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Pneumothorax
Pneumothorax Reginald EPIDEMIOLOGY
Greene, AND
M.D.,
Theresa
ETIOLOGY
Spontaneous pneumothorax frequently occurs in apparently healthy males during the third or fourth decade of life (Fig. 1). For many years it was thought to be tuberculous in origin, but in 1932 Kjaergaard emphasized that the common cause was rupture of an apical bleb.“6 Blebs have been defined as gas pockets within the elastic fibers of the visceral pleura that form as a result of rupture and centrifugal dissection of air from subpleural alveoli that are involved with paraseptal emphysema.“” These gas pockets are usually small and are covered by a thin layer of visceral pleura. The abnormality is localized and not necessarily associated with generalized pulmonary emphysema. Alternatively, air from a ruptured bleb may dissect centripetally from the bleb toward the lung hilus, producing a pneumomediastinum. The fact that blebs tend to occur and rupture at the lung apices, especially in tall people, is explained by the very large stresses that are believed to act on the lung apex.53 The majority of these cases of pneumothorax are truly spontaneous, but on occasion straining or sneezing has been implicated as a precipitating cause.s’ When pleural adhesions are present, straining may precipitate pneumothorax by pulling on localized areas of visceral pleural weakness. The frequent coexistence of hemothorax with pneumothorax (about one-fifth of cases) is explained by rupture of small subpleural bronchial vessels (Fig. 2).32 Clinical onset of spontaneous pneumothorax is most often heralded by sudden development of dyspnea and chest pain, aggravated by deep breathing and body movement. Not infrequently, however, asymptomatic pneumoReginald Greene, M.D.: Deparfment of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, Mass. Theresa C. McLoud, M.D.: Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, Mass. Paul Stark, M.D.: Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, Mass. Reprint requests should be addressed to Reginald Greene, M.D., Depariment of Radiology, Massachusetts General Hospital, Boston. Mass. 02114. 0 1977 by Grune & Stratton. Inc. ISSN:0037-198X. Seminars
in Roeorgenology,
Vol. XII, No. 4 (October).
1977
C. McLoud,
M.D.,
and
Paul
Stark,
M.D.
thorax is discovered incidentally. The incidence of pneumothorax is approximately the same in the two lungs. Bilateral pneumothorax is rare.]* Spontaneous pneumothorax is reported to recur in about 30% of patients on the ipsilateral side and in 10% of patients on the contralateral side.1’,45 Spontaneous pneumothorax can be treated successfully with bedrest, but the time required for full lung expansion often makes this approach impractical. With normal lungs, the average rate of pneumothorax gas resorption is only about 1.25% per day.‘” Treatment by thoracotomy tube suction or water seal usually results in full reexpansion within 24 to 48 hr in the absence of a persistent leak. Surgical treat-
ment by pleurectomy or pleurodesis is generally reserved for recurrent or persistent pneumothorax.15.?’ In addition to apical blebs, there are many other causes of spontaneous pneumothorax that are related to underlying lung disease or trauma. Chronic obstructive pulmonary disease, especially chronic bronchitis and emphysema, accounts for a second peak in the incidence of pneumothorax that occurs between 45 and 65 years of age.13 In these conditions, the pneumothorax results from rupture of peripheral emphysematous areas (Fig. 3).‘* In asthma, the presumed mechanism of pneumothorax and pneumomediastinum is related to air trapping and alveolar rupture distal to bronchiolar mucous plugs.“,32 Air dissects centripetally along the perivascular sheaths to the hilum and mediastinum, with subsequent rupture into the pleural space. Unlike spontaneous pneumothorax occurring in otherwise healthy young adults, spontaneous pneumothorax associated with chronic obstructive lung disease is potentially lethal and may lead to respiratory failure.13 The clinical presentation may be misleading, because the signs and symptoms of pneumothorax often resemble those of the underlying obstructive lung disease. Pneumothorax should always be suspected as a possible cause of sudden clinical deterioration in chronic obstructive lung disease. Recurrent pneumothorax may be associated 313
GREENE,
MC LOUD,
AND
STARK
Fig. 1. Spontaneous pneumothorax in a 22-year-old man. The right lung is totally collapsed except for blebs at its apex. Note air bronchograms in the collapsed lung. There is no evidence of tension. A soft tissue density of unknown significance overlies the right anterior second rib.
with chronic interstitial lung disease of any cause, including idiopathic pulmonary fibrosis, sarcoidosis, histiocytosis X, lymphangiomyomatosis, radiation pneumonitis, silicosis, and tuberous sclerosis (Fig. 4).4,12*30,37 Pneumothorax is rarely the first indication of the interstitial lung disorder. It generally occurs late in the course of the disease, after organization, fi-
Fig. 3. A 70-year-old man with chronic bronchitis, emphysema, and coronary artery disease. (A) A bulla in the right upper lobe, coronal narrowing of the trachea, and cardiac enlargement are present. (B) Subsequent film. Right pneumothorax has appeared. The right hemidiaphragm is now more depressed, and the mediastinal pleura is displaced to the left (arrows), indicating some degree of tension.
Fig. 2. Spontaneous pneumothorax in a 21-year-old man. Note the thin line of the visceral pleura and the avascular pneumothorax space. An air-fluid level seen through the right hemidiaphragm indicates hydrothorax or hemothorax. There is no evidence of tension.
brosis, and architectural distortion have developed. The late stages of many interstitial lung diseases are characterized by the formation of cystic spaces of variable size and extent, the result of alveolar septal dissolution, bronchiolectasis, and obstructive emphysema. Rupture of one of the subpleural cysts into the pleural cavity leads to pneumothorax. This is a particularly common complication of histiocytosis X (20%-50% of patients). Patients with lymphangiomyomatosis, a rare condition of
315
PNEUMOTHORAX
Fig. 4. Spontaneous old man with diffuse tosis X.
pneumothorax lung involvement
(arrow) caused
in a 33-yearby histiocy-
young or middle-aged women in whom honeycomb lung and chylous effusion occur, also show a high incidence of pneumothorax.‘2~27 Pneumothorax resulting from radiation pneumonitis tends to occur 3 to 8 months following
Fig. 5. Spontaneous with multiple nodular (arrows).
pneumothorax metastases from
in a PI-year-om man osteogenic sarcoma
completion of therapy, when fibrosis develops and subpleural cysts form.3o Malignant neoplasms, particularly metastatic sarcoma, are occasional causes of spontaneous pneumothorax (Fig. 5). They are said to account for about 1% of cases.gv56Most are in children, and the most common primary form of the tumor is osteogenic sarcoma. Pulmonary metastases from almost every type of primary tumor have been reported in association with spontaneous pneumothorax.8*20~2s,“7 Two mechanisms have been implicated in the development of pneumothorax with malignant tumor: (1) rapid growth and ischemic necrosis of a peripheral tumor, leading to rupture into the pleural space; (2) bronchiolar obstruction by tumor, leading to alveolar rupture, dissection of air along tissue planes, and rupture into the pleural space. 2o Occasionally, pneumothorax may by the first sign of pulmonary metastasis. Unless chronic obstructive airway disease is also present, pneumothorax rarely occurs in association with primary lung tumors.‘3*5” In these cases, the rupture of a preexisting overdistended bulla distal to an endobronchial obstruction may be the precipitating event.” Pneumothorax is not an uncommon complication of infected infarct, lung abscess, or septic embolus.‘g~‘O There have been isolated reports of pneumothorax complicating alveolar proteinosis, Marfan syndrome, and diabetic ketoacidosis.‘,‘0*5L Catamenial pneumothorax (ie, recurrent spontaneous pneumothorax concurrent with menses) is a rare but interesting manifestation of intrathoracic endometriosis.36.39.12 The right side has been more frequently involved; bilateral pneumothorax has been described.“” Pneumothorax occurs in the interval from 3 days prior to onset of menses to 3 days after onset. In the neonate, pneumothorax has been reported in association with hyaline membrane disease, renal malformation, and Potter syndrome.7.“.‘6 Both open- and closed-chest trauma is often associated with pneumothorax. In blunt trauma, pneumothorax can occur without evidence of rib fracture, as a result of lung laceration from spalling phenomena or implosion.6~1” When rib fractures are present, pneumothorax is usually the result of laceration by a rib fragment. Occasionally, pneumothorax occurs in the apparently undamaged lung, presumably as
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Fig. 6. latrogenic pneumothorax in a 35-year-old man a result of lung puncture during subclavian line insertion.
GREENE,
MCLOUD,
AND
STARK
as
a result of contrecoup injury.34,“4 Pneumothorax along with pneumomediastinum may occur with tracheobronchial and esophageal rupture.‘” In adults, a tracheobronchial tear is sometimes accompanied by fracture of one or more of the first three ribs. It should be suspected when a large air leak continues in spite of apparently adequate thoracotomy tube drainage, or when an area of massive posttraumatic atelectasis persists.“’ A penetrating thoracic injury from a knife or bullet wound often induces pneumothorax. The cauterizing effect of a bullet, however, may prevent the escape of air into the pleural space.‘” Iatrogenic pneumothorax is becoming increasingly frequent. This occurs from inadvertent entry of air into the pleura1 space during thoracentesis, puncture of the lung during subclavian line placement, liver biopsy, kidney biopsy, renal cyst puncture, and needle aspiration biopsy of the lungb3 (Fig. 6). Approximately 20% of closed needle aspiration biopsies of the lung are complicated by pneumothorax.“4 Acupuncture is an esoteric cause of pneumothorax. Pneumothorax is the most common form of barotrauma, occurring in about 25% of patients maintained on mechanical ventilation and positive end-expiratory pressure. Its incidence is related to the level of inspiratory pressure employed, the du-
Fig. 7. Effect of respiration. Pleuritic a 2Cyear-old man. (A) lnspiratory chest suspicious but indefinite linear density rows). (B) Expiratory film confirms the apical pneumothorax (arrow).
left shoulder pain in radiograph shows a at the left apex (arpresence of a small
ration of mechanical ventilation, and the development of complicating infection or infarction. Pneumothorax associated with mechanical ventilation may be antedated by interstitial or mediastinal emphysema. It is frequently bilateral and under tension. CLINICAL
AND PHYSiOLOGlC
EFFECTS
A thorough understanding of the clinical consequences and radiologic findings in pneumothorax depends on a knowledge of the anatomy
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PNEUMOTHORAX
and incomplete. If only a small amount of gas enters the pleural space, the chest wall will expand a little and the lung will collapse a little. The exact proportions of chest wall expansion and lung retraction depend on the relative compliances. Ordinarily, more of the pneumothorax volume is provided by chest wall expansion than by lung collapse. In the absence of a ball-valve mechanism or a persistent rent in the visceral pleura, the pneumothorax gas volume will not change much during respiration (Fig. 7). However, a sudden fall in atmospheric pressure, such as occurs during accidental decompression in airplane flight, is life-threatening to the patient with a closed pneumothorax because the volume of the pneumothorax will greatly increase.
Fig. basilar
8. Small spontaneous portions of the pleural
right surfaces
pneumothorax. remain coupled.
The
and physiology of the lungs. The same mechanisms that keep the normal pleural space totally
gas-free
and relatively
liquid-free
are
also responsible for efficient ventilation. The normal trace amount of pleural fluid strongly couples the lung to the chest wall in the same manner that a liquid tilm tightly binds two plates of glass together. This coupling of the pleural surfaces allows direct transmission of inflationary forces from the chest wall (ie, rib cage and diaphragm) to the lung and provides frictionless slippage between the visceral and parietal surfaces during respiration. The low total gas pressure of the tissues surrounding the pleural space (70 mm Hg below atmospheric) keeps the pleural space gas-free by tending to drive out any atmospheric gas. When the lowpressure pleural space is opened to the atmosphere, air enters and uncouples the pleural surfaces. The lung is then free to retract toward the hilus as a result of its elastic recoil. The rib cage is also free to spring outward. When the elastic recoil of the lung is normal, collapse of the lung may be rapid and complete. However, when the lung recoil is decreased, as in emphysema,
pulmonary
or when the lung is stiff, as in
fibrosis, lung collapse may be slow
The pathophysiologic consequences depend on the size of the pneumothorax, the presence of tension, and the condition of the underlying lung. In the young healthy patient with a very small pneumothorax, gas exchange is nearly normal. Ventilation and perfusion matching is maintained, since ventilation tends to be reduced in step with blood how, which is diminished by hypoxic vasoconstriction and lung collapse. In patients with more than 50% lung collapse, however, there is a transient hypoxemia that tends to disappear within 24 hr.“s,r9 Ventilation of the pneumothorax lung is reduced because the gas buffer between the pleural surfaces results in an indirect transmission of inflationary forces. The larger the
Ins pi rat ion
Expiration
Fig. 9. Diagram of a flaplike pleural defect with a ballvalve effect. producing tension pneumothorax. The pleural flap opens during inspiration, allowing air to enter the pleural space. The flap closes during expiration, trapping the pleural gas. This process generally leads to tension. Note the displacement of the mediastinum and depression of the left hemidiaphragm.
318
pneumothorax, the less efficient the transmission and the smaller the ventilation. In a small pneumothorax, the dependent pleural surfaces usually remain coupled, and partial ventilation continues (Fig, 8). Otherwise healthy people with pneumothorax easily compensate for reduced ventilation in the affected lung by increased ventilation in the other lung. However, patients with markedly decreased vital capacity from underlying lung disease have limited ability to compensate. The volume of the pneumothorax occurs at the expense of the functional residual capacity of the affected lung, thereby reducing the vital capacity. In these patients, the increased work of breathing and the reduced vital capacity resulting from a small pneumothorax can lead to respiratory failure. When the pleural defect is in the form of a flap, as with a ruptured bulla, a ball-valve phenomenon may allow air to enter the pleural space during inspiration and prevent free exit during expiration (Fig. 9). The volume and pressure of gas in the pleural space will then increase, achieving supraatmospheric levels (tension pneumothorax). The presence of tension has very significant physiologic consequences in pneumothorax. Compression of the normal lung markedly increases the work of breathing and contributes to regional ventilation and perfusion imbalance by increasing the resistance to blood flow. When the compressive effect is pronounced, the result is somewhat analogous to asphyxia. Distortion of the mediastinum also reduces systemic venous return to the heart. In contrast to the relatively benign effect of simple pneumothorax in otherwise healthy people, tension pneumothorax always produces serious adverse functional changes. In an open pneumothorax with a large pleural defect (eg, a gunshot wound that forms a continuous connection between the atmosphere, pleural space, and lung), the gas volume in the pleural space varies with respiration (Fig. 10). Air freely enters the pleural space and is in competition with air entering the lungs via the airways. In the case of a large opening in the chest wall, the chest bellows may not ventilate the lungs adequately, because the resistance of air flow into the pleural space may actually be lower than the resistance of normal air flow into the lungs. In a large open pneumothorax, ventilation of the pleural space is life-
GREENE,
lnspirat
ion
MC LOUD,
AND
STARK
Expiration
Fig. 10. Open wound of the chest wall. During inspiration, air enters the pleural space in competition with the lung. The normal lung tends to inspire some of the used gas from the affected lung (pende//ult). During expiration, pleural gas exits through the hole in the chest wall. Note the marked mediastinal swing to the ipsilateral side during expiration.
threatening, and emergency occlusion of the hole in the chest wall is required. Gas exchange in open pneumothorax is further aggravated by the tendency of the oxygen-poor expired gas from the affected lung to mix with the inspired gas of the normal lung (pendellufi). RADIOLOGIC
DIAGNOSIS
The radiologic findings in pneumothorax vary considerably, depending on the degree of pulmonary collapse, the presence of tension, and other associated conditions. The basic observation consists of recognizing that the outer margin of the visceral pleura (and lung) is separated from the parietal pleura (and chest wall) by a lucent gas space devoid of pulmonary vessels (Figs. 1, 2, and 8). A small pleural tear or puncture that quickly seals itself will result in a small pneumothorax with limited lung collapse. Its detection is difficult because the lung tends to maintain its normal radiolucency because of an increase in the overall gas volume of the hemithorax and vasoconstriction in the affected lung. It is not often appreciated that the degree of true lung collapse is trifling in a small pneumothorax because only about a third of the pneumothorax gas is compensated by lung collapse.” Although most of the pneumothorax is accommodated by expansion of the chest wall (lateral, diaphragmatic, and mediastinal aspects), in a small pneumothorax this expansion is not obvious. When a suspected pneumothorax is not defi-
319
PNEUMOTHORAX
Fig. 11. Skin folds causing densities that parallel the chest wall (arrows). The broad band of increased density favors the diagnosis of skin fold rather than pneumothorax.
nitely seen on an inspiration study, then an expiration radiograph may be diagnostic (Fig. 7). The constant volume of the pneumothorax gas is accentuated by an overall reduction in the size of the hemithorax on expiration. Similar accentuation of a small pneumothorax can be obtained with lateral decubitus studies of the appropriate side. From a practical point of view, it is very important to differentiate a small pneumothorax from a skin fold, clothing, tubing artifacts, abnormalities of the chest wall, and cavitary and bullous lung disease. An incorrect diagnosis may result in unnecessary, hazardous chest tube insertion. The thin visceral pleural tangent of true pneumothorax closely parallels the shape of the chest wall in the absence of un-
derlying lung disease. Artifactual densities may simulate the visceral pleural tangent, but they generally do not exactl~~ parallel the course of the chest wall over their whole length. Careful inspection may also show that the artifact extends beyond the thorax. Skin fold artifacts can be particularly troublesome in a recumbent portable film (Fig. 11). The density characteristics of a skin fold are quite different from those of the visceral pleural tangent (Fig. 12). The “lung” density of a skin fold progressively increases until it reaches a maximum at its tangent and then abruptly becomes lucent. This is quite different from the uniform lucency of the pneumothorax lung and pleural space, interrupted by the thin visceral pleural tangent. Other artifacts that cause excessive lucency of a hemithorax only superficially simulate pneumothorax. Careful inspection with a bright light will often demonstrate the presence of normal pulmonary vasculature distal to the artifact. Large avascular emphysematous bullae or thin-walled cysts cause greater problems in
VISCERAL -PLEURA
CHEST WA
CHEST WA
Fig. 12. Diagram of true pneumothorax on the left and skin fold pseudopneumothorax on the right. The upper crosssectional drawings are correlated with the radiographic density profiles below. In pneumothorax, the lucency of the lung and pneumothorax space is interrupted by the thin line density of the visceral pleura. With skin folds, the density of the skin fold progressively increases until a peak is reached and sudden lucency appears. Bright light examination will generally demonstrate pulmonary vessels beyond the skin fold pseudopneumothorax.
Fig. 13. Spontaneous pneumothorax in a 55-year-old man with chronic obstructive lung disease. Bullae are present in the right apex and at the right base. The concave inner margin of the basilar bulla is easily differentiated from a loculated pneumothorax.
320
Fig. zontal edges bulla.
GREENE,
14. Spontaneous pleural synechia at of the synechia are which have rounded
tension pneumothorax with a horithe right base (arrow). The straight to be distinguished from a cyst or edges.
differentiation. Bullae have concave rather than convex inner margins and do not exactly conform to the normal shape of the costophrenic sulcus when they occur at the lung base (Fig. 13).’ A pneumothorax with a pleura1 adhesion may simulate a lung cyst or bulla (Fig. 14). A synechia tends to form a straight line connecting the lung to the parietal pleura; cysts and bullae have rounded edges. When lung collapse is nearly complete from pneumothorax, the lung hangs limply from the
Fig. 15. Spontaneous man. The margins of the (arrows) as the lung hangs can be identified.
pneumothorax in a IO-year-old lobes can be separately identified from the hilum. Right apical blebs
MC LOUD,
AND
STARK
hilum, and the margins of the separate lobes can often be seen (Fig. 15). This finding is accentuated in the presence of a ruptured bronchus to the extent that the lung may appear to have fallen into the cardiophrenic sulcus.“” In contrast to the lucency of the lung with a small pneumothorax, a lung that is totally airless from pneumothorax will have an increased density. Air-filled bronchi are often visible in the atelectatic lung when no bronchial occlusion is present (Fig. 1). It is important to remember that the lung does not always collapse uniformly. Nonuniform atelectasis is explained by residual areas of pleural contact that maintain adjacent aeration or by underlying lung disease that promotes or prevents localized atelectasis. With partial reexpansion, atelectatic areas may simulate infarction, tumor, or pneumonia (Fig. 16). When a flaplike pleural defect results in tension pneumothorax, the pleural space becomes expanded. The most common manifestations of tension pneumothorax are mediastinal shift, diaphragmatic depression, and rib cage expansion (Fig. 17). Any significant degree of displacement of the mediastinum from the midline position on maximum inspiration, or any depression of the diaphragm, should be taken as evidence of tension. The degree of lung collapse is not a dependable sign for or against tension. As mentioned previously, underlying lung disease may prevent total collapse even if tension is present. An additional word of caution about tension pneumothorax in patients on mechanical ventilation is warranted. Because positive airway pressure is used for ventilation, little if any midline shift of the mediastinum may occur even in the presence of significant tension. The depressed position of the hemidiaphragm is a much more reliable sign of tension when mechanical ventilation is used. In the supine patient, pneumothorax gas will migrate along the broad ventral surface of the lung, making detection on the frontal radiograph, difficult. In this position, the most ventral portions of the lower thorax, especially along the juxtacardiac area, the lateral chest wall, and the base, are the best places to search for evidence of pneumothorax (Fig. 18).:S3.50The collapsed lung falls against the posterior chest wall in the supine position (Fig. 19). Occa-
PNEUMOTHORAX
Fig. 16. Nonuniform atalectasis carcinoma. (6) Hydropneumothorax middle lobe and its bronchus. Note
in pneumothorax. after thoracentesis. the fixed configuration
(A)
PA chest film showing a right pleural effusion from metastatic breast The airless lung (single arrow) is the result of tumor invasion of the right of the pleural margin after thoracentesis (three arrows).
Fig. 17. Tension pneumothorax in an 16-year-old woman on mechanical ventilation for severe acute respiratory failure. There is marked depression of the ipsilateral diaphragm. The contralateral displacement of the mediastinum is less marked. Note the incomplete collapse of the consolidated right lung.
Fig. 18. the small costophrenic
Persistent air leak after right thoracotomy. accumulation of pleural air in the sulcus (arrows).
Note medial
322
GREENE.
MC LOUD,
AND
STARK
Fig. 19. Effect of body position on the appearance of hydropneumothorax. (A) In the supine position, the air-fluid interface of the right basilar hydropneumothorax is parrallel to the plane of the film and is therefore not seen. The homogeneous density just above the right hemidiaphragm (arrow) which is devoid of vasculature is caused by superimposition of the hydroand pneumothorax. Note that the costophrenic portion of the diaphragm is obscured by fluid. The wedge-shaped density in the upper lung is a loculation of fluid and an area of associated atelectasis. (9) In the erect position. the air-fluid level of the hydropneumothorax is obvious (arrows).
Fig. 20. Encapsulated spontaneous pneumothorax in a 52-year-old man with chronic obstructive pulmonary disease. Note the lateral and medial basilar location of the left pneumothorax on this upright film. A previous pneumothorax may have been responsible for obliterating the upper portion of the pleural space.
sionally, the accumulation of air along the medial pleural space will simulate pneumomediastinum. Cross-table lateral or decubitus views are most helpful when an erect film cannot be obtained. With previous pleural scarring pneumothorax may be encapsulated and may remain at the lung base even in the erect position (Fig. 20).44 Associated findings are important to identify. A hydrothorax or hemothorax frequently coexists with the pneumothorax (Figs. 2 and 22). When the pneumothorax is small and pleural contact is maintained at the lung base, the fluid will appear as a meniscus on the erect radiograph. When the pneumothorax is larger, a typical air-fluid interface will be identified. A bleb responsible for spontaneous pneumothorax can usually be identified on a properly exposed radiograph with careful search (Fig. 1). Similarly, offending bullae, interstitial lung disease, and metastatic pulmonary nodules should be carefully searched for when the source of pneumothorax is not apparent (Figs. 3, 4, and
PNEUMOTHORAX
Fig. 21. (A) Spontaneous pneumothorax in a 19-year-old man. (8) Three days later. lpsilateral pulmonary edema after sudden reexpansion of the lung. (Courtesy of Dr. E. F. Parsons.1
5).Pulmonary edema is occasionally identified in the affected lung and rarely in the contralateral lung after reexpansion of a pneumothorax (Fig. 21).48 Pulmonary edema is more apt to occur when a longstanding pneumothorax is suddenly reexpanded.‘7*57 Fluoroscopic examination (or inspiration/expiration radiographs) of a small nontension pneumothorax shows a variable degree of mediastinal shift toward the normal lung during expiration (Fig. 22). The findings in tension pneumothorax are similar, except that the
323
Fig. 22. Inspiration-expiration films of right spontaneous pneumothorax in a 19-year-old man. (A) Inspiration. The mediastinum and ipsilateral hemidiaphragm are in normal position. Note the small hydrothorax or hemothorax. (B) Expiration accentuates the pneumothorax. The trachea and right heart border show a slight shift to the left.
mediastinum extends beyond the midline at maximum inspiration, and the degree of displacement toward the normal lung during expiration is reduced, Accurately estimating the size of a pneumothorax is very difficult. It is not often realized that a pneumothorax that occupies the peripheral inch of the lung amounts to about 30% of the total lung volume.35 Percentage estimations are, generally speaking, inaccurate and most often underestimate the true size of the
324
GREENE,
pneumothorax. When the size of a pneumothorax is being periodically monitored, it is probably best to relate the position of the lung apex to a particular rib and measure the thickness of the pneumothorax rim at the same reference point.
MC LOUD,
AND
STARK
ACKNOWLEDGMENTS The authors acknowledge the kind assistance of Dr. Helga Stark in the preparation of the diagrams. Radiographs for Figure 19 were generously provided by Dr. Edward F. Parsons.
REFERENCES I. Anton HC, Gray B: Pulmonary alveolar proteinosis presenting with pneumothorax. Clin Radio1 18:428-431, 1967 2. Berg RA: Giant congenital hronchogenic cyst, “Pseudopneumothorax.” Postgrad Med48:121-126, 1970 3. Chretien J, Bignon J, Choffel C, et al: Recurrent spontaneous pneumothorax with miliary appearance of the lungs in an arc-welder. J Fr Med Chir Thorac 19:481I494, 1965 4. Christensen EE, Dietz GW: Subpulmonic pneumothorax in patients with chronic obstructive pulmonary disease. Radiology 121:33-37, 1976 5. Christie RV, McIntosh CA: Lung volume and respiratory exchange after pneumothorax. Q J Med 5:4455454, 1936 6. Crawford WO Jr: Pulmonary injury in thoracic and non-thoracic trauma. Radio1 Clin North Am 11:527-541, 1973 7. Deaton WR, Doyle OW: Pneumothorax in infants and children. South Med J 53:1487-1494, 1960 8. D’Ettorre A, Babini L: Pneumothorax from pulmonary metastases. Ann Radio1 Diag 38:595-601, 1965 9. Dines DE, Cortese DA, Brennan MD, et al: Malignant pulmonary neoplasms predisposing to spontaneous pneumothorax. Mayo Clin Proc 48:541I544, 1973 10. Dwyer EM Jr, Troncale F: Spontaneous pneumothorax and pulmonary disease in the Marfan syndrome. Report of two cases and review of the literature. Ann Intern Med62:128551292, 1965 I I. Fletcher SL, Dunbar JS, Levant MN, et al: Pneumothorax and pneumomediastinum associated with renal malformations in newborn infants. Am J Roentgen01 116:7855791, 1972 12. Fraser RG, Pare JAP: Diagnosis of Diseases of the Chest. Philadelphia, WBSaunders, 1970, pp 1159-l 161 13. George RB, Herbert SJ, Shames JM, et al: Pneumothorax complicating pulmonary emphysema. JAMA 234:389-393, 1975 14. Gerblich AA, Kleinerman J: Blunt chest trauma and the lung (editorial). Am Rev Respir Dis 115:3699370, 1977 15. Hickok DF, Ballenger FP: The management of spontaneous pneumothorax due to emphysematous blebs. Surg Gynecol Obstet 120:499-502, 1965 16. Hilgenberg F: Spontaneous pneumothorax. Radiologe8:310-312, 1968 17. Humphreys RL, Berne AS: Rapid re-expansion of pneumothorax: A cause of unilateral pulmonary edema. Radiology 96:50995 12, 1970 18. Izaguirre SFS, Haggerty JT, Eckert G: Spontaneous ruptureof the esophagus. Surgery 67:6077613, 1970 19. Jaffe RB, Koschmann EB: Septic pulmonary emboli. Radiology 96:5277532, 1970
20. Janetos GP, Ochsner SF: Bilateral pneumothorax in metastatic osteogenic sarcoma. Am Rev Respir Dis 88:73-76, 1963 21. Jorgensen JR, Falliers CJ, Bukantz SC: Pneumothorax and mediastinal and subcutaneous emphysema in children with bronchial asthma. Pediatrics 31:824-832, 1963 22. Kellen DA, Gobbel WG Jr: Spontaneous Pneumothorax. Boston, Little, Brown, 1968, pp 80-85 23. Khan F, Seriff NS: Pneumothorax: A rare presenting manifestation of lung cancer. Am Rev Respir Dis 108:1397- 1400, 1973 24. Kircher LT Jr, Swartzel RL: Spontaneous pneumothorax and its treatment. JAMA l55:24,-29, 1954 25. Kittredge RD, Geller A, Finby N: The reticuloendothelioses in the lung. Am J Roentgen01 100:588-592, 1967 26. Kjaergaard H: Spontaneous pneumothorax in apparently healthy. Acta Med Stand [Suppl] 43:1-159, 1932 27. Kruglik GD, Reed JC, Daroca PJ: Radiologicpathologic correlation from the Armed Forces Institute of Pathology. Lymphangiomyomatosis. Radiology 120: 583-588, 1976 28. Laucius JF, Brodovsky HS, Howe CD: Spontaneous pneumothorax and pneumomediastinum as complications of sarcoma. J Thorac Cardiovasc Surg 64:467747 I, 1972 29. Laws HL, Fox LS, Younger JB: Bilateral catamenial pneumothorax. Arch Surg 112:6277628, 1977 30. Libshitz HI, Banner MP: Spontaneous pneumothorax as a complication of radiation therapy to the thorax. Radiology ll2:199 201, 1974 31. Lindskog GE, Halasz NA: Spontaneous pneumothorax: A consideration of pathogenesis and management with review of seventy-two hospitalized cases. Arch Surg 75:693-698, 1957 32. Macklin CC: Pneumothorax with massive collapse from experimental local over-inflation of lung substance. Can Med Assoc J 36:414--420, 1937 33. Moskowitz PS, Griscom NT: The medial pneumothorax. Radiology 120:143- 147, 1976 34. Paredes S, Hipona FA: The radiologic evaluation of patients with chest trauma. Respiratory system. Med Clin North Am 59:37 63, 1975 35. Peter RM: The Mechanical Basis of Respiration. Boston, Little, Brown, 1969 36. Piiron R, Bonnet JL, Demay C, et al: Pneumothorax, puis hthmthorax r6cidivants rCvClateurs d’une endombtriose. J Fr Mcd Chir Thorac 23:1477161, 1969 37. Portner MM, Gracie WA Jr: Rheumatoid lung disease with cavitary nodules, pneumothorax and eosinophilia. N Engl J Med 275:6977700, 1966 38. Richards DW Jr, Riley CB, Hiscock M: Cardiac
PNEUMOTHORAX
output following artificial pneumothorax in man. Arch Intern Med 49:99441006, 1932 39. Ripstein CB, Robman M, Wallach JB: Endometriosis involving the pleura. J Thorac Surg 37:464471, 1959 40. Schweich A, Fierstein J: Staphylococcal septicemia with recurrent spontaneous pneumothorax. Ann Intern Med 50:819-828, 1959 41. Seremetis MG: The management of spontaneous pneumothorax. Chest 57:65-68, 1970 42. Shearin RP, Hepper NG, Payne WS: Recurrent spontaneous pneumothorax concurrent with menses. Mayo Clin Proc 49:98- 101, 1974 43. Silver TM, Thornbury JR: Pneumothorax: A complication of percutaneous aspiration of upper pole renal masses. Am J Roentgen01 128:45ll452, 1977 44. Sinner WN: Complications of percutaneous transthoracic needle aspiration biopsy. Acta Radio1 Diagn 17:813-827, 1976 45. Smith WG, Rothwell PPG: Treatment of spontaneous pneumothorax. Thorax 17:342-349, 1962 46. Spencer H: Pathology of the Lung. New York, Pergamon, 1968 47. Spittle MF, Heal J, Harmer C, et al: The association of spontaneous pneumothorax with pulmonary metastases in bone tumours of children. Clin Radio1 19:400-403, 1968 48. Steckel RJ: Unilateral pulmonary edema after pneumothorax. N Engl J Med 289:62ll622, 1973 49. Stewart HJ, Bailey RL Jr: The effect of unilateral
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spontaneous pneumothorax on the circulation in man. J Clin Invest 19:321l326, 1940 50. Swischuk LE: Two lesser known but useful signs of neonatal pneumothorax. Am J Roentgen01 127:623-627, 1976 51. Toomey FB, Chinnock RF: Subcutaneous emphysema, pneumomediastinum, and pneumothorax in diabetic ketoacidosis. Radiology 116:543-545, 1975 52. Weber WN, Margolin FR, Nielsen SL: Pulmonary histiocytosis X: A review of 18 patients with reports of 6 cases. Am J Roentgen01 107:280-289, 1969 53. West JB: Distribution of mechanical stress in the lung, a possible factor in localization of pulmonary disease. Lancet 1:839-841, 1971 54. Williams JR, Bonte FJ: The Roentgenological Aspect of Nonpenetrating Chest Injuries. Springfield, III, Charles C Thomas, 196 1 55. Williams HO, Kidner PH: Alveolar cell carcinoma presenting as a pneumothorax. Am Rev Respir Dis 103:108112, 1971 56. Wright FW: Spontaneous pneumothorax and pulmonary malignant disease-a syndrome sometimes associated with cavitating tumours. Report of nine new cases, four with metastases and five with primary bronchial tumours. Clin Radio1 27:21 l-222, 1976 57. Ziskind MM, Weill H, George RA: Acute pulmonary edema following the treatment of spontaneous pneumothorax with excessive negative intrapleural pressure. Am Rev Respir Dis 92:632-636, 1965
Greene, AND
M.D.,
Theresa
ETIOLOGY
Spontaneous pneumothorax frequently occurs in apparently healthy males during the third or fourth decade of life (Fig. 1). For many years it was thought to be tuberculous in origin, but in 1932 Kjaergaard emphasized that the common cause was rupture of an apical bleb.“6 Blebs have been defined as gas pockets within the elastic fibers of the visceral pleura that form as a result of rupture and centrifugal dissection of air from subpleural alveoli that are involved with paraseptal emphysema.“” These gas pockets are usually small and are covered by a thin layer of visceral pleura. The abnormality is localized and not necessarily associated with generalized pulmonary emphysema. Alternatively, air from a ruptured bleb may dissect centripetally from the bleb toward the lung hilus, producing a pneumomediastinum. The fact that blebs tend to occur and rupture at the lung apices, especially in tall people, is explained by the very large stresses that are believed to act on the lung apex.53 The majority of these cases of pneumothorax are truly spontaneous, but on occasion straining or sneezing has been implicated as a precipitating cause.s’ When pleural adhesions are present, straining may precipitate pneumothorax by pulling on localized areas of visceral pleural weakness. The frequent coexistence of hemothorax with pneumothorax (about one-fifth of cases) is explained by rupture of small subpleural bronchial vessels (Fig. 2).32 Clinical onset of spontaneous pneumothorax is most often heralded by sudden development of dyspnea and chest pain, aggravated by deep breathing and body movement. Not infrequently, however, asymptomatic pneumoReginald Greene, M.D.: Deparfment of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, Mass. Theresa C. McLoud, M.D.: Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, Mass. Paul Stark, M.D.: Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, Mass. Reprint requests should be addressed to Reginald Greene, M.D., Depariment of Radiology, Massachusetts General Hospital, Boston. Mass. 02114. 0 1977 by Grune & Stratton. Inc. ISSN:0037-198X. Seminars
in Roeorgenology,
Vol. XII, No. 4 (October).
1977
C. McLoud,
M.D.,
and
Paul
Stark,
M.D.
thorax is discovered incidentally. The incidence of pneumothorax is approximately the same in the two lungs. Bilateral pneumothorax is rare.]* Spontaneous pneumothorax is reported to recur in about 30% of patients on the ipsilateral side and in 10% of patients on the contralateral side.1’,45 Spontaneous pneumothorax can be treated successfully with bedrest, but the time required for full lung expansion often makes this approach impractical. With normal lungs, the average rate of pneumothorax gas resorption is only about 1.25% per day.‘” Treatment by thoracotomy tube suction or water seal usually results in full reexpansion within 24 to 48 hr in the absence of a persistent leak. Surgical treat-
ment by pleurectomy or pleurodesis is generally reserved for recurrent or persistent pneumothorax.15.?’ In addition to apical blebs, there are many other causes of spontaneous pneumothorax that are related to underlying lung disease or trauma. Chronic obstructive pulmonary disease, especially chronic bronchitis and emphysema, accounts for a second peak in the incidence of pneumothorax that occurs between 45 and 65 years of age.13 In these conditions, the pneumothorax results from rupture of peripheral emphysematous areas (Fig. 3).‘* In asthma, the presumed mechanism of pneumothorax and pneumomediastinum is related to air trapping and alveolar rupture distal to bronchiolar mucous plugs.“,32 Air dissects centripetally along the perivascular sheaths to the hilum and mediastinum, with subsequent rupture into the pleural space. Unlike spontaneous pneumothorax occurring in otherwise healthy young adults, spontaneous pneumothorax associated with chronic obstructive lung disease is potentially lethal and may lead to respiratory failure.13 The clinical presentation may be misleading, because the signs and symptoms of pneumothorax often resemble those of the underlying obstructive lung disease. Pneumothorax should always be suspected as a possible cause of sudden clinical deterioration in chronic obstructive lung disease. Recurrent pneumothorax may be associated 313
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Fig. 1. Spontaneous pneumothorax in a 22-year-old man. The right lung is totally collapsed except for blebs at its apex. Note air bronchograms in the collapsed lung. There is no evidence of tension. A soft tissue density of unknown significance overlies the right anterior second rib.
with chronic interstitial lung disease of any cause, including idiopathic pulmonary fibrosis, sarcoidosis, histiocytosis X, lymphangiomyomatosis, radiation pneumonitis, silicosis, and tuberous sclerosis (Fig. 4).4,12*30,37 Pneumothorax is rarely the first indication of the interstitial lung disorder. It generally occurs late in the course of the disease, after organization, fi-
Fig. 3. A 70-year-old man with chronic bronchitis, emphysema, and coronary artery disease. (A) A bulla in the right upper lobe, coronal narrowing of the trachea, and cardiac enlargement are present. (B) Subsequent film. Right pneumothorax has appeared. The right hemidiaphragm is now more depressed, and the mediastinal pleura is displaced to the left (arrows), indicating some degree of tension.
Fig. 2. Spontaneous pneumothorax in a 21-year-old man. Note the thin line of the visceral pleura and the avascular pneumothorax space. An air-fluid level seen through the right hemidiaphragm indicates hydrothorax or hemothorax. There is no evidence of tension.
brosis, and architectural distortion have developed. The late stages of many interstitial lung diseases are characterized by the formation of cystic spaces of variable size and extent, the result of alveolar septal dissolution, bronchiolectasis, and obstructive emphysema. Rupture of one of the subpleural cysts into the pleural cavity leads to pneumothorax. This is a particularly common complication of histiocytosis X (20%-50% of patients). Patients with lymphangiomyomatosis, a rare condition of
315
PNEUMOTHORAX
Fig. 4. Spontaneous old man with diffuse tosis X.
pneumothorax lung involvement
(arrow) caused
in a 33-yearby histiocy-
young or middle-aged women in whom honeycomb lung and chylous effusion occur, also show a high incidence of pneumothorax.‘2~27 Pneumothorax resulting from radiation pneumonitis tends to occur 3 to 8 months following
Fig. 5. Spontaneous with multiple nodular (arrows).
pneumothorax metastases from
in a PI-year-om man osteogenic sarcoma
completion of therapy, when fibrosis develops and subpleural cysts form.3o Malignant neoplasms, particularly metastatic sarcoma, are occasional causes of spontaneous pneumothorax (Fig. 5). They are said to account for about 1% of cases.gv56Most are in children, and the most common primary form of the tumor is osteogenic sarcoma. Pulmonary metastases from almost every type of primary tumor have been reported in association with spontaneous pneumothorax.8*20~2s,“7 Two mechanisms have been implicated in the development of pneumothorax with malignant tumor: (1) rapid growth and ischemic necrosis of a peripheral tumor, leading to rupture into the pleural space; (2) bronchiolar obstruction by tumor, leading to alveolar rupture, dissection of air along tissue planes, and rupture into the pleural space. 2o Occasionally, pneumothorax may by the first sign of pulmonary metastasis. Unless chronic obstructive airway disease is also present, pneumothorax rarely occurs in association with primary lung tumors.‘3*5” In these cases, the rupture of a preexisting overdistended bulla distal to an endobronchial obstruction may be the precipitating event.” Pneumothorax is not an uncommon complication of infected infarct, lung abscess, or septic embolus.‘g~‘O There have been isolated reports of pneumothorax complicating alveolar proteinosis, Marfan syndrome, and diabetic ketoacidosis.‘,‘0*5L Catamenial pneumothorax (ie, recurrent spontaneous pneumothorax concurrent with menses) is a rare but interesting manifestation of intrathoracic endometriosis.36.39.12 The right side has been more frequently involved; bilateral pneumothorax has been described.“” Pneumothorax occurs in the interval from 3 days prior to onset of menses to 3 days after onset. In the neonate, pneumothorax has been reported in association with hyaline membrane disease, renal malformation, and Potter syndrome.7.“.‘6 Both open- and closed-chest trauma is often associated with pneumothorax. In blunt trauma, pneumothorax can occur without evidence of rib fracture, as a result of lung laceration from spalling phenomena or implosion.6~1” When rib fractures are present, pneumothorax is usually the result of laceration by a rib fragment. Occasionally, pneumothorax occurs in the apparently undamaged lung, presumably as
316
Fig. 6. latrogenic pneumothorax in a 35-year-old man a result of lung puncture during subclavian line insertion.
GREENE,
MCLOUD,
AND
STARK
as
a result of contrecoup injury.34,“4 Pneumothorax along with pneumomediastinum may occur with tracheobronchial and esophageal rupture.‘” In adults, a tracheobronchial tear is sometimes accompanied by fracture of one or more of the first three ribs. It should be suspected when a large air leak continues in spite of apparently adequate thoracotomy tube drainage, or when an area of massive posttraumatic atelectasis persists.“’ A penetrating thoracic injury from a knife or bullet wound often induces pneumothorax. The cauterizing effect of a bullet, however, may prevent the escape of air into the pleural space.‘” Iatrogenic pneumothorax is becoming increasingly frequent. This occurs from inadvertent entry of air into the pleura1 space during thoracentesis, puncture of the lung during subclavian line placement, liver biopsy, kidney biopsy, renal cyst puncture, and needle aspiration biopsy of the lungb3 (Fig. 6). Approximately 20% of closed needle aspiration biopsies of the lung are complicated by pneumothorax.“4 Acupuncture is an esoteric cause of pneumothorax. Pneumothorax is the most common form of barotrauma, occurring in about 25% of patients maintained on mechanical ventilation and positive end-expiratory pressure. Its incidence is related to the level of inspiratory pressure employed, the du-
Fig. 7. Effect of respiration. Pleuritic a 2Cyear-old man. (A) lnspiratory chest suspicious but indefinite linear density rows). (B) Expiratory film confirms the apical pneumothorax (arrow).
left shoulder pain in radiograph shows a at the left apex (arpresence of a small
ration of mechanical ventilation, and the development of complicating infection or infarction. Pneumothorax associated with mechanical ventilation may be antedated by interstitial or mediastinal emphysema. It is frequently bilateral and under tension. CLINICAL
AND PHYSiOLOGlC
EFFECTS
A thorough understanding of the clinical consequences and radiologic findings in pneumothorax depends on a knowledge of the anatomy
317
PNEUMOTHORAX
and incomplete. If only a small amount of gas enters the pleural space, the chest wall will expand a little and the lung will collapse a little. The exact proportions of chest wall expansion and lung retraction depend on the relative compliances. Ordinarily, more of the pneumothorax volume is provided by chest wall expansion than by lung collapse. In the absence of a ball-valve mechanism or a persistent rent in the visceral pleura, the pneumothorax gas volume will not change much during respiration (Fig. 7). However, a sudden fall in atmospheric pressure, such as occurs during accidental decompression in airplane flight, is life-threatening to the patient with a closed pneumothorax because the volume of the pneumothorax will greatly increase.
Fig. basilar
8. Small spontaneous portions of the pleural
right surfaces
pneumothorax. remain coupled.
The
and physiology of the lungs. The same mechanisms that keep the normal pleural space totally
gas-free
and relatively
liquid-free
are
also responsible for efficient ventilation. The normal trace amount of pleural fluid strongly couples the lung to the chest wall in the same manner that a liquid tilm tightly binds two plates of glass together. This coupling of the pleural surfaces allows direct transmission of inflationary forces from the chest wall (ie, rib cage and diaphragm) to the lung and provides frictionless slippage between the visceral and parietal surfaces during respiration. The low total gas pressure of the tissues surrounding the pleural space (70 mm Hg below atmospheric) keeps the pleural space gas-free by tending to drive out any atmospheric gas. When the lowpressure pleural space is opened to the atmosphere, air enters and uncouples the pleural surfaces. The lung is then free to retract toward the hilus as a result of its elastic recoil. The rib cage is also free to spring outward. When the elastic recoil of the lung is normal, collapse of the lung may be rapid and complete. However, when the lung recoil is decreased, as in emphysema,
pulmonary
or when the lung is stiff, as in
fibrosis, lung collapse may be slow
The pathophysiologic consequences depend on the size of the pneumothorax, the presence of tension, and the condition of the underlying lung. In the young healthy patient with a very small pneumothorax, gas exchange is nearly normal. Ventilation and perfusion matching is maintained, since ventilation tends to be reduced in step with blood how, which is diminished by hypoxic vasoconstriction and lung collapse. In patients with more than 50% lung collapse, however, there is a transient hypoxemia that tends to disappear within 24 hr.“s,r9 Ventilation of the pneumothorax lung is reduced because the gas buffer between the pleural surfaces results in an indirect transmission of inflationary forces. The larger the
Ins pi rat ion
Expiration
Fig. 9. Diagram of a flaplike pleural defect with a ballvalve effect. producing tension pneumothorax. The pleural flap opens during inspiration, allowing air to enter the pleural space. The flap closes during expiration, trapping the pleural gas. This process generally leads to tension. Note the displacement of the mediastinum and depression of the left hemidiaphragm.
318
pneumothorax, the less efficient the transmission and the smaller the ventilation. In a small pneumothorax, the dependent pleural surfaces usually remain coupled, and partial ventilation continues (Fig, 8). Otherwise healthy people with pneumothorax easily compensate for reduced ventilation in the affected lung by increased ventilation in the other lung. However, patients with markedly decreased vital capacity from underlying lung disease have limited ability to compensate. The volume of the pneumothorax occurs at the expense of the functional residual capacity of the affected lung, thereby reducing the vital capacity. In these patients, the increased work of breathing and the reduced vital capacity resulting from a small pneumothorax can lead to respiratory failure. When the pleural defect is in the form of a flap, as with a ruptured bulla, a ball-valve phenomenon may allow air to enter the pleural space during inspiration and prevent free exit during expiration (Fig. 9). The volume and pressure of gas in the pleural space will then increase, achieving supraatmospheric levels (tension pneumothorax). The presence of tension has very significant physiologic consequences in pneumothorax. Compression of the normal lung markedly increases the work of breathing and contributes to regional ventilation and perfusion imbalance by increasing the resistance to blood flow. When the compressive effect is pronounced, the result is somewhat analogous to asphyxia. Distortion of the mediastinum also reduces systemic venous return to the heart. In contrast to the relatively benign effect of simple pneumothorax in otherwise healthy people, tension pneumothorax always produces serious adverse functional changes. In an open pneumothorax with a large pleural defect (eg, a gunshot wound that forms a continuous connection between the atmosphere, pleural space, and lung), the gas volume in the pleural space varies with respiration (Fig. 10). Air freely enters the pleural space and is in competition with air entering the lungs via the airways. In the case of a large opening in the chest wall, the chest bellows may not ventilate the lungs adequately, because the resistance of air flow into the pleural space may actually be lower than the resistance of normal air flow into the lungs. In a large open pneumothorax, ventilation of the pleural space is life-
GREENE,
lnspirat
ion
MC LOUD,
AND
STARK
Expiration
Fig. 10. Open wound of the chest wall. During inspiration, air enters the pleural space in competition with the lung. The normal lung tends to inspire some of the used gas from the affected lung (pende//ult). During expiration, pleural gas exits through the hole in the chest wall. Note the marked mediastinal swing to the ipsilateral side during expiration.
threatening, and emergency occlusion of the hole in the chest wall is required. Gas exchange in open pneumothorax is further aggravated by the tendency of the oxygen-poor expired gas from the affected lung to mix with the inspired gas of the normal lung (pendellufi). RADIOLOGIC
DIAGNOSIS
The radiologic findings in pneumothorax vary considerably, depending on the degree of pulmonary collapse, the presence of tension, and other associated conditions. The basic observation consists of recognizing that the outer margin of the visceral pleura (and lung) is separated from the parietal pleura (and chest wall) by a lucent gas space devoid of pulmonary vessels (Figs. 1, 2, and 8). A small pleural tear or puncture that quickly seals itself will result in a small pneumothorax with limited lung collapse. Its detection is difficult because the lung tends to maintain its normal radiolucency because of an increase in the overall gas volume of the hemithorax and vasoconstriction in the affected lung. It is not often appreciated that the degree of true lung collapse is trifling in a small pneumothorax because only about a third of the pneumothorax gas is compensated by lung collapse.” Although most of the pneumothorax is accommodated by expansion of the chest wall (lateral, diaphragmatic, and mediastinal aspects), in a small pneumothorax this expansion is not obvious. When a suspected pneumothorax is not defi-
319
PNEUMOTHORAX
Fig. 11. Skin folds causing densities that parallel the chest wall (arrows). The broad band of increased density favors the diagnosis of skin fold rather than pneumothorax.
nitely seen on an inspiration study, then an expiration radiograph may be diagnostic (Fig. 7). The constant volume of the pneumothorax gas is accentuated by an overall reduction in the size of the hemithorax on expiration. Similar accentuation of a small pneumothorax can be obtained with lateral decubitus studies of the appropriate side. From a practical point of view, it is very important to differentiate a small pneumothorax from a skin fold, clothing, tubing artifacts, abnormalities of the chest wall, and cavitary and bullous lung disease. An incorrect diagnosis may result in unnecessary, hazardous chest tube insertion. The thin visceral pleural tangent of true pneumothorax closely parallels the shape of the chest wall in the absence of un-
derlying lung disease. Artifactual densities may simulate the visceral pleural tangent, but they generally do not exactl~~ parallel the course of the chest wall over their whole length. Careful inspection may also show that the artifact extends beyond the thorax. Skin fold artifacts can be particularly troublesome in a recumbent portable film (Fig. 11). The density characteristics of a skin fold are quite different from those of the visceral pleural tangent (Fig. 12). The “lung” density of a skin fold progressively increases until it reaches a maximum at its tangent and then abruptly becomes lucent. This is quite different from the uniform lucency of the pneumothorax lung and pleural space, interrupted by the thin visceral pleural tangent. Other artifacts that cause excessive lucency of a hemithorax only superficially simulate pneumothorax. Careful inspection with a bright light will often demonstrate the presence of normal pulmonary vasculature distal to the artifact. Large avascular emphysematous bullae or thin-walled cysts cause greater problems in
VISCERAL -PLEURA
CHEST WA
CHEST WA
Fig. 12. Diagram of true pneumothorax on the left and skin fold pseudopneumothorax on the right. The upper crosssectional drawings are correlated with the radiographic density profiles below. In pneumothorax, the lucency of the lung and pneumothorax space is interrupted by the thin line density of the visceral pleura. With skin folds, the density of the skin fold progressively increases until a peak is reached and sudden lucency appears. Bright light examination will generally demonstrate pulmonary vessels beyond the skin fold pseudopneumothorax.
Fig. 13. Spontaneous pneumothorax in a 55-year-old man with chronic obstructive lung disease. Bullae are present in the right apex and at the right base. The concave inner margin of the basilar bulla is easily differentiated from a loculated pneumothorax.
320
Fig. zontal edges bulla.
GREENE,
14. Spontaneous pleural synechia at of the synechia are which have rounded
tension pneumothorax with a horithe right base (arrow). The straight to be distinguished from a cyst or edges.
differentiation. Bullae have concave rather than convex inner margins and do not exactly conform to the normal shape of the costophrenic sulcus when they occur at the lung base (Fig. 13).’ A pneumothorax with a pleura1 adhesion may simulate a lung cyst or bulla (Fig. 14). A synechia tends to form a straight line connecting the lung to the parietal pleura; cysts and bullae have rounded edges. When lung collapse is nearly complete from pneumothorax, the lung hangs limply from the
Fig. 15. Spontaneous man. The margins of the (arrows) as the lung hangs can be identified.
pneumothorax in a IO-year-old lobes can be separately identified from the hilum. Right apical blebs
MC LOUD,
AND
STARK
hilum, and the margins of the separate lobes can often be seen (Fig. 15). This finding is accentuated in the presence of a ruptured bronchus to the extent that the lung may appear to have fallen into the cardiophrenic sulcus.“” In contrast to the lucency of the lung with a small pneumothorax, a lung that is totally airless from pneumothorax will have an increased density. Air-filled bronchi are often visible in the atelectatic lung when no bronchial occlusion is present (Fig. 1). It is important to remember that the lung does not always collapse uniformly. Nonuniform atelectasis is explained by residual areas of pleural contact that maintain adjacent aeration or by underlying lung disease that promotes or prevents localized atelectasis. With partial reexpansion, atelectatic areas may simulate infarction, tumor, or pneumonia (Fig. 16). When a flaplike pleural defect results in tension pneumothorax, the pleural space becomes expanded. The most common manifestations of tension pneumothorax are mediastinal shift, diaphragmatic depression, and rib cage expansion (Fig. 17). Any significant degree of displacement of the mediastinum from the midline position on maximum inspiration, or any depression of the diaphragm, should be taken as evidence of tension. The degree of lung collapse is not a dependable sign for or against tension. As mentioned previously, underlying lung disease may prevent total collapse even if tension is present. An additional word of caution about tension pneumothorax in patients on mechanical ventilation is warranted. Because positive airway pressure is used for ventilation, little if any midline shift of the mediastinum may occur even in the presence of significant tension. The depressed position of the hemidiaphragm is a much more reliable sign of tension when mechanical ventilation is used. In the supine patient, pneumothorax gas will migrate along the broad ventral surface of the lung, making detection on the frontal radiograph, difficult. In this position, the most ventral portions of the lower thorax, especially along the juxtacardiac area, the lateral chest wall, and the base, are the best places to search for evidence of pneumothorax (Fig. 18).:S3.50The collapsed lung falls against the posterior chest wall in the supine position (Fig. 19). Occa-
PNEUMOTHORAX
Fig. 16. Nonuniform atalectasis carcinoma. (6) Hydropneumothorax middle lobe and its bronchus. Note
in pneumothorax. after thoracentesis. the fixed configuration
(A)
PA chest film showing a right pleural effusion from metastatic breast The airless lung (single arrow) is the result of tumor invasion of the right of the pleural margin after thoracentesis (three arrows).
Fig. 17. Tension pneumothorax in an 16-year-old woman on mechanical ventilation for severe acute respiratory failure. There is marked depression of the ipsilateral diaphragm. The contralateral displacement of the mediastinum is less marked. Note the incomplete collapse of the consolidated right lung.
Fig. 18. the small costophrenic
Persistent air leak after right thoracotomy. accumulation of pleural air in the sulcus (arrows).
Note medial
322
GREENE.
MC LOUD,
AND
STARK
Fig. 19. Effect of body position on the appearance of hydropneumothorax. (A) In the supine position, the air-fluid interface of the right basilar hydropneumothorax is parrallel to the plane of the film and is therefore not seen. The homogeneous density just above the right hemidiaphragm (arrow) which is devoid of vasculature is caused by superimposition of the hydroand pneumothorax. Note that the costophrenic portion of the diaphragm is obscured by fluid. The wedge-shaped density in the upper lung is a loculation of fluid and an area of associated atelectasis. (9) In the erect position. the air-fluid level of the hydropneumothorax is obvious (arrows).
Fig. 20. Encapsulated spontaneous pneumothorax in a 52-year-old man with chronic obstructive pulmonary disease. Note the lateral and medial basilar location of the left pneumothorax on this upright film. A previous pneumothorax may have been responsible for obliterating the upper portion of the pleural space.
sionally, the accumulation of air along the medial pleural space will simulate pneumomediastinum. Cross-table lateral or decubitus views are most helpful when an erect film cannot be obtained. With previous pleural scarring pneumothorax may be encapsulated and may remain at the lung base even in the erect position (Fig. 20).44 Associated findings are important to identify. A hydrothorax or hemothorax frequently coexists with the pneumothorax (Figs. 2 and 22). When the pneumothorax is small and pleural contact is maintained at the lung base, the fluid will appear as a meniscus on the erect radiograph. When the pneumothorax is larger, a typical air-fluid interface will be identified. A bleb responsible for spontaneous pneumothorax can usually be identified on a properly exposed radiograph with careful search (Fig. 1). Similarly, offending bullae, interstitial lung disease, and metastatic pulmonary nodules should be carefully searched for when the source of pneumothorax is not apparent (Figs. 3, 4, and
PNEUMOTHORAX
Fig. 21. (A) Spontaneous pneumothorax in a 19-year-old man. (8) Three days later. lpsilateral pulmonary edema after sudden reexpansion of the lung. (Courtesy of Dr. E. F. Parsons.1
5).Pulmonary edema is occasionally identified in the affected lung and rarely in the contralateral lung after reexpansion of a pneumothorax (Fig. 21).48 Pulmonary edema is more apt to occur when a longstanding pneumothorax is suddenly reexpanded.‘7*57 Fluoroscopic examination (or inspiration/expiration radiographs) of a small nontension pneumothorax shows a variable degree of mediastinal shift toward the normal lung during expiration (Fig. 22). The findings in tension pneumothorax are similar, except that the
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Fig. 22. Inspiration-expiration films of right spontaneous pneumothorax in a 19-year-old man. (A) Inspiration. The mediastinum and ipsilateral hemidiaphragm are in normal position. Note the small hydrothorax or hemothorax. (B) Expiration accentuates the pneumothorax. The trachea and right heart border show a slight shift to the left.
mediastinum extends beyond the midline at maximum inspiration, and the degree of displacement toward the normal lung during expiration is reduced, Accurately estimating the size of a pneumothorax is very difficult. It is not often realized that a pneumothorax that occupies the peripheral inch of the lung amounts to about 30% of the total lung volume.35 Percentage estimations are, generally speaking, inaccurate and most often underestimate the true size of the
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GREENE,
pneumothorax. When the size of a pneumothorax is being periodically monitored, it is probably best to relate the position of the lung apex to a particular rib and measure the thickness of the pneumothorax rim at the same reference point.
MC LOUD,
AND
STARK
ACKNOWLEDGMENTS The authors acknowledge the kind assistance of Dr. Helga Stark in the preparation of the diagrams. Radiographs for Figure 19 were generously provided by Dr. Edward F. Parsons.
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