occur with atelectasis, must be ruled out in all patients older than 35 years. A spontaneous pneumothorax produces clinical findings that are similar to those of atelectasis, but the percussion note is tympanic, the heart and mediastinum are pushed to the opposite side, and the radiographic results are diagnostic. A massive pleural effusion may cause absent breath sounds, dyspnea, cyanosis, weakness, and dullness over the hemithorax. However, the heart and mediastinum are deviated away from the involved area. RADIOGRAPHSection 4 of 11
FindingsChest radiographs and CT scans show 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, a mediastinal shift toward the side of collapse, loss of volume in the ipsilateral hemithorax, elevation of the ipsilateral diaphragm, crowding of the ribs, compensatory hyperlucency of the remaining lobes, and silhouetting of the diaphragm or heart border. Complete atelectasis Complete atelectasis of an entire lung is characterized as follows: complete collapse of a lung leads to opacification of the entire hemithorax and an ipsilateral shift of the mediastinum. The mediastinal shift separates atelectasis from a massive pleural effusion (see Images 8 and 13). RUL collapse The collapsed RUL shifts medially and superiorly, resulting in elevation of the right hilum and the minor fissure. The RUL may also collapse laterally, producing a pleural-based opacity that may look like a loculated pleural effusion. The minor fissure in an RUL collapse is usually convex at its superior aspect, but it may appear concave because of an underlying mass lesion. This is called the Golden sign of S (also known as the Golden S sign and the S sign of Golden). Tenting of the diaphragmatic pleura, called the juxtaphrenic peak sign, is another helpful sign of RUL atelectasis (see Images 2, 15, and 17).14 RML collapse RML collapse obscures the right heart border on a posteroanterior (PA) image. The lateral view shows a triangular opacity overlying the heart because the major fissure shifts upward and the minor fissure shifts downward. With worsening collapse, the opacity diminishes in size, and it may be barely perceptible (see Images 3 and 20). RLL collapse The collapsed RLL shifts posteriorly and inferiorly, resulting in a triangular opacity that obscures the RLL pulmonary artery. The major fissure, normally not visible on a PA radiograph, is evident with an RLL collapse. The superior mediastinal structure shifts to the right, causing a superior triangle sign. Laterally, the collapsed RLL obliterates the posterior one third of the right hemidiaphragm and projects as an opacity over the normally lucent area (see Images 4 and 21). Concomitant RML and RLL atelectasis may appear as an elevated right hemidiaphragm or a subpulmonic effusion. An attempt to identify the fissures usually leads to the accurate diagnosis (see Image 19). LUL collapse An atelectatic LUL shifts anteriorly and superiorly. In one half of the cases, a hyperexpanded superior segment of the LLL is positioned between the atelectatic upper lobe and the aortic arch. This gives the appearance of a crescent of the aerated lung, called the luftsichel sign. On PA views, an atelectatic LUL produces a faint opacity in the left upper hemithorax, obliterating the left heart border. On lateral views, the major fissure is displaced anteriorly behind the sternum (see Images 4, 6, and 9-11). LLL collapse On frontal views, an increased retrocardiac opacity obliterates the LLL pulmonary artery and the left hemidiaphragm. The hilar structures shift downward, and the rotation of the heart produces flattening of the cardiac waist, which is known as the flat-waist sign. The superior mediastinum may shift and obliterate the aortic arch; this is the top-of-the-aortic-knob sign. On the lateral radiographs, an opacity silhouettes the posterior third of the left diaphragm, and an opacity is projected over the normally lucent area (see Images 5 and 14). Rounded atelectasis In cases of rounded atelectasis, segmental or subsegmental atelectasis occurs secondary to visceral pleural thickening and entrapment of the lung tissue. Rounded atelectasis manifests as a subpleural mass, and bronchovascular structures radiate out of the mass toward the hilum. An associated parietal pleural plaque may be present. The swirl appearance of the bronchovascular shadows is called the comet-tail sign and establishes the diagnosis (see Image 22).15 Degree of ConfidenceChest radiography has the highest sensitivity when direct signs of atelectasis can be detected. More specifically, the identification of a displaced fissure is of significant advantage in diagnosing lobar collapse. The presence of several indirect signs further corroborates the direct signs in the diagnosis of atelectasis. False Positives/NegativesModest loss of volume may occur secondary to lobar consolidation; this may lead to the erroneous diagnosis of lobar collapse. A loculated pleural effusion or pleural effusion with passive collapse may be mistakenly identified as a collapse secondary to an endobronchial lesion. False-negative results may occur if the collapse does not involve the whole lobe; this situation may be secondary to an incompletely obstructive bronchial lesion or partial ventilation of the lobe. Platelike atelectasis or postoperative atelectasis may often be missed on chest radiographs because it may be obscured by other thoracic structures. A false-negative diagnosis may also occur if the patient cannot take a full breath or if the anteroposterior or lateral chest radiograph is not available. CT SCANSection 5 of 11
FindingsRadiographic changes of lobar collapse are more obvious on CT scans than on plain radiographs. CT scans are additionally helpful in identifying and localizing an obstructing bronchial lesion. Correlation with a chest radiograph helps in the evaluation, as does careful examination of the mediastinum, hilum, and pleura. The primary changes of lobar collapse on CT scan are as follows:
RUL collapse The RUL is bordered medially by the mediastinum, superiorly by the chest wall, inferiorly by the minor fissure, and posteroinferiorly by the superior portion of the oblique fissure. On CT scanning, RUL collapse appears as a right paratracheal opacity, and the minor fissure appears concave laterally. The RUL collapses against the mediastinum, and this is identified as a wedge of uniform attenuation extending along the mediastinum to the anterior chest wall. Concomitant hyperinflation of the middle and lower lobes is present. A bulge in the contour of the collapsed RUL occurs secondary to an endobronchial tumor and gives an S-shaped configuration. Endobronchial obstruction is readily identifiable on the CT scan (see Image 18). RML collapse The RML is bounded medially by the right heart border; anteriorly and laterally by the chest wall; posteriorly by the major fissure; and superiorly, the minor fissure. As the RML collapses, the minor fissure shifts downward and the oblique fissure is displaced forward. With a progressive loss of volume, the middle lobe collapses medially against the right heart border. The collapsed middle lobe is a wedge-shaped opacity that extends laterally from the hilum toward the lateral chest wall. It is bounded posteriorly by the RLL and anteriorly by the hyperinflated RUL. On CT scans, a triangular opacity along the right heart border, with the apex pointing laterally, is a characteristic finding. This appearance resembles a tilted ice-cream cone. RLL collapse The RLL is bordered inferiorly by the hemidiaphragm, posteriorly and laterally by the chest wall, medially by the heart and mediastinum, and anteriorly by the major fissure. The RLL generally collapses in a posteromedial direction against the posterior mediastinum and spine. An endobronchial lesion may result in a convex lateral contour of the collapsed RLL. The major fissure is displaced posteromedially. LUL collapse The LUL is bounded medially by the mediastinum, inferiorly by the left heart border, superiorly and laterally by the chest wall, and posteriorly by the major fissure. CT scanning shows the inferior location of the collapsed lobe and the shift of the RUL across the midline. LUL collapse occurs anterosuperiorly. As opposed to the RUL, the collapsed LUL maintains more contact with the anterior and lateral chest wall. Hyperaeration of the superior segment of the LLL may cause displacement and superior movement; these changes may account for periaortic lucency or the luftsichel sign on PA images. The LUL maintains its contact with the mediastinum and remains attached to the left hilum by a wedge of collapsed tissue. The anterosuperior direction of the collapse projects a wedge-shaped triangular opacity, with the apex pointing posteriorly. Endobronchial obstruction is easily identified on CT scans. LLL collapse The LLL is bordered inferiorly by the hemidiaphragm, posteriorly and laterally by the chest wall, medially by the heart and mediastinum, and anteriorly by the major fissure. The LLL collapses medially toward the mediastinum and maintains contact with the hemidiaphragms. The major fissure moves posteriorly. The LLL has an opacity situated against the posterior mediastinum. CT scanning shows the atelectatic LLL in the inferior posterior location (see Image 12). Passive atelectasis Passive atelectasis is likely the most common form of atelectasis. It occurs secondary to the presence of air or fluid in the pleural space. The CT scan easily depicts pleural effusion and the underlying collapsed lung. Differentiation may be made easier with the use of contrast medium. The pattern of collapse secondary to an endobronchial lesion is distorted in the presence of pleural fluid. CT scanning may be of some help in distinguishing benign causes from malignant causes of pleural effusion. An irregular or nodular pleural surface may indicate an underlying malignancy. Cicatrization atelectasis Scarring or fibrosis from an inflammatory disease may lead to cicatrization collapse, the most common example being previous tuberculosis. In cicatrization atelectasis, an endobronchial lesion is not seen and the bronchial tree in the collapsed lobe is hidden. Marked volume loss is present, and bronchiectatic changes frequently occur in the involved lobe. Chronic middle-lobe syndrome results in a patent bronchus. Significant bronchiectasis and scarring may be observed in the collapsed lobe. Adhesive atelectasis Adhesive atelectasis occurs secondary to the loss of surfactant. A common cause is lung collapse due to radiation pneumonitis. The CT scan appearance is a sharp line demarcating the normal pulmonary parenchyma from the irradiated lung, which is generally paramediastinal. Replacement atelectasis Replacement atelectasis is a form of volume loss in which the pulmonary parenchyma is replaced by tumor infiltration. In this situation, the CT scan shows uniform attenuation throughout the involved lobe. This finding generally mimics consolidation. The tumor may grow into the edges and structures, such as the chest wall or mediastinum. Rounded atelectasis Rounded atelectasis is a form of chronic atelectasis that may appear as a mass lesion on chest radiographs. Although this form is most commonly associated with asbestos exposure, other benign conditions may also be present. These conditions include tuberculosis, uremic pleuritis, pulmonary infarction, and other causes of pleuritis. Because of adhesions between the visceral pleura and parietal pleura, the atelectatic lung becomes trapped and folds onto itself. In cases of rounded atelectasis, the CT scan results are diagnostic and definitive; therefore, further investigations to exclude lung cancer are not required.. The CT scan findings are a peripheral oval or wedge-shaped attenuating area with smooth lateral edges and a medial irregular or ill-defined border that points to the hilum. Distortion and displacement of the blood vessels and bronchi appear in a characteristic curvilinear configuration that leads to the rounded atelectasis (ie, comet-tail sign). In most cases, bronchograms are seen on the CT scan, and calcification is also common. Degree of ConfidenceThe common etiologies of lobar collapse include central endobronchial tumor, long-standing infection, pleural disease, and previous irradiation. CT scanning may play an important role in differentiating obstructive endobronchial lesions from other forms of collapse. By identifying the exact location of an endobronchial lesion and the presence of peribronchial spread, CT scans may be helpful in planning bronchoscopy and transbronchial biopsy. Evaluation of the mediastinum, pleura, chest wall, and adrenal glands plays a role in the staging process. In evaluating patients with radiographically atypical forms of collapse, CT scans further help in accurately delineating the collapse and in identifying any additional pathology.16, 17 CT scans are particularly helpful in patients who have a pleural effusion associated with atelectasis, and these images have a significant advantage over plain radiographs in the assessment of pleural malignancy. Finally, CT scans are especially useful in evaluating patients with cicatrization atelectasis. These patients have underlying bronchiectasis and present with atypical plain radiographic findings. False Positives/NegativesDetermining the cause of an endobronchial obstruction on the basis of CT scans alone may be difficult. CT scans may not be useful in distinguishing among an endobronchial malignancy, a benign tumor, mucus plug, blood clot, and another nonopaque foreign body. Significant lung collapse associated with pleural effusion may not have the characteristic findings of lobar collapse; therefore, discerning whether an endobronchial lesion is present may be difficult. CT scans may not be accurate in identifying benign and malignant causes of pleural effusion. CT scanning is also limited in differentiating a consolidation secondary to an infectious cause from a replacement collapse in which a tumor has infiltrated the entire lobe. CT scans do not obviate bronchoscopy, which is a mandatory procedure to accurately localize an endobronchial lesion and to characterize its nature. Bronchoscopy may also serve a therapeutic role. MRISection 6 of 11
FindingsThe role of MRI in differentiating a central obstructing tumor from a peripheral collapsed lung has been evaluated. T2-weighted sequences are useful in identifying an endobronchial lesion.13 Because lipid-laden macrophages accumulate in the subacute phase of lobar collapse, progressive lymphocytic infiltration and collagen deposition occur within the pulmonary interstitium. In these situations in which the ratio of lung to fat in the collapsed lung is greater than 1, T2-weighted MRIs are most useful in differentiating a tumor from lung collapse. MRI may have a role in the evaluation of adhesive atelectasis. T2-weighted sequences may help in differentiating fibrosis secondary to an endobronchial obstruction from radiation-induced pneumonitis. Furthermore, MRI may have a role in diagnosing rounded atelectasis because MRIs may more accurately depict curvilinear vessels in the folded lung. Degree of ConfidenceMRI is an excellent imaging modality in situations in which intravenous contrast material cannot be administered. MRIs may delineate the extent and the location of a tumor; this modality may also have a role when CT scans are not helpful in differentiating between a tumor and a collapsed lung. False Positives/NegativesIn a study of 10 patients, MRI was useful in identifying a tumor due to a collapsed lung in 5 (50%) patients, as compared with CT scanning. In the same study, CT scanning successfully differentiated between tumor and lung collapse in 8 (80%) of 10 patients. Interestingly, MRI was successful in 2 cases in which differentiation was not possible with CT scanning. ULTRASOUNDSection 7 of 11
FindingsUltrasonography has a limited role in the evaluation of atelectasis. The only potential role for this modality is in differentiating a basal lung collapse from a loculated pleural effusion. However, there are data to support the use of bedside ultrasonography in cases in which the clinical history and findings as well as the radiologic studies of critically ill patients are inconclusive.18, 19 Degree of ConfidenceCT scanning is preferred to ultrasonography because CT scanning is more accurate, delineates the surrounding structures better, and is also more useful in identifying the cause of atelectasis. INTERVENTIONSection 8 of 11
Medical care The treatment of atelectasis depends on the underlying etiology. The 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 to reexpand the collapsed lung. When these efforts are not successful within 24 hours, flexible fiberoptic bronchoscopy should be performed. Bronchoscopy When a mechanically obstructed bronchus is suspected and when coughing or suctioning is not successful, bronchoscopy should be performed. If bronchoscopy is successful, any underlying infection should be treated. Prevention of further atelectasis involves (1) placing the patient in a position such that the uninvolved side is dependent to promote increased drainage of the affected area, (2) providing vigorous chest physiotherapy, and (3) encouraging the patient to cough and to breathe deeply. Patients may require repeat bronchoscopy if atelectasis recurs. This is particularly true in patients with neuromuscular disease and a poor cough. Bronchoscopy is the most important diagnostic procedure in the evaluation of atelectasis; this procedure is useful not only in detecting and localizing an obstructive lesion, but also in obtaining tissue samples for the histologic confirmation of bronchogenic carcinoma. Bronchoscopy has therapeutic value in obstructive lesions other than tumors, and it is urgently indicated in patients with hypoxemia or respiratory distress. A pulmonary specialist performs the bronchoscopic procedure. Flexible fiberoptic bronchoscopy can be a useful diagnostic and therapeutic procedure. Bronchoscopy helps in evaluating the cause of bronchial obstruction. In addition, bronchoscopy helps clear mucus plugs when they cause bronchial obstruction. However, bronchoscopy has limitations; because only the subsegmental bronchi are visualized, a distal endobronchial lesion is not accessible by means of this procedure. Airway stenting Patients with obstructing airway lesions either secondary to benign or malignant lesions can be treated with the use of airway stents. Initially designed to relieve tracheal stenosis, these stents have proven to be beneficial in lobar collapses secondary to large airway obstruction. The nature of the underlying pathologic condition and the location of the obstructing lesion influences the stenting methods and the techniques. Airway obstructions caused by malignant lesions are best treated by a multimodality approach utilizing debridement and/or stenting of the lesion. Debridement of malignant endobronchial lesions provides effective short-term relief of the obstruction and reexpansion of the collapsed lobe. The presence of significant residual luminal narrowing requires placement of a stent. Primary airway stenting is used in cases in which the lesions are caused by external compression without endobronchial obstruction because in such situations, the role of debridement is limited. Other treatment modalities such as adjuvant radiotherapy, either external beam or brachytherapy, may also be applied in these conditions. Subsequent mechanical or laser debridement can be employed if the tumor overgrowth occurs after the stenting. For benign tracheobronchial stenoses that cannot be treated with endoscopic debridement, these conditions are best managed with tracheobronchial stents. Either the Y-stents or the straight silicone stents of the Hood or Dumon variety are selected for patients with distal tracheal or mainstem bronchial lesions that invade the carina. The stents are generally well tolerated and have been shown to offer significant palliation of symptoms. A variety of stents are available; these include silicone, metallic, and mixed stents. The silicone stents are easy to place but require rigid bronchoscopy with general anesthesia.20 The advantages of metallic stents are that flexible fiberoptic bronchoscopy and local anesthetic are utilized in their placement; the disadvantages are the difficult removal and occlusion from tissue proliferation. The other complications of silicone stents are migration, granuloma formation, obstruction, cough, mucociliary alteration, and rupture. Metallic stents can cause complications such as cough, hemoptysis, bronchial obliteration, and occlusion by tumor growth. Medical/Legal Pitfalls
Related Medscape topic: ACKNOWLEDGMENTSSection 9 of 11
The authors and editors of eMedicine gratefully acknowledge the contributions of previous coauthor Dr Sean Tsuyuki to the development and writing of this article. MULTIMEDIASection 10 of 11
REFERENCESSection 11 of 11
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