Seurnal of Thorac Imaging ‘13241080 1956 Lippincott Raven Publishers, Philadephia Types and Mechanisms of Pulmonary Atelectasis John H. Woodring, M.D., and James C. Reed, M.D. ‘Summary: Atelectasis is one of the most commonly encountered abnormalities in chest radiology and remains a daly diagnostic challenge. At times atelectasis can be overlooked, particularly when pulmonary opacification is minimal or absent, and at other times it might be interpreted as being some other form of intrathoracic pathology, particularly pneumonia. The direct signs of atelectasis, are crowded pulmonary vessels, crowded air bronchograms, and displacement of the interlobar fissures. Indirect signs of atelectasis are pulmonary opacifi- cation; elevation of the diaphragm; shift of the trachea, heart, and mediast ‘num; displacement of the hilus; compensatory hyperexpansion of the sur- rounding lung; approximation of the ribs; and shifting granolomas. For descrip- tive purposes, atelectasis can be divided into the following types: segmental, lobar, or whole lung; subsegmental; platelike, linear, or discoid; round; and generalized or diffuse. Resorption atelectasis is caused by resorption of alve- lar air distal to obstructing lesions of the airways; adhesive atelectasis stems from surfactant deficiency; passive atelectasis is caused by simple pneumo- thorax, diaphragmatic dysfunction, or hypoventilation; compressive atelecta sis is due to tension pneumothorax, space-occupying intrathoracic lesions, or abdominal distention; cicatrization atelectasis stems from pulmonary fibrosis; and gravity-dependent atelectasis isthe result of gravity-dependent alterations in alveolar volume. Whenever signs of volume loss are present on a chest radiograph, the radiograph should be interpreted as showing atelectasis. By understanding the various mechanisms leading to atelectasis, and by consid~ ering the underlying conditions, the radiologist should be able to develop an appropriate list of the possible causes of atelectasis. The diagnosis of atelec- {atic pneumonia should be based upon the presence of clinical signs and symp. toms of pneumonia coupled with the identification of pathogenic bacteria in sputum, tracheal aspirates, or protected bronchoalveolar lavage or bronchial brush specimens rather than on the radiographic identification of atelectasis alone. Key Words: Atclectasis—Mechanisms—Radiographic signs—Pulmon- ary collapse. The term atelectasis is derived from the Greek words ateles and ektasis meaning “incomplete ex- pansion’ (1-3), In current usage, atelectasis refers to acquired diminution in volume of part or all of a lung, with or without opacification of the affected From the Department of Diagnostic Radiology, University of| Kentucky Medical Center, Lexington, Kentucky, U.S.A. ‘Address correspondence and reprint requests to Dr. J. Woodring, Department of Diagnostic Radiology, University of Kentucky’ Medical Center, 800 Rose Street, Lexington, KY 40536-0084, U.S.A. 2 portion of the lung (I,2,4). Acceptable synonyms for atelectasis are loss of volume and collapse; how- ever, the term collapse is often reserved to denote total atelectasis of the affected part of the lung (4) Based upon different mechanisms, pulmonary at- electasis can be divided into six types: resorption, adhesive, passive, compressive, cicatrization, and gravity-dependent atelectasis (1,3,5-10). The pur- pose ofthis article isto review the mechanisms and etiologies of these types of atelectasis and to pro- vide a broad overview of the radiographic signs and the various radiographic-morphologic types.PULMONARY ATELECTASIS 93 ‘TYPES OF ATELECTASIS BASED UPON MECHANISM Resorption atelectasis, Resorption atelectasis is the most common type (J); it stems from resorption of gas from the alveoli (1,2). This resorption occurs when communications between the alveoli and the trachea are obstructed (1,2). For this reason, resorption atelectasis is also referred to as obstructive atelectasis (2,5). Resorp- tion atelectasis can be divided into two groups, de- pending on whether bronchial obstruction involves ‘a large airway, such as a segmental, lobar, or main bronchus, or the smaller peripheral bronchi and bronchioles (1,5). Resorption atelectasis from obstruction of a large airway When acute obstruction of a large airway occurs, blood circulating through the capillary bed of the obstructed portion of lung begins to resorb air from it, resulting in progressive diminution in size of the alveoli (1,2). In an otherwise healthy lung, complete resorption of air will take place within 24 bh after acute bronchial obstruction (11). Since the diffusion rate for oxygen is much faster than that of nitrogen, atelectasis can develop even more rapidly in pa- tients ventilated with high concentrations of oxygen (1,2). In patients receiving 100% oxygen, complete atelectasis of a lobe can occur within an hour after acute bronchial obstruction (12,13). It is important to note that diminished alveolar volume is not the sole accompaniment of acute bronchial obstruction (1,2). Since intrapleural pres- sure represents the balance between the elastic re- coil of the lung and the outward pull of the chest wall, intrapleural pressure becomes more negative when air is resorbed and atelectasis ensues (1). This increased negative pressure is transmitted to the i terstitial compartment of the atelectatic lung and draws some edema fluid from the capillary bed of the atelectatic lung into the collapsed alveoli (1,2). An additional volume of blood will be drawn into and sequestered in the vascular bed and interstitium of the atelectatic lung (1,2) These two factors combine to produce atelectatic Tung that weighs more than a similar volume of nor- mal lung (1,2). Although the amount of trapped edema fluid and blood within the obstructed lung is often slight, in some circumstances, rather than los- ing a significant amount of volume, the affected por- tion of lung will predominantly fill with fluid, This condition has been termed “drowned lung” (I-3). Since a drowned lobe can be reduced in volume (1,2), remain normal in size (2), or be enlarged (3), the diagnosis of drowned lung often remains a pathologic one; however, lobar enlargement distal to an obstructing lesion of the bronchus should be considered strong radiologic evidence of the diag- nosis (3). In cases in which bronchial obstruction is of slow onset and atelectasis develops over a long period of time, such as happens in many cases of bron- chogenic carcinoma, obstructive pneumonitis is of- ten found distal to the obstructing lesion in the bronchus (1,2,14). In these cases the predominant pathologic features are those of a noninfectious pro- cess: bronchiectasis with distal mucoid impaction of the bronchi, alveolar volume loss, retention of edema fluid, and lymphocytic infiltration of the bronchial walls (1,2,14); polymorphonuclear leuko- cytes and parenchymal necrosis, features typical of acute bacterial pneumonia, are absent (14). AS the process becomes more chronic, the affected lung develops a yellow or golden hue from a combination of thickening of the interstitium of the affected lung by collagen and mononuclear inflammatory cells and filling of the alveoli by numerous foamy mac- rophages containing intracytoplasmic lipid (1,2, 14). This condition has been termed golden pneu- monia, cholesterol pneumonia, or endogenous lipid pneumonia (2,14), In later stages, marked atelecta- sis ensues after progressive interstitial fibrosis and lymphocytic infiltration of the obstructed lungs this condition is accompanied by a marked decrease in the number of lipid-laden mactophages in the alveolar spaces, and the affected lung assumes a gray-white appearance (I,14). If bacterial infection accompanies obstructive pneumonitis, it primarily affects the airways and cannot be detected radio- sraphically (14). Because of a combination of resorption of air, retained edema fluid and sequestered blood and ob- structive pneumonitis which can follow obstruction of a large airway, most cases demonstrate radio- graphic opacification of the involved lung (1-3) (Fig, 1). On plain films, air bronchograms are typi- cally absent in the atelectatic lung (1,2) (Fig. 1); however, they may be evident on computed tomog- raphy (CT), even in the face of long-standing central bronchial obstruction (15). It should be noted that obstruction of a large bronchus does not always result in atelectasis (1,2). Collateral air drift readily occurs between segments Journal of Thoracic Imaging, Vo. I, No.2 19964 J. H, WOODRING AND J. C. REED within a lobe and can also take place between con- tiguous lobes separated by an incomplete fissure. When collateral air drift arises, the lung distal to an obstructing endobronchial lesion can remain nor- mally ventilated or might even become hyperin- flated (1,2). Furthermore, if the obstructing bron- chial lesion acts as a check valve, allowing air to enter the lung on inspiration but not to leave on expiration, there can also be postobstructive hyper- inflation of the lung distal to the obstructing lesion (. ‘A number of conditions are known to result in resorption atelectasis from obstruction of a large airway; they are summarized in Table 1. Of those conditions producing intrinsic bronchial obstruc- tion, the most important is bronchogenic carcinoma G,5,6,16) (Fig. 1). All cell types of bronchogenic carcinoma have been shown to cause obstruction of Journal of Thoracic Imaging, Vol. 1, No.2, 19% FIG. 1. Resorption atelectasis ofthe et-upper lobe stem= ting from obstruction of the left-upper lobe broneius by lange cell carcinoma is evident in a 4S-yearold female smoker. The posteroanterior radiograph (A) shows ho rogenous opacification of the medial aspect of the lef. hemithoran, obscuration ofthe left heart border, and el ‘vation ofthe left hemidiaphragm (arrowheads) the lat- ‘ral radiograph (B) shows marked anterior displacement fof the left major fissure (arrows) and homogenous opac {ication of te aelectatic lef-upper lobe. No air broncho grams are visible within the stelectatic lobe’ on either \iew. CT (C) shows abrupt termination ofthe lef-upper lobe bronchus (curved arrow), distal atelectasis othe lft. upper lobe (arrowheads), and absence of ait broncho- rams in the atelecaticleft-upper lobe. By fiberoptic Bronchoscopy @ large cell carcinoma arising within and ‘obstructing the let-upper-lobe bronchus was found, the large airways and can become evident as seg- mental, lobar, or whole lung atelectasis (16). When a middle-aged or elderly smoker has symptoms of unexplained segmental, lobar, or whole lung at- electasis, the diagnosis of bronchogenic carcinoma should be considered until it is categorically ex- cluded (5). Occasionally, resorption atelectasis is evidence of the presence of other endobronchial tu- mors, including bronchial carcinoids (5,6,16), ade- noid cystic carcinoma (17), endobronchial me- tastases (3,5,16), lymphoma (5,6,16), and, rarely, benign endobronchial tumors, such as lipoma 6,18), hamartoma (19,20), granular cell myoblas- toma (5,21), papilloma (22,23), endometrioma (22), fibroma (22), neurofibroma (22), and neurilemmoma (22,24), Although endobronchial metastases are un- common, certain extrapulmonary malignancies have a propensity to metastasize to the bronchialPULMONARY ATELECTASIS 95 TABLE 1, Etiologies of resorption atelectasis 1. Large airway obstruction A Intrinsic obstruction 1. Tumor 2, Bronchogenie eaeinoma b. Bronchial carcinoid ©. Adenoid cystic carcinoma 4. Metastases : Lymphoma Benign endobronchial tumors 2. nlammatory 1 Tuberculosis or fungal infection (endobronchial granuloma, broncholith, bronchostenosis) b, Sarcoidosis 3. Other “Aspitated foreign bodies, food, and gastric contents Malpositioned endotracheal tubes Mucous plugs |. Bronchial torsion Bronchial transection Amyloidosis| Wegener's granulomatosis Tracheobronchopathia osteochondroplastica BB. Exirinsc obstruction 1. Invasionlcompression of bronchus by adjacent bronchogenic eareinoma 2. Metastatic hilar lymphadenopathy 53. Granulomatous Iymphadenitis 4 Mediatinal masses 5. Mediastinal fibrosis 6 7 Aortic aneurysm Cardiac enlargement IL Small airway obstruction ‘A. Altered mucociliary clearance 1 Thoracic and abdominal pain, trauma, or surgery 2. Central nervous system depression 53, Respiratory depressant drugs (morphine, codeine) 4 Antcholinergic medication 5. General anesthesia 6 5 8 Endotracheal intubation Ventilation with dry gases High inspired 0, Smoke inhalation B. Chronic obstructive airway disease 1. Asthma 2. Chronic bronchitis 3. Emphysema 4 Bronchioltis obliterans 5. Bronchiectais 1. Cystic fbrosis Acute infection 1. Actte bronchitis and bronchiolitis 2. Pneumonia ‘Modified with permission from ref. 5 lumen; among them, renal cell carcinoma, breast carcinoma, melanoma, colon carcinoma, and sarco- mas (3,5). Certain inflammatory conditions are also known to produce intrinsic obstruction ofthe large airways. (Fable 1), including tuberculosis and fungal infec- tions, which can cause bronchial obstruction from the formation of endobronchial granulomas, bron- cholithiasis, or bronchial stenosis (3,5,15,25), and sarcoidosis, which can rarely produce obstructing endobronchial granulomas (5,6). A number of mis- cellaneous conditions can also cause intrinsic ob- struction of a large airway (Table 1): aspirated for- eign bodies, food, and gastric contents (3,5,6,26); malpositioned endotracheal tubes (5,6); mucous plugs (3,4,6,16,27); bronchial torsion (6); bronchial transection (3,5); amyloidosis (5,22,28); Wegener's granulomatosis (5,29-31); and tracheobroncho- pathia osteochondroplastica (32). Extrinsic compression of the bronchus can also result in obstruction of a large airway with resorp- tion atelectasis of the distal lung (Table 1). This condition arises from compression and invasion of the bronchus by an adjacent bronchogenic carci noma, hilar lymphadenopathy, mediastinal masses, mediastinal fibrosis, aortic aneurysms, or cardiac enlargement (3,5,6,33-35). Chronic atelectasis of the right-middle lobe, due to granulomatous Iym- phadenitis with bronchial stenosis from histoplas- mosis or tuberculosis has been given the name “middle lobe syndrome” G,6). Middle lobe syn- drome, however, can also be due to nongranuloma- tous inflammatory bronchostenosis or bronchiecta- sis (6) and can affect any lobe (). Hilar lymphadenopathy from metastatic disease to an adjacent Iymph node can cause atelectasis from extrinsic compression of the bronchus (5,6); this is particularly true for metastatic breast and Jung cancer (6). In sarcoidosis and lymphoma, both ‘of which commonly appear as massive hilar lymph- adenopathy, atelectasis is seldom caused by com- pression of the bronchi from the enlarged lymph nodes alone (5,6). In those cases in which atelecta- sis does develop, it usually stems from associated endobronchial involvement by the disease (5,6). Resorption atelectasis from obstruction of the small airways Obstruction of the small peripheral bronchi and bronchioles is by far the most common cause of resorption atelectasis (5). Impairment of mucocili- ary transport causes pooling of retained secretions in the smaller airways with resultant bronchial and bronchiolar obstruction and distal resorption at- electasis (36). In a study of postoperative clearance of insufflated tantalum powder following major ab- dominal surgery, Gamsu and co-workers (36) found that when mucociliary clearance was impaired, tan- talum-labeled mucus migrated in a retrograde fash- ion into the peripheral airways and was retained there for <6 days. The pooling and retention of mu- Journal of Thoracic Imaging, Vo. I, No.2, 199896; J. H, WOODRING AND J. C. REED cus was most severe in the gravity-dependent por- tions of the lungs (36). Peripheral migration and reten- tion of tantalum-labeled mucus occurred in 78% of the patients and was associated with the development of radiographically visible atelectasis in all cases (36). Clearance of the retained tantalum did not commence Until the atelectatic lung began to reexpand (36). In resorption atelectasis stemming from periph- eral airway obstruction, the larger airways are often patent and filled with air (1,2,36). This condition will result in the formation of air bronchograms within the atelectatic lung (1,2) (Fig. 2). However, rapid accumulation of secretions can cause filling of | the bronchi all the way to the main bronchus, lead- ing to complete disappearance of air bronchograms in the atelectatic lung (37) (Fig. 3). Although the presence of air bronchograms within the atelectatic lung on plain films implies the absence of a central obstructing neoplasm (2), this sign is not completely reliable (2), particularly on CT, where air broncho- grams are not infrequently identified in atelectatic lung distal to a central obstructing neoplasm (15), Harris (37) has noted the importance of air bron- chogram formation in the treatment of resorption atelectasis due to impaired mucociliary transport and mucous plugging of the bronchi. He has classi- fied air bronchograms into three categories: (a) proximal air bronchogram, where air is visible only to the level of the main bronchi (Fig. 3), bronchus FIG. 2, Resorption atelectasis is evident in the lease lobe, stemming from impaired mucociliary transport with smal tway obstruction after nephrectomy. A posteroanterior chest radio- {raph shows the atelectaticleft-iower lobe asa triangular opacity behind the heart. The lef-loweriobe bronchus is patent, and ‘humerous crowded distal ar bronchograms are visible ia the atelectati leftlower lobe. Journal of Thoracic Imaging, Vol. I, No. 2,19 FIG. 3. Proximal air bronchogram stems from filling ofthe left bronchial tree by secretions and mucus. This 55-year-old mai underwent prolonged surgery for removal of carcinoma of the right face and neck. The immediate postoperative chest radio- raph shows complete atelectasis ofthe let lung, with opacif- ‘ation ofthe let lung and marked shift ofthe trachea, hear, and mediastinum tthe eft. An illdefined proximal air bronchogram (arrow) is seen in the left main bronchus, indicating that the elt bronchial tree is filled with secretions. Twelve hours after bron- choscopic suctioning, the left lung completely reexpanded, intermedius, or lobar bronchi; (b) intermediate air bronchogram, where air is visible down to the level of the segmental bronchi; and (c) distal air broncho- ‘gram, where air is visible down to the level of the subsegmental bronchi or beyond (37) (Fig. 2). Proximal or intermediate air bronchograms sig- nify the accumulation of secretions in the central bronchi and indicate the need for fiberoptic bron- choscopy (37). A distal air bronchogram signifies peripheral bronchial obstruction, thus precluding fi beroptic bronchoscopy as an effective means of treating the atelectasis; in such cases chest physio- therapy is a more appropriate treatment (37). The proximal air bronchogram can rapidly change in ex- tent or definition (37). A receding or increasingly ill-defined proximal air bronchogram indicates pro- gressive accumulation of secretions in the central airways and may be a harbinger of impending respi- ratory arrest; in such cases emergent fiberoptic bronchoscopy may be indicated (37) A number of conditions are known to impair mu- cociliary clearance (Table 1), among them, thoracic ‘and abdominal pain (5), thoracic and abdominal sur- gery or trauma (5,36), central nervous system de- pression (5), respiratory depressant medications such as morphine and codeine (5,36), anticholin- ergic medication (36), general anesthesia (36), en-PULMO) dotracheal intubation (36), ventilation with dry ‘gases (36), inspired oxygen in concentrations higher than that of room air (36), and inhalation of toxic fumes or smoke (38). In addition to impairment of mucociliary transport, high concentrations of oxy- ‘gen also contribute to the development of atelecta- sis by accentuating airway closure because of the rapid rate at which oxygen is resorbed from the alveoli compared with nitrogen (10-13). In postop- erative patients, patients who have sustained severe thoracic or abdominal trauma, and patients in the in- tensive care unit, a number of these factors can com- bine to overwhelm the normal mucociliary transport mechanisms and cause resorption atelectasis Resorption atelectasis may arise during the course of certain chronic obstructive airway dis- eases (Table 1) (including asthma, chronic bronchi- tis, and emphysema) from a combination of chronic changes in the airway walls and loss of elastic re- coil, which lead to luminal narrowing and the for- mation of intraluminal mucous plugs (5,10). Al though the radiographic findings of atelectasis in these conditions are usually minimal, significant ar- eas of atelectasis may be present during acute ex- acerbations (5) ‘Volume loss can also be a prominent feature of bronchiolitis obliterans, bronchiectasis, and cystic fibrosis (1,5,26,39-47). Histologically, bronchiolitis obliterans is characterized by the presence of in- traluminal granulation tissue plugs in the bronchi- oles and alveolar ducts and by obliterative scarring and destruction of the small airways, often associ- ated with areas of organizing pneumonia (39-46). The small-airway obstruction often contributes to diffuse volume loss in the lungs (40.44,47); how- ever, scattered areas of linear atelectasis (44,47) or even segmental or lobar atelectasis can occasionally be evident (40). In addition, postobstructive hyperinflation is of ten a prominent feature of bronchiolitis obliterans (41-43). This is particularly true in cases of unilat- eral bronchiolitis obliterans from Swyer-James or MacLeod syndrome (41). In early bronchiectasis, inflammatory stenosis and obliteration of small bronchi and bronchioles and mucous plugging of the airways combine to produce resorption atelectasis (1,5). As bronchiectasis becomes chronic, ing degrees of pulmonary fibrosis also contribute to atelectasis (1). In young infants with cystic fibrosis, thick mucous secretions can obstruct the small ar ways, resulting in both widespread hyperinflation and scattered areas of atelectasis (26). VARY ATELECTASIS 7 Resorption atelectasis can be seen in acute bron- chitis, bronchiolitis, and pneumonia from obstruc- tion of small bronchi and bronchioles by inflamma- tory exudate (5,6,26,48) (Table 1). This condition is found more often in children than in adults (26,49), presumably owing to the relatively smaller size of the airways in children. Although atelectasis is not common manifestation of pneumonia in adults, endobronchial and peribronchial inflammation from bronchopneumonia can result in small-airway ob- struction followed by atelectasis (5). It has been referred to as “atelectatic pneumonia” (5). ‘The diagnosis of atelectatic pneumonia is usually straightforward in previously healthy outpatients (Fig. 4); however, the distinction between atelectat- ic pneumonia and simple atelectasis can be difficult to make in hospitalized patients who develop seg- mental or lobar atelectasis, especially those on ven- tilators and those who have just had surgery. While nosocomial pneumonia is found to be the cause of segmental or lobar atelectasis in some cases, in the majority, it stems from simple mucous plugging of the bronchi from impaired mucociliary transport. In such cases, the radiographic identification of at- electasis is a nonspecific finding that should not prompt an automatic diagnosis of pneumonia (50). Instead, the diagnosis of pneumonia should be based, whenever possible, on the presence of clin- ical signs and symptoms of pneumonia coupled with identification of pathogenic bacteria in the patient's sputum or pulmonary secretions (5,50,51). In some patients on ventilators, the diagnosis of pneumonia may require fiberoptic bronchoscopy with culturing of material obtained from tracheal aspirates, pro- tected bronchoalveolar lavage, or protected spe ‘men brushing (50,52,53). Adhesive atelectasis Adhesive atelectasis is the term used to describe a type of atelectasis stemming from surfactant de- ficiency (1,5,6,10,54). Surfactant deficiency can re- sult either from destruction of the type II pneumo- cytes (6,55) or from the destruction or inactivation of surfactant by a number of factors (1,10,55). Nor ‘mally, surfactant acts to reduce surface tension in the alveoli and helps maintain alveolar expansion (1). When there is a deficiency of surfactant, there is a much greater tendency for the alveoli to col lapse (1,5). Once collapsed, the alveolar walls tend to adhere, making reexpansion difficult (5). Ini ally, surfactant deficiency produces diffuse loss of volume without significant pulmonary opacifica- Journal of Thoracic tmaging, Vol. 1, No.2, 19%98 J. H, WOODRING AND J. C. REED tion, manifested primarily by high positioning of the diaphragm and marked arteriovenous shunting (1). Later in the course of adhesive atelectasis, diffuse pulmonary opacification can arise, particularly when there is associated pulmonary edema (1,5,55, 56), ‘A number of conditions have been shown to pro- duce adhesive atelectasis due to surfactant defi- ciency (Table 2), among them, hyaline membrane disease, adult respiratory distress syndrome, smoke inhalation, cardiac bypass surgery, uremia, pro- longed shallow breathing, pulmonary embolism, acute radiation pneumonitis, and pneumonia (1,5,6,10,38,54-57). In hyaline membrane disease, adult respiratory distress syndrome (Fig. 5), smoke inhalation, cardiac bypass surgery, uremia, and prolonged shallow breathing, the deficiency of sur- factant and resultant adhesive atelectasis are often widespread throughout the lungs (1,5,10,38,55,57). In pulmonary embolism (Fig. 6), focal ischemia of the lung distal to the embolus can result in marked reduction of surfactant levels in the affected lung, leading to subsegmental, segmental, or lobar at electasis (1,5,10). Similarly, in acute radiation pneu- monitis, the deficiency in surfactant and resulting adhesive atelectasis are limited to the irradiated portion of lung (54,56). In this case, atelectasis is sharply demarcated from normal lung and conforms to the radiation ports (54,56). Rarely, acute pneu- ‘monia can result in surfactant depletion in the af- fected lung (6). In these cases atelectasis of the af- fected segment or lobe can persist for months or years following successful treatment of the acute infection (1,6) (Fig. 7). Journal of Thoracic Imasing, Vo. H, No, 2, 1986 FIG. 4. A case of atelectatic preumonia is shown, ‘This 21- Year-old man had a tay history of fever, chills. anorexia, and pro- ‘ductive cough. Gram stain of the sputum showed gram-positive deci. The posteroanterior radon raph (A) demonstrates opacifica tion ofthe leftemidung zone with ‘obscuration ofthe lowerleft heart ‘border. The lateral radiograph (8) shows a typical triangular shaped ‘opacity (arrows) with anterior bowing of the inferior aspect of the left major fissure, from at- electass of the lingula ofthe let. Upper lobe. Following a full ‘ours of antibiotics the patient's Symptoms and imgular atelectasis resolved. Passive atelectasis ‘Normally, the elastic recoil of the lung is opposed by the outward pull of the chest wall and downward pull of the diaphragm (1,10,54,58). These opposing forces make for negative intrapleural pressure (10,58). In the presence of simple pneumothorax, intrapleural pressure becomes atmospheric, and in- traalveolar pressure and intrapleural pressure are ‘equalized (58). This situation allows the lung to col lapse and the thorax to spring out (10,58) (Fig. 8). Loss of volume in the lung is referred to as passive or relaxation atelectasis (1,5,54) (Table 2). In simple pneumothorax, when intrapleural pressure is atmo- spheric or remains slightly negative, the underlying lung remains partly aerated even in the presence of a large amount of pneumothorax (59) (Fig. 8) Similarly, paralysis of the diaphragm (10,57) and congenital eventration of the diaphragm (60) are as- sociated with loss of the normal downward pull of the diaphragm, thereby allowing for passive at- clectasis of the underlying lung. Diffuse passive at- electasis of the lungs can also develop during peri- ods of pulmonary hypoventilation, when the patient is unable to generate sufficient diaphragmatic ex- cursion to fully expand the lungs (6,10); this condi- tion can resolve rapidly following deep inspiration (0). Compressive atelectasi ‘Any space-occupying lesion of the thorax can compress the lung and squeeze air out of the alveoli (1,5-7). This phenomenon has been called compres- sive atelectasis (5-7). In many cases, the amount of ‘compressed lung is slight and inapparent on plainPULMONARY ATELECTASIS 99 TABLE 2. Etiologies of adhesive, passive, compressive, ‘and cicatrization atelectasis 1. Adhesive atelectasis AL Ditfuse surfactant deficiency 1. Hyaline membrane disease 2. Adult respiratory distress syndrome 53, Smoke inhalation 4 Cardi bypass surgery 5. Uremia 6. Prolonged shallow breathing B. Localized surfactant deficiency 1. Pulmonary embolism 2. Acute radiation peumonitis 3, Preumon TL Passive atelectasis ‘A. Simple pneumothorax B. Diaphragmatic abnormalities 1. Paralysis ofthe diaphragm 2, Congenital eventration of the diaphragm CC. Hypoventilation I. Compressive atelectasis ‘A. Inrathoracie space-oecupying lesions 1. Tension pneumothorax 2; Pleural effusion 5. Empyema 4 Pletal tumors 5, Large pulmonary masses 6. Emphysematous bullae 7. Diaphragmatic herias B. [Abdominal distention 1: Morbid obesity 2, Lage intraabdominsl tumors 53: Hepatosplenomesaly 4 Matsive ascites 5. Intestinal obstruction 6, Pregnaney 1V, Cieatization atelectasis ‘A. Generalized pulmonary fibrosis 1. Idiopathic pulmonary fibrosis 2, Sarcoidosis 3 Silicosis 4 Coal worker's pneumoconiosis 5. Asbestosis 6 Scleroderma and other collagen vascular diseases B. Localized pulmonary florosis 1. Bronchiectasis 2, Chronie tuberculosis and fungal diseases 53, Radiation fibrosis Modified with permission from ret. 5 radiographs (1); however, in certain contexts there can be complete collapse of the lung (6,54). In- trathoracic causes of compressive atelectasis in- clude pleural effusion (Fig. 9), empyema, pleural tumors, large pulmonary masses, large emphysema- tous bullae, lobar emphysema, and diaphragmatic hernias (1,5-7,54) (Table 2). Similarly, abdominal distention from morbid obesity, large intraabdomi- nal tumors, hepatosplenomegaly, massive ascites, intestinal obstruction, and pregnancy can push the iaphragm upward, causing compressive atelectasis of the lower lobes (6,10) (Table 2) In tension pneumothorax (Fig. 10), positive intra- pleural pressure forces all the air out of the alveoli, leaving the atelectatic lung completely airless (59) This finding is helpful in distinguishing tension pneumothorax from a large simple pneumothorax, a condition in which the atelectatic lung remains partly aerated (59), Cicatrization atelectasis Cicatrization atelectasis denotes volume loss stemming from decreased pulmonary compliance due to localized or diffuse pulmonary fibrosis (1,5, 6,54). Cicatrization atelectasis is usually associated with some degtee of bronchiectasis and bronchi- ‘olectasis in the affected lung (1,54,61); itis thought to result from traction on the airways from sur- rounding pulmonary fibrosis and may not indicate primary bronchial disease (61). Diffuse pulmonary volume loss can be seen in a number of conditions that cause diffuse pulmonary fibrosis, including id- iopathic pulmonary fibrosis (Fig. 11), sarcoidosis, silicosis, coal worker's pneumoconiosis, asbesto- sis, and scleroderma and other collagen vascular diseases (1,5,6) (Table 2) Localized cicatrization atelectasis can be seen in chronic bronchiectasis, chronic tuberculosis and fungal infections, and radiation fibrosis (Fig. 12) (1, 5,6,54) (Table 2). In localized cicatrization atelecta- sis, the degree of volume loss is generally more se- vere than that seen in other forms of atelectasis (1,54), Localized cicatrization atelectasis stemming from bronchiectasis or chronic tuberculosis or fun- al disease is also frequently associated with de- monstrable pleural thickening (5,54), Gravity-dependent atelectasis CT measurements of photon attenuation in nor- mal lungs invariably demonstrate a gradient in at- tenuation between dependent and nondependent portions of the lungs, with gravity-dependent por- tions of the lung being of higher attenuation than nondependent areas (62,63). The increased attenu- ation in the dependent portions of the lungs reflects both greater perfusion and decreased alveolar ex- pansion in the dependent areas and is greatest at Jow lung volumes (10,63). In the erect position, the alveolar volume gradient between the lung apex and base is ~4:1 at end-expiration (10); in the supine position, the alveolar volume gradient between the anterior lung and posterior lung is ~2.5:1 at end- expiration (10). These gravitational gradients in al- veolar volume are accentuated by disease processes that increase lung weight (10), Journal of Thoracic Imaging, Vol. 11, No. 2,196100 J. H, WOODRING AND J.C. REED weg FIG. 5. A case of adhesive atelectasis stemming from adult respiratory distress syndrome (ARDS) with diffuse surfactant deficiency is shown. This 37-year-old man had ARDS due to gram-negative bacterial sepsis. A chest radiograph obtained shorty after the onset of lachypnea (A) shows indistinetnss of the perihilar vasculature from early pulmonary edema, A seccnd radiograph obtained? Jays later (8) shows diffuse opacification of both lungs, suggesting ARDS. Note the higher positioning of the diaphragm {arows) in B compared With A, indicating difluse adhesive atelectasis doe to the surfactant deliciency associated with ARDS. Although gravity-dependent alterations in alveo- Jar volume are normal, they exacerbate atelectasis in the dependent portions of the lungs, particularly in bedridden hospitalized patients with prolonged shallow breathing, in patients with impaired muco- ciliary transport, and in patients with conditions that increase the weight of the lungs, such as pneu- monia, increased blood volume, and pulmonary edema (8-10,36), 6a Summary As can be seen from the foregoing discussion, many factors can contribute to or play a part in pulmonary atelectasis. While atelectasis can be di- vided into types based upon different mechanisms, in any given patient several mechanisms can work together to cause the condition. For example, in patients who have undergone cardiac bypass sur- gery, extrinsic compression of the left-lower-lobe FIG. 6, Acase of adhesive atelectasis due to pulmonary embolism is shown. The chest radiograph (A) of this 48-year-old man with deep ‘venous thrombosis and pleritie chest pain shows moderate atelectasis of he rght-and left-lower lobes; several areas of plate atelectasis in the right-middle, rightlower, and eftlower lobes; and a small right pleural effusion. Pulmonary arteriggniphy (B) shows a large embolus (arrow) in the descending branch ofthe right pulmonary artery. Note vascular crowding in the rghtemiddle and lower lobes, particularly in the ares of plate atelectasis (arrowheads) Journal of Torate Imaging, Vol. I, No-2, 19PULMONARY ATELECTASIS JO FIG. 7. Prolonged lobar atelectasis stemming from surfactant depletion from preumonia is evident. This 63-year-old man developed sram-negative bacterial pneumonia in the lef-lower lobe while in the hospital for renal insufficiency. Despite successful antibiotic therapy, the lef-lower lobe collapsed. A posteroanterior radiograph (A) obtained after 2 weeks of anibiotie therapy shows marked lefelower-lobe atelectasis with opacification of the left-over lobe, inferior displacement ofthe let hlus (large white arrow), and inferior snd medial displacement ofthe lett major fissure (three small white arrows). Note the paucity of pulmonary vessels in the letpper lobe, indicating compensatory hyperexpunsion. The lateral radiograph (B) shows marked posterior displacement ofthe left major fissure (arrows). Fiberoptic bronchoscopy showed thick mucus inthe leftlowerlobe bronchi but no evidence of endobronchial neoplasm However, suctioning of the mucus did not reslt in reexpansion of the lobe. The lelower lobe finally reexpanded 3 months later. bronchus, impaired mucociliary transport, surfac- tant deficiency, paralysis of the left hemidiaphragm, and gravity-dependent changes in the lung can com- bine to produce lefi-lower-lobe atelectasis. It is important for the radiologist to understand. the mechanisms of atelectasis and to diagnose it correctly. Despite the frequency with which at- electasis develops in ill and hospitalized patients, many radiologists have trouble both in recognizing atelectasis and in distinguishing atelectasis from other intrathoracic abnormalities. Herein we review the radiographic signs and categories of atelectasis. RADIOGRAPHIC SIGNS OF ATELECTASIS Direct signs of atelectasis The direct signs of atelectasis are crowding to- gether of the pulmonary vessels, crowded air bron- chograms, and displacement of the interlobar fis- sures (13,64) (Table 3). If the collapsing portion of lung still contains some air, the pulmonary vessels within the atelectatic area will remain visible and can be noted to lie close together (3,64) (Figs. 6 and 12). This is one of the earliest signs of atelectasis and is often best appreciated when comparison is ‘made to a normal baseline study. As the airlessness of the affected portion of the lung increases, the pulmonary vessels within the atelectatic area will disappear; however, if the bronchi remain filled with air, crowded air bronchograms will be visible G,64) (Figs, 2 and 9). In addition, as a segment or Jobe of the lung loses volume, the interlobar fissures will be displaced from their normal positions (Figs 1,4,7, and 12), Therefore, crowding together of the pulmonary vessels, crowded air bronchograms, and displacement of the interlobar fissures serve as the primary indicators of atelectasis (I-3,64). If the proximal bronchi are occluded or filled with secre- tions, air within the bronchi can also disappear. When this happens, displacement of the interiobar fissures could be the only direct sign of atelectasis (2. Indirect signs of atelectasis Indirect signs of atelectasis include pulmonary opacification; elevation of the diaphragm; shift of the trachea, heart, and mediastinum; displacement of the hilus; compensatory hyperexpansion of the surrounding lung; approximation of the ribs; and shifting granulomas (1-3,64-66) (Table 3). The indi- Journal of Thoracic Imaging. Vo. 1, No.2, 1998102 J. H. WOODRING AND J. C. REED FIG. 8. A case of passive atelectasis due to simple pneumotho sux is shown, There is large paeumothorax with medially ds placed visceral pleura (arrows) and reduced volume of the right Jung. Also note inferior displacement of the right hemidia- Phraam, wide separation of the right Hibs, and shift of the medi Aastinum and heart to the left, The fat thatthe right lung remains aerated indicates that intrapleural pressure and inrsalveolar pressure are equal and atmosphere. The inferior displacement of the sight hemidiaphragm, wide separation ofthe right ribs, and shift ofthe mediastinum and heart simply reflect the natural tendency of the thorax to spring qutward when unopposed by the elastic recoil of the lung. 9A FIG, 10, A case of compressive atelectasis due to tension ped ‘mothorax is shown. There is @ large sight pneumothorax with inferior displacement ofthe right hemidiaphragm, wide sepe lion ofthe right ribs, and shift ofthe mediastinum and heart to the lef. The ght lung (arrows) is markedly atelectatic and com. pletely airless. The ailess condition of the right lung indicates that inrapeural pressure is greater than intaalveolar pressure (tension) and that the air has been squeezed out of the lung. ‘Compare with Fig 8 rect signs of atelectasis are not constant, and in any given case of atelectasis, one or more of the indirect signs might be absent. Because of the large amount of air contained within normal lung, when the lung loses volume, 9B FIG. 9. A case of compressive atelectasis stems from massive pleural effusion. The chest radiograph (A) of this 43-year-old woman in blast crisis from chronic myefogenous leukemia shows a massive right pleural effusion with mild shift of the heart to the lefts A small Sournal of Thorac Imaging, Vol 11, No.2, 1998 amount of aerated lung is visible at the right apex. A small let pleural effusion is also evident. CT (B) demonstrates massive right and small eft pleural effusions. The right lung (arrows) is markedly atlectatic and containe numerous crowded air bronchogramns.PULMONARY ATELECTASIS 103 opacification of the collapsing lung may not be apparent until a considerable amount of volume loss has occurred (1,64) (Fig. 12). In cases in which edema fluid and sequestered blood are drawn into the collapsing lung (1,2), or when pneumonia has resulted in atelectasis (5,64), or where there is pos- tobstructive pneumonitis (1,2,14), there can be sig- nificant opacification of the lung with only minimal evidence of volume loss (64). Although opacifica- tion of the affected lung is not required to make the diagnosis of atelectasis (4), most cases do show a degree of pulmonary opacification (1,64) (Figs. 4, 6, and 7). For this reason, pulmonary opacification ‘is considered to be the most important of the indi- rect signs of atelectasis (1) Elevation of the diaphragm is also an important indirect sign of atelectasis (1) (Figs. 1, 5, and 11); this condition can best be appreciated when com- parison is made to a normal baseline study. In cases of adhesive atelectasis from diffuse surfactant defi- ciency, resorption atelectasis from diffuse obstruc- tion of the small airways, passive atelectasis due to diaphragmatic dysfunction, compressive atelectasis from abdominal distention, and cicatrization at- electasis from diffuse pulmonary fibrosis, elevation of the diaphragm can be one of the earliest indica- tions of volume loss (1,6,8.9.36). In unilateral seg- mental, lobar, or whole lung atelectasis, elevation of the ipsilateral hemidiaphragm can be present, de- pending upon the degree of volume loss (1-3,64,66) ig. 0, When atelectasis involves only one lung, the tra- chea, heart, and mediastinum may be shifted to- ward the side of atelectasis (1-3,64,65) (Fig. 3). The degree of displacement of these structures is di- rectly related to the severity of the atelectasis (3). When atelectasis is bilateral, the trachea, heart, and mediastinum usually remain in the midline. Dis- placement of the hilus can be an important clue to the diagnosis of atelectasis (1-3,68). In upper-lobe atelectasis the hilus can be displaced superiorly Gig. 12); in lower-lobe atelectasis the hilus can be displaced inferiorly (Figs. 7, 13, and 14) (13,64). In atelectasis of the right-midile lobe or lingula, hilar displacement is usually absent (3). In segmental and lobar atelectasis, as the affected segment or lobe loses volume, the surrounding nor- mal lung often hyperexpands in an attempt to fill in the missing volume of lung (1-3,64). This phenom- enon is referred to as compensatory hyperexpan- sion (64). In cases in which the volume loss is mild, the degree of compensatory hyperexpansion may be so slight as to be inapparent on plain films. How- ever, as the degree of volume loss progresses, com- pensatory hyperexpansion often becomes radio- sraphically apparent both by alterations in vascular markings and increased lung translucency from a greater air-blood ratio in the hyperexpanded lung (1). The increased lung translucency might be diffi- cult to appreciate on plain films but is usually easily seen on CT (1). Alterations in the vascular markings in compensatory hyperexpansion include wide sep- aration of the vessels and a decrease in number of visible vessels in the hyperexpanded lung compared with the normal contralateral lung (Figs. 7 and 14) (13). If atelectasis affects only one lung, the ribs on that side may come to lie closer together than the ribs on the contralateral, normal side (I-3). Since close approximation of the ribs can also occur from oor positioning of the patient at the time the radio- graph is obtained (1), this sign by itself is an unre- liable indicator of atelectasis. Another sign of atelectasis that can be of diagnos- tic value is that of the “shifting granuloma” (1,64, 67) (Fig. 13). When a calcified granuloma changes its position within the chest between two radio- graphs, itis usually due to either atelectasis within the lobe containing the granuloma or atelectasis within one of the adjacent lobes (1,67). RADIOGRAPHIC TYPES OF ATELECTASIS For descriptive purposes, atelectasis can be vided into several types, including segmental, lo- bar, or whole lung atelectasis; subsegmental at- clectasis; platelike atelectasis; round atelectasis; and generalized or diffuse atelectasis (1,2,4,10,64, 68,69). The anatomic localization of atelectasis to a bronchopulmonary segment, one or more lobes of the lungs, or an entire lung is usually readily accom- plished from plain films or CT and will be reviewed in the subsequent article. However, subsegmental atelectasis, plate atelectasis, round atelectasis, and generalized atelectasis bear special mention here. ‘The radiographic identification of subsegmental atelectasis can be difficult (2). Because of collateral air drift, which readily takes place both between lobar segments and between alveoli within a seg- ‘ment (1) when atelectasis is present at the subseg- mental level, many secondary pulmonary lobules within the affected segment or lobe may remain aer- ated while others collapse (2). In such cases the Journal of Thorate Imaging, Vo. H, No.2, 1996104 J. H. WOODRING AND J.C. REED FIG, 11. Cicarization atelectasis from diffuse interstitial fibrosis is shown. The posteroantrior chest radiograph ofa 45-year-old man with bopsy-confirmed idiopathic pulmonary fibrosis (A) shows a coarse reticular patter in the mid- and lower-lung zones of both ngs. A followup radiograph obtained 3 years later (B) shows interval progression of the interstitial disease bilaterally, especially inthe midlung zones. Note the higher positioning ofthe diaphragm (arrows) in B compared with A, indicating diffuse volume loss due to progressive interstitial fibrosis degree of volume loss can be very slight, and the radiograph may evidence only patchy opacities that resemble bronchopneumonia (2) (Fig. 14). As more secondary pulmonary lobules collapse within FIG. 12, Cicatrization atelectasis stemming from radiation fbro- sis is shown. The posteroanteior chest radiograph of this 28- year-old woman obtained } year after completion of mantle ir {adiation for Hodgkin's lmphonra shows moderate atelectasis of the rahtupperlobe without associated pulmonary opacification ‘The volume loss from radiation fibrosis evidenced by superior lsplacement of the right hilas (curved aro), superior displace ment ofthe right minor fissure (arrow), and erowded vessels in the right-upper lobe Journal of Thoracic Imasing, Vol H, No 2,198 the affected segment or lobe, crowded vessels and bronchi, hilar displacement, or fissural displace- ment will become apparent, allowing for a correct diagnosis of atelectasis (Fig. 14). Platelike atelectasis, also called linear or discoid atelectasis, is one of the most common types (10) (Figs. 6, 14, and 15). It can be limited to a bron- chopulmonary segment or subsegment, or extend over a greater distance to involve a lobe, or even extend across fissures to affect several lobes (1,2, 10). Platelike atelectasis can be oriented in a hori- zontal, oblique, or vertical plane (2,10) In the past it was thought that platelike atelectasis might represent either atelectasis distal to obstruct- ing mucous plugs in the small bronchi and bronchi- oles (2) or thrombosed small pulmonary vessels TABLE 3. Radiographic signs of atelectasis 1, Direct signs of atelectasis A. Crowding together ofthe pulmonary vessels fe ai bronchograms I. indirect signs of atelectasis 's. Pulmonary opacification 1B, Elevation of the diaphragm CC Displacement ofthe trachea, heart, and mediastinum D. Displacement of the hit E, Compensatory hyperexpansion ofthe surrounding lung E. Approximation of the nbs G. Shiting granPULMONARY ATE! 105 FIG. 13. A case of sifting granuloma is shown, A routine chest radiograph obisined before abdominal surgery (A) inthis 76-year-old ‘woman shows f large grandloma in the rig midlung zone (arowhead). A postoperative radiograph (B) obtained 2 days later shows ‘moderate right-lowerlobe atelectasis. Compared with A, not inferior displacement ofthe granuloma (arrowhead) and inferior displace meat ofthe right hilus (open arrow). (70). Westcott and Cole (10), in a pathologic study Instead, the typical radiographic findings of plate- of 10 cases of platelike atelectasis, found that bron- like atelectasis corresponded to sheets of atelectasis chial and bronchiolar obstruction were not present in the subpleural region of the lung, which extended in any of their cases of platelike atelectasis. In ad- to the pleural surface and were always associated dition, thrombosed vessels were not the cause of with linear invagination of the overlying pleura (10). the line shadows seen on the radiographs in any ‘The alveoli within the atelectatic plate were not uni- case (10). formly decreased in volume, but rather were flat- hac FIG. 14. Subsegmental atelectasis is shown. The admission chest radiograph (A) of tis 60-year-old man obtained before coronary artery bypass graft surgery is normal. Note the position ofthe descending branch of the right pulmonary artery (arrow. The first postoperative fadiograph (B) demonstrates subsegmental atelectasis f the rightlower lobe. There is inhomogenous opacification of the right-lower Tobe sith indistnctness of the vasculature; two small line shadows are noted above the right hemidiaphragm, AU this point the radiographic appearance could easily be confused with early-stage bronchopneumonis; however, the diagnosis of atelectasis is supported by alight downward and medial shift ofthe descending branch ofthe right pulmonary artery (arrow) compared with the normal baseline iograph in A. A second ragigraph ablained 24 ate (C) shows more typical ight lower labe atelectasis, Note the further downward medial displacement ofthe descending branch of the right pulmonary artery (arrow), In addition, there is a paueity of vascular rarkings inthe riahtupperlobe compared with A, indicating compensatory hyperexpansion ofthe right-upper lobe. Joarnal of Tioracie Imaging. Vol. I, No.2, 1986106 J. H. WOODRING AND J. C. REED FIG. 15. The chest raaiograph of his 39-year-old man with night chest pain after insertion of a rightintemaljugular deep line shows abroad band of platlike atelectasis (arrowheads) bligue- ly oriented in the right-midlung and lower lung zones. This con lion resolved several day later tened (10). The pleural component in some patients consisted of a shallow linear invagination superfi- cial to the atelectasis (10). In others, the platelike atelectasis was deep to incomplete fissures or ex- tended to preexisting pleural clefts (10). These pathologic features suggest that in persist- ing low-volume states, platelike atelectasis devel- ‘ops as the subpleural lung buckles and folds in along. lines of acquired or preexisting pleural invagination (10). Gravity-dependent alterations in alveolar vol- lume, coupled with surfactant deficiency and hypov- entilation, appear to be the main predisposing fac- tors to the development of platelike atelectasis (10). Platelike atelectasis can accompany a variety of, thoracic and abdominal conditions, including pul- monary thromboembolism and infarction; pneumo- nia; pulmonary edema; prolonged shallow breath- ing: diaphragmatic dysfunction; thoracic or abdom- inal pain, trauma, or surgery; general anesthesia; pregnancy; abdominal masses and distention; and morbid obesity (10). Although platelike atelectasis is common and often unimpressive in appearance, it frequently indicates more widespread peripheral at- electasis than is radiologically apparent and can be associated with significant disturbances in ventila- tion and hypoxemia (10). Round or helical atelectasis is another form of atelectasis associated with folding of the lung along an area of pleural invagination (1,68,69). When pleural effusion accumulates rapidly, the basal por- tion of the lower lobe will be pushed upward and folded inward on itself along a cleft or invagination on the lung surface (168,69). If it is not complicated by the development of fibrinous pleural adhesions within the pleural cleft, round atelectasis probably spontaneously resolves in most cases as the pleural effusion recedes and the atelectatic area unfolds (1, 68,69). However, when adhesions arise in the pleu- ral cleft, the lung cannot unfold, and round atelecta- sis can persist for prolonged periods of time follow- FIG. 16, Generalized or difuse atelectasis is shown. The admission chest radiograph (A) ofthis 24-year-old man with bacterial sepsis and panhypopitutarism after resection ofa craniopharyngioma is normal. Over the next 2 days the patient experienced progressive decline in his mental status and became unresponsive, with hypoxia, tachYpnea, and sbored respirations. A chest radiograph at that me (@) showed generalized atelectasis of both lungs with diffise pulmonary opacification and marked high positioning ofthe diaphragm (arrows). After intubation and mechanical ventilation, the atelectasis resolved in IZ h, The patient was tested for sepsis and hypo, tuitarism and did well, ournal of Thoracic Imaging, Vol. I, No.2, 1996PULMONARY ATEI ing resolution of the pleural effusion (1,68,69), ‘When this happens, the atelectatic portion of lung, can be seen as a rounded, subpleural mass contain- ing curvilinear air bronchograms, with pulmonary vessels gathered together in a curvilinear fashion as they course toward the mass (1,68,69).. Generalized or diffuse atelectasis is a term em- ployed to describe widespread volume loss in the lungs without specific evidence of segmental or lo- bar atelectasis (Fig. 16). In generalized atelectasis, there can be marked arteriovenous shunting; how- ever, opacification of the lungs may be mild or in- apparent, and high positioning of the diaphragm may be the sole radiographic clue to the presence of the volume loss (1). When pulmonary opacification is absent, most cases of generalized atelectasis are probably written off as simply a poor inspiratory effort on the patient's part at the time the radi graph was obtained. Conversely, when generalized atelectasis is associated with diffuse pulmonary opacification, most cases are probably interpreted as diffuse pneumonia or pulmonary edema. High positioning of the diaphragm should, however, be the clue to the correct diagnosis (Fig. 16). CONCLUSION Pulmonary atelectasis is one of the most com- monly encountered abnormalities in chest radiology and remains a daily diagnostic dilemma for many radiologists. At times, atelectasis can be over- looked entirely, particularly when pulmonary opacification is minimal or absent. At other times atelectasis can be interpreted as some other form of intrathoracic pathology, particularly pneumonia, Whenever signs of volume loss are present on a chest radiograph, the radiograph should be intet- preted as showing atelectasis. By understanding the mechanisms that can lead to the development of atelectasis, an appropriate list of its possible etiol- ogies can be generated. The diagnosis of atelectatic pneumonia should be based upon the presence of cal signs and symptoms of pneumonia, coupled with the identification of pathogenic bacteria in spu- tum, tracheal aspirates, or protected bronchoalve- olar lavage or bronchial brush specimens, rather than on the radiographic identification of atelectasis alone. REFERENCES 1. Fraser RG, Paré JAP, Paré PD, Fraser RS, Genereux GP. Diagnosis of diseases of the chest, 3nd e4, vo. I. Philadel hiss WB Saunders, 1988:472-545, ‘CTASIS 107 Heitzman ER. The lang: radiologic pathologic correlations, 2nd ed, St. Lous: Mosby, 1984:457-501, Felson B. Chest roentgenology. Philadelphia: WB Saunders, 197392133 Glossary of terms for thoracic radiology: recommendations of the nomenclature committee of the Fleisehner Society ‘AUR 1988;183:509-17. Reed JC. Chest radiology: pla film patterns and differen tial diagnoces, 3rd ed, St. Lovisi Mosby-Vear Book, 1991 167-93 Freundlich IM. Atelectasis. In: Freundlich IM, Bragg DG, es, A radiologic approach to diseases of the chest. Balti more: Williams and Wilkins, 192:60-71 Paling MR, Grifin GK. Lower lobe collapse due to ple effusion: © CT analysis. J Comput Assist Tomogr 1985‘: 1079-83. Morimoto S, Takeuchi N, Imanska H, et al. Gravity- dependent atelectasis: radiologic, physiologic, and patholog- ic correlation in rabbits on high-frequency oscillation venti lation, Iavest Radiol 1989,24:522-30, ‘Tomiyama N, Takeuchi N, Imanaks H, etal, Mechanism of| sravity-dependent atelectasis: analysis by nonradioactive ‘enon-enhanced dynamic computed tomography. Invest Ra io 193:28:633-8, ‘Westeot 3, Cote S, Plat atelectasis, Radiolony 1985185 Coulter WW Jr. Experimental massive pulmonary collapse. Dis Chest 1980:18:186-53, Lansing AM. Radiologic changes in pulmonary atelectasis. Arch Surg 196530:32-6 Stein LA, McLoud TC, Vidal J, Hogg 18, Fraser RG. Acute lobar caliapse in canine lungs. fnvest Radiol 1976;11:518-27 Burke M, Fraser R, Obstructive pneumonitis: a pathologic and pathogenetic reappraisal. Radiology 1988;166:699-703 Woodring JH. Determining the cause of pulmonary atelecta- sista comparison of plain radiography and CT. AJR 1988; 15075783 Naidich DP, McCauley DI, Khouri NF, Leitman BS, Hul- nick DH, Siegelman SS, Computed tomography of lobar col- Tapse, I. Endobronchial obstruction. J Comput Assist To- opr 19837745-37 Spizatny DL, Shepard 10, MeLoud TC, Grillo HC, Dedtick CG. CT of adenowd cystic carcinoma of the trachea. AJR 196146112932, Mendelsohn SL. Fagelman D, Zwvanaga-Mendelsohn S. En dabronchial lipoma demonstrated by CT. Radiology 1983; 148790, Davis WK, Roberts LJ, Foster WL Ir, Peyton RB, Hal: vorsen R ir, Computed tomographic diagnosis of an en- Sobronchial hamartoma, Invest Rado! 1988'23:981-4, ‘Ahn JM, Im -G, Seo TW, etal, Endobronchil hamartoma: CCT findings in three patients. AJR 1994;163:49-50, Robinson IM, Kaoll R, Henry DA. Intrathoracie granular cell myablastoma, South Med J 1988381: 1453-7, Madevell JE, Feigin DS. Benign tumors of the lung, Semin Roenigenol 19TTI2175-86. ‘Anderson KC, Roy TM, Fields CL, Collins LC. Juvenile laryngeal papillomatosis’ a new complication. South Med J 198864879 Feidhaus RJ, Anene C, Bogard P. A rare endobronchial neu- rilemmoma (schwannoma). Chest 1989,95:461-2. Han JK, Im J-G, Park JH, Han MC, Kim YW, Shim Y-S. Bronchial stenosis due to endobronchal tuberculosis: sic: cessful treatment with seifexpanding metallic stent. AJR 1992:159:97 ‘Swischuk LE, Radiology of the newborn and young infant, 2nd ed. Balimore: Willams and Wikins, 1980:(67=75. Pham DH, Huang D, Korwan A, Greyson ND. Acute uni- Journal of Thoracic Imaging, Vo. Il, No.2, 1998108 28. a. 2. x. 4%. 6. M. 3. 2. 4. 2. 6 4s, ro lateral pulmonary nonventilation due to mucous plugs. Rae diology 1987.165-138-7 Cordier JP, Loire R, Brune J. Amyloidosis of the lower re- Spiratory tract clinical and pathologic features in a series of 21 patients: Chess 1986;90:827-31 Maguire R. Fauci AS, Doppman JL, Wolf SM. Unusual Tadiographic features ‘of Wegener's granulomatosis. AJR 1978:130:233-8. Aberie DR, Gamsu G, Lynch D. Thoracie manifestations of ‘Wegener granulomatosis: diagnosis and course. Radiology 1980;174:708.9. Cordier JF, Valeyre D, Gullevin L, Loire R, Brechot JM, Pulmonary’ Wesener's granulomatosis: lineal and imag’ ing stady of 77 cases. Chest 199097:906-1 Hodges MK, IsaelE. Tracheobronchopathis osteachndro- plastica presenting a sight middle lobe collapse: diagnosis by bronchoscopy and computed tomography. Chest 18834, aa, Kirchner SG, Hernanz-Schulman M, Stein SM, Wright PP, Heller RM, Imaging of pediatric mediastinal histoplasmosis RadioGraphics 191:11365-81 Landay MJ, Rollins NK, Mediastinal histoplasmosis granu Toma: evaluation with CT. Radiology 1989:172:657-9, Weinstein JB, Aronberg DJ, Sagel SS. CT of fibrosing me- iastinitis: findings and their uly. AJR 1983;141:247-51, Gamsu G, Singer MM, Vincent HH, Berry 8, Nadel JA Postoperative impairment of mucous transport ‘Am Res Respir Dis 1976;116:673-9, Harris RS. The importance of prox chograms ia the management of atelectasis. J Can Assoc. Radiol 1985:36:105-9, Putman CE, Lake J, Matthay RA, Ravin CE. Radiographic manifestations of smoke inhalation. AJR 1977:129:865-70. Miller NL, Staples CA, Miller RR. Bronchioliis obliterans ‘organizing pneumonia: CT features in 14 patients. AJR 1990; [54985-7 Bouchardy LM, Kublmen JE, Ball WC Jr, Hroban RE, ‘Askin FB, Siegelman SS. CT findings in bronchiolitis bli ‘tans organizing pneumonia (BOOP) wit radiographic, clin- lea, histologic correlation. J Comput Assist Tomogr 1993; 17352-7. McLoud TC, Epler GR, Colby TV, Gaensler FA, Carrington CB. Bronchiolts obliterans. Radiology 1986:159:1-8 Muller NL, Guerry-Force ML, Staples CA. et al. Differen al diagnosis of bronchiolitis obliterans with organizing ‘pneumonia and usual interstitial pneumoni: clinical, func tional, and radiologic findings. Radiology 1987:162:151-6 Seggev IS, Mason UG Ill, Worthen S, Stanford RE, Fertan ez E, Bronchiolis obliterans: report of three cases with detailed physiologic studies. Chest 1983:83:168-74 Chandler PW. Shin MS, Friedman SE, Myers JL, Katzen. Stein A:L. Radiographic manifestations of bronchiolitis obliterans with organizing pneumonia Vs usual intersttl peumonia, AJR 1986;147-899-906. Miki Y, Hatabu H, Takahashi M, Sadatoh N, Kuroda Y. Computed tomography of bronehishitis obliterans. J Comput Assist Tomogr 1988125124 Epler GR. Colby TV. The spectrum of bronchiolitis obliter- ans. Chest 1983:83:1611-162 Holt RM, Schmidt RA, Godwin JD, Raghu G. High resolu. tion CT in respiratory bronchiolits-associated interstitial lung disease. J Comput Assist Tomogr 1993;17:46-50. ournl of Thoracic Imaging, Vo. 1, No.2, 19 J. H, WOODRING AND J. C. REED 48. Coblentz CL, Babeook Cl, Alton D, Riley BJ, Norman G. Observer variation in detecting the ratiologe features asso- ciated with bronchiolitis. Tnvest Radiol 1991;26:115-8 49, Condon VR, Preumonia in chiléren. J Thorac Imaging 1991; 60):31-44 50, Meduri GU, Mauldin GL, Wunderink RG, et al. Causes of fever and pulmonary densities in patients with clinical man- ifestations of ventilator associated pneumonia. Chest 1994; 106:221-35, 51, Niedetman MS, Torres A, Summer W. Invasive diagnostic testing is not needed routinely to manage suspected venti lorassociated pneumonia. Am J Respir Crt Care Med 1998; 15015659, 52. Rumbak MJ, Bass RL. Tracheal aspirate correlates with pro- tected specimen brs in long-term ventilated patients Who have elnical pneumonia. Chest 1984:106:331-4, 58. Chastre J, Fagon JY. Invasive diagnostic testing should be routinely used To manage ventilated patients with suspected ‘pneumonia. Am J Respir Crt Care Med 1994:150°570-4, 54, Naidich DP, McCauley DI, Khouri NF, Leitman BS, Hul- nick DH, Siegelman SS. Computed tomography of lobar col lapse. 1 Collapse in the absence of endobronchial obstuc- tion. J Comput Assist Tomogr 1983; 758-67, 55. lannuazi M, Petty TL. The diagnosis, pathogenesis, and ‘westment of adult respiratory distress syndrome. J Thorac Imaging 1986318): 1-10. 56. Davis SD, Yankelevitz DF, Henschke CI. Radiation effects ‘om the lung: clinical features, pathology, and imaging find- ings. AJR 1992;159:1157-64, 57. Wilcox P, Baile EM, Hards J, et al. Phrenic nerve function and is relationship to atelectasis after coronary artery by- pass surgery. Chest 198;93:693-8. 58. West IB. Respiratory physiology: she essential, 2nd ed. Baltimore: Wiliams and Wilkins, 1979:98-109 59. Milne ENC, Pistolesi M. Reading the chest radiograph: a Physiologic approach. St. Louis: Mosby, 1993:333-4, 60, Tarver RD, Conces I Jr, Cory DA, Vik VA. Imaging the dlapragm ad is disorders J Thor Imaging 980) 1 61. Westcott JL, Cole SR. Traction bronchiectasis in end-stage pulmonary fibrosis. Radiology 1985;161:655-9 (62, Rosenblum Li, Mauceri RA, Wellen:tein DE, eal. Density pattems inthe normal lung as determined by computed 10- ‘ography. Radiology 1980;137:409-16. (63, Verschakelen JA, Van Fraeyenhoven L, Laureys G, Demedts M, Baert'AL. Differences in CT density between dependent and nondependent portions of the lng: influence of lung volume. AUR 1993:161 713-7, (64, Proto AV, Tocino I. Radiographic manifestations of lobar collapse, Semin Roentgenol 1980:15:117-73, 65. Kattan KR. Upper mediastinal changes in lower lobe col. lapse. Semin Roenigenol 1980;18:183-6, 66. Kattan KR, Eyler WR, Felson B. The juxtaphrenic peak in upper lobe collapse, Semin Roenigencl 1980:18:187-93, 67, Roblfing BM. The shifting granuloma: an internal marker of atelectasis. Radiology 1977123:283-5, 68, Hanke R, Kretzschmar R. Round atelectasis, Semin Roent- geno! 1980;15:174-82. 68, Woodring JH. Round atelectasis. Ausralas Radiol 198731: a 70, Simon G. Further observations on the long line shadow sctoss a lower zone ofthe lung. Br J Radiol 1970;43:327-82