Unilateral hyperlucent lung

Unilateral Hyperlucent Lung* (Swyer-James Syndrome J . RAKOWER, M .D . and E . MORAN, M .D . Jerusalem, Israel

the past few years there have been several reports [1-12] describing a new nosologic entity under the headings "unilateral pulmonary emphysema" [1-5] or "abnormal transradiancy of one lung" [6-12] . Other papers describing cases identical with these were published under the headings "hypoplasia or agenesis of pulmonary arteries" [73-19] or "unilateral bronchiectasis without atelectasis" [20] . This entity, first reported by Swyer and James in 1953 [1], has a benign clinical course characterized by recurrent pulmonary infections . Diminished expansion, faint breath sounds and fine rales are found over the abnormal lung . The roentgenographic features consist essentially of by perlucency of the affected lung or lobe, a small hilar shadow and decreased peripheral vascular markings (oligemia) . The affected lung is of normal size or smaller than the contralateral lung . Fluoroscopy shows shifting of the heart and Inediastinum in the direction of the hyperlucent lung during inspiration and away

D

from it on expiration, as is seen in obstructive emphysema . Bronchoscopy does not show signs of bronchial obstruction in the major bronchi . On bronchography the filling is scanty or even absent in the periphery. There may also be a bronchial crowding . An unusual bronchiectatic pattern confined to the hyperlucent lung is frequently seen, the smaller bronchi terminating in the form of small clubs or pools . Angiography shows the pulmonary artery of the affected side to be much diminished in caliber, or there may be complete absence of filling . In the few available pathologic specimens [1,2,7] the pulmonary artery, surprisingly, was found to be of normal size . Histologically there was evidence of recent and old bronchitis and bronchiolitis with bronchiolectasis . Some alveoli were collapsed while others were emphysematous . A striking feature was widespread obliteration of the peripheral lung capillaries in the walls of emphysematous alveoli [1] . The purpose of this paper is to present five

URING

1 . Case I . Inspiratory and expiratory roentgenograms . There is hypcrlucency of the left lung . On expiration the right lung becomes clouded, but the left lung remains radiolucent . The mediastinum shifts to the right . The excursion of the left hemidiaphragm is limited FIG .

a From m the Dcpartments of Chest Diseases and Pathology, Rothschild Hadassah University Hospital and Hebrew University Hadassah Medical School, Jerusalem, Israel . Manuscript received January 19, 1962 .

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additional cases of hyperlucent lung and to discuss the controversial etiologic and pathophysiologic aspects of this condition . CASE REPORTS CASE t . An eighteen year old boy was admitted to the hospital in June 1960, with the complaint of exceptional dyspnea of eight months' duration . At the age of nine, he had a cough productive of large amounts of sputum, and in the following years he had occasional episodes of bronchitis . Physical examination revealed a normally developed patient with diminished expansion of the left hemithorax . Breath sounds were decreased over the entire left side of the chest and numerous small crepitant rales were heard posteriorly and anteriorly over the lower half of the lung . The heart showed no abnormality . Inspiratory and expiratory roentgenograms (Fig. 1) showed distinct hyperlucency of the left lung . On expiration the right lung became normally clouded whereas the left lung remained radiolucent . There was simultaneous shift of the mediastinal structures towards the right hemithorax . The excursion of the left hemidiaphragm was very limited . Bronchoscopy revealed that the main bronchi were normal except for the presence of some secretions . Bronchograms demonstrated that there was no alveolar filling, the subsegmental bronchi terminating abruptly in blind saccular expansions, like small pools . This peculiar pattern was uniform and was present throughout the entire left bronchial tree. (Fig . 2 .) Tomograms demonstrated that the left pulmonary artery was of a normal size but its lobar branches were sparse, thin and very short . There was a considerable decrease in vascular markings . Pulmonary function studies revealed the vital capacity to be 87 per cent of the predicted value and the maximum breathing capacity 70 per cent of the predicted value . Bronchospirometry confirmed that the impairment was unilateral . 'I he minute ventilation of the abnormal lung was almost normal, contributing to 40 per cent of the ventilation (instead of 45 per cent) but only to 25 per cent of the vital capacity and 10 per cent of the oxygen uptake . The systemic arterial oxygen saturation was normal . There were no pathologic changes in the electrocardiogram. The administration of antibiotics favorably influenced the clinical symptoms, but the roentgenographic findings remained unchanged .

n . S. C ., a thirteen year old boy was admitted to the hospital in January 1959 . One year prior to admission he had had an episode of rheumatic fever accompanied by a high temperature and pains in the joints . On that occasion, a routine roentgenogram of the chest showed a striking difference in the radiolucency of the two lungs . Past history revealed that he had inhaled a bean at the age of one year and was subsequently acutely ill. Since that time, a mild CASE

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2 . Case L . Bronchograms showing a "leafless tree" and peripheral pooling . There is no alveolar filling, the peripheral bronchi terminating abruptly in blind saccular expansions . chronic cough with some shortness of breath had been noted . Physical examination revealed a thin boy with markedly diminished expansion of the left hemithorax . Breath sounds were distinctly decreased and numerous crepitations were heard over the entire



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FIG . 3. Case IF. Inspiratory and expiratory roentgenograms reveal hyperlucency and air trapping in the left lung . left side of the chest . Accentuation of the first sound at the apex of the heart and a systolic murmur in this area were audible . The electrocardiogram showed right ventricular strain . Inspiratory and expiratory roentgenograms confirmed the hyperlucency of the left lung and revealed air trapping during expiration . (Fig . 3 .) Bronchoscopy showed normal openings of the major bronchi. Bronchograms demonstrated absence of filling of the peripheral bronchi of the affected lung with very numerous stops forming a sharp line of demarcation between the peripheral unfilled and the proximal filled parts of the lung . Some of the bronchi showed terminal bud-like formations . (Fig . 4 .) Tomograms demonstrated that the left pulmonary artery was small and its branches

Fm . 4. Case n . Bronchogram shows "peripheral pooling" : terminal bud-like formations without atelectasis .

decreased in caliber and number . The right lung showed increased vascularity. Pulmonary function studies showed a vital capacity of 80 per cent of the normal predicted value and a maximum breathing capacity of 55 per cent of the normal predicted value . Bronchospirometry revealed that the affected lung contributed 32 per cent of minute ventilation, 38 per cent of vital capacity and 18 per cent of oxygen uptake . The arterial oxygen saturation was normal . Four weeks of antibiotic therapy brought about a clinical improvement in the patient's condition . CASE in . A twenty-nine year old male machinist was admitted to the hospital in April 1961, with complaints of pains in the lower part of the thorax and of cough productive of large amounts of purulent sputum . Three months prior to admission he had had some episodes of hemoptysis . Past history revealed that from early childhood he had been prone to recurrent attacks of bronchitis . He was a chain smoker, smoking 60 cigarettes per day, and was also addicted to alcohol, hashish and morphine . Physical examination revealed a well developed man with diminished expansion of the left side of the chest . Breath sounds were distinctly diminished over the lower left side of the chest and sonorous rales were heard over this area . Inspiratory and expiratory roentgenograms showed a markedly hyperlucent lower lobe of the left lung which trapped air on expiration . (Fig . 5 .) Tomograms showed that the left main pulmonary artery and its upper branch were normal, while the lower lobar artery was small and its branches considerably decreased in caliber and number. (Fig . 6 .) Bronchographic examination revealed patency of the left main stem and of the lobar and segmental bronchi . The peripheral bronchi terminated in club-like formations ; there was absence of alveolar filling . Bronchoscopy showed normal bronchial openings and there was considerable hypersecretion . Pulmonary function studies showed the vital capacity to be 93 per cent of the predicted

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Frc. 5 . Case or. Fxpiratory roentgenograms showing air trapping in the left lower hyperlucent lobe . value, and the three second timed vital capacity 87 per cent of the predicted value. The maximum breathing capacity was reduced to 82 per cent of the predicted value . An attempt to perform bronchospirometry was unsuccessful because of the marked hypersecretion of the bronchial tree . The heart and the electrocardiogram were within normal limits. On May 25, 1961, left lower lobectomy was performed . At operation the pleural space was found to be obliterated . The lower lobe of the left lung was emphysematous, abnormally pink and showed no anthracotic changes . The bronchus of the lower lobe of the left lung was of normal size, but the accompanying pulmonary artery was rather smaller than normal and surrounded by enlarged lymph nodes . On gross pathologic examination the resected lobe was of normal size . The pleural surface of the basal segments contained many emphysematous blebs, measuring up to 2 cm . in diameter . The more centrally situated bronchi showed cylindrical bronchiectasis and fibrous thickening of their wall, while the more peripheral bronchi showed marked saccular bronchicctasis . These sacs in the ectatic bronchi were filled with viscous mucus and intercommunicated by narrow passages, forming the classic "string bead" or "necklace" bronchial deformity . (Fig . 7 .) The most striking feature on microscopic examination was chronic emphysema ; scattered atelectatic areas were also observed. In the emphysematous areas the bronchioles showed the picture of bronchiolectasis and chronic peribronchiolitis . (Fig . 8 .) Their lumens contained desquamated epithelial cells, mucus and a few leukocytes . Dilated and thick-walled bronchioles were also found in the immediate subpleural area . In the atelectatic areas a large number of pigmentladen macrophages were seen within the collapsed voc .

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Fro . 6 . Case in . Tomogram of the left lung showing normal vascularization of the upper lobe and marked oligemia of the lower lobe . alveoli and also within the respiratory bronchioles . The small arteries showed mild thickening of their walls but without obvious luminal narrowing . The patient made an uneventful recovery and was discharged two weeks after operation . CASE Iv . F . M., a thirty year old woman, was referred to the hospital for investigation in January 1955, after recovering from an acute pulmonary infection . She gave a history of recurrent infections of the respiratory tract and thoracic pains while in Nazi concentration camps during 1942-1945 . In 1953, following an acute pneumonic episode, a roentgenogram of the chest revealed increased hyperlucency of the lower lobe of the left lung . On examination, there was diminished expansion of the left side of the chest over which breath sounds were weak and accompanied by crepitations . A roentgenogram of the left side of the chest confirmed the abnormal

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Flu . 7. Case m . Saccular bronchiolcctasis intercommunicating by narrow passages ("string bead" appearance of the bronchus) . Fm . 8 . Case HT . Microphotograph showing chronic emphysema, bronchiolectasis and chronic peribronchitis (X 33) . translucency of the lower lobe and demonstrated a decrease of peripheral vessels in this area . On bronchoscopy, the major bronchi were normal . Bronchography revealed crowding of the bronchial tree in the lower lobe of the left lung without bronchiectasis . Studies of the ventilatory function of both lungs indicated reduction of the vital capacity (74 per cent of the normal predicted value) and of the maximum breathing capacity (62 per cent of the normal predicted value) . These values were only slightly improved after vaponephrin inhalation . The arterial oxygen saturation was normal . The patient was hospitalized again five years later because of a further infection of the respiratory tract . The findings on clinical and roentgenological examination remained unchanged, but she continues to refuse surgery . CASE V. M. F ., a thirty-nine year old woman, was admitted to the hospital in June 1961, with complaints of diffuse pains in the thorax and of cough productive of small quantities of purulent sputum .

Three months prior to admission she had suffered from high temperature and recurring hemoptysis . Her past history was not contributory . Physical examination revealed a well developed woman with diminished expansion of the left side of the chest . Breath sounds were very faint over the upper left part of the chest. Inspiratory and expiratory roentgenograms showed a markedly hyperlucent upper lobe compressing the lower lobe . (Fig . 9 .) Bronchoscopy revealed excess secretions in the left bronchial tree and normal openings of the main bronchi . Bronchography was performed twice but it was impossible to fill the upper lobe of the left lung . On October 5, 1961, a left upper lobectomy was performed . The pleural cavity was partially obliterated by fibrous adhesions . The entire upper lobe of the left lung was markedly emphysematous, pink and showed no anthracotic changes . The lower lobe was compressed by the overdistended upper lobe . The left pulmonary artery, as well as its branches, were of normal size . Enlarged lymph nodes surrounded the main arterial branches . On pathologic examination, the resected lobe was of spongy consistency . The medium-sized bronchi were filled with thick mucous plugs and the more peripheral bronchi showed saccular bronchiolectasis . The lack of filling with contrast medium at bronchography can be explained by obstruction of the medium-sized bronchi with mucous plugs, or by the high pressure of the trapped air in the emphysematous area . The patient made an uneventful recovery, although reexpansion of the lower lobe of the left lung was very slow . COMMENTS

Fm . 9. Case v . Marked hyperlucency of the left upper lobe and compression of the lower lobe .

Two hypotheses have been put forward to explain the condition of unilateral hyperlucent AMERICAN JOURNAL OF MEDICINE



Unilateral Hyperlucent lung . One maintains that this disease represents primary hypoplasia of a main branch of the pulmonary artery with bronchiectasis as a result of superimposed infection . The other postulates that the primary abnormality is an acquired obstructive process in the small peripheral bronchi, the emphysema being explained on the basis of multiple check-valve mechanisms . Hyperlucent lung with its decreased size and small pulmonary artery differs distinctly from the emphysematous lung which is usually enlarged in size and with a pulmonary artery dilated rather than contracted . However, the small size of the lung and of its pulmonary artery is not a constant feature of unilateral hyperlucent lung . In the cases in this report, for example, the affected lung was always of normal size and the pulmonary artery was diminished in size in Cases n and in only . The smallness of the pulmonary artery, or even its absence as visualized in angiograms, does not necessarily mean vascular hypoplasia or agenesis . The patient of Swyer and James [1] had a much larger pulmonary artery at surgery than was suspected from the preoperative angiogram . We had an opportunity to study a patient in whom the left lung was destroyed by bronchiectasis and no filling of the left pulmonary artery was evident on the angiogram . However, at thoracotomy, the artery was patent and of normal size . (Fig. 10 .) This discrepancy is due to the hemodynamic changes associated with the development of the pulmonary collateral circulation, which consists mainly of marked enlargement of the bronchial arteries and of their anastomoses with pulmonary arteries . The object of this collateral circulation, which frequently occurs in chronic pulmonary diseases, is to block the inflow of unoxygenated pulmonary arterial blood to the diseased portions of the lung, thus helping to maintain a normal arterial oxygen saturation [21] . Studies of blood oxygen saturation at various sites in the pulmonary arteries during surgery for removal of a destroyed lung showed that there was a retrograde flow of blood from bronchial to pulmonary arteries [22,23] . At angiography in these instances, all the contrast medium flows to the normal lung . In this way, the illusion of agenesis of one of the pulmonary arteries arises, while in reality this vessel is filled with arterialized blood coming from the bronchial arteries . It is probable that some of the cases in which the diagnosis of agenesis of the main branch of VOL . 33, DECEMBER 1962

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Fm . 10 . Left bronchieetatic destroyed lung . Bronchography demonstrates typical "dove nests ." Angiography shows lack of filling of the left pulmonary artery . At operation, this vessel was found to be completely patent and of normal size .

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the pulmonary artery was made on the basis of the angiogram only [15,17,18] were in reality unilateral hyperlucent lung, the clinical, roent genological and bronchographical features being consistent with this diagnosis . In some cases of unilateral hyperlucent lung the small pulmonary artery corresponds to an actual failure of growth of this vessel (Case m) . This malformation should be considered as secondary to reduced lung function from early childhood, as the lung is known to continue its postnatal growth up through middle childhood . The high incidence of pneumonic episodes occurring in this growing phase, and which has been noted in most series of unilateral hyperlucent lung, suggests that bronchiolar obstruction during these infections causes permanent bronchiolar and capillary damage and arrests the development of the vessel . The case of Oswald [10], the only one in whom the actual onset of the disease was observed, provides evidence that such pneumonic episodes may be the cause of unilateral hyperlucent lung . Absence of the pulmonary artery as an isolated congenital defect is an extremely rare condition . Of thirteen published case reports of this condition [29,30] only six cases were actually proved surgically or at autopsy . In the others the diagnosis was made on an angiographic basis only . The lung of true congenital hypoplasia or agenesis of the pulmonary arteries differs greatly from the unilateral hyperlucent lung . It, too, is an oligemic lung, but not an emphysematous one . It is commonly associated with major congenital cardiac defects when the pulmonary vascular malformation is present on the left, and pulmonary defects when the malformation is present on the right [26,27] . We investigated two cases of congenital absence or hypoplasia of the right pulmonary artery, which were associated with unilobar hypoplastic lung, anomalous drainage of the pulmonary vein into the inferior vena cava and dextroversion of the heart . The bronchograms revealed a hypoplastic bronchial tree with abnormal distribution of the bronchi, but no bronchiectasis . Moreover, the expiratory roentgenograms showed no air trapping in the affected lung [28] . The histologic examination in such cases shows uniform fibrosis with thickening of intra-alveolar septums but no emphysema [26] . Faulty development of the pulmonary artery is accompanied also by anomalous pulmonary arteries arising from the aorta . The aortic com-

ponents compensate for the deficiency in the pulmonary artery channels . 'these congenital abnormalities have never been found in the unilateral hyperlucent lung . The fact that the left lung was the affected one in all five cases in this report should be considered a coincidence . In thirty-eight cases of unilateral hyperlucent lung reported in the literature, the disease was localized on the right in seventeen cases and on the left in twenty-one . Bronchospirometry in unilateral hyperlucent lung shows that although the affected lung ventilates well, there is a poor oxygen uptake . However, the arterial oxygen saturation is normal . There is no shunt of non-aerated blood because the normal lung offers an alternative route for the pulmonary arterial blood . Bronchography shows that the site of the check-valve obstruction lies in the medium-sized bronchi, i .e ., the first, second and third order bronchi, distal to the segmental bronchi . Pathologic examination confirms these findings showing "string bead" appearance of the bronchus . The peripheral "pool" observed in our bronchograms was only the first sac in a long "necklace" of sacs, the lipiodol being unable to pass through the narrow communications linking the sacs of the ectatic bronchus . The entire bronchial tree is affected, including the smaller bronchi of 2 mm . or less in diameter . The small peripheral buds joined to the bronchial ramifications by very fine connections, seen especially in Case I, correspond to the emphysematous spaces of centrilobular type described by Leopold and Seal [25] . As seen in the pathologic specimens in Cases in and v, many bronchial passages are completely obstructed by mucous plugs . The absence of larger areas of atelectasis in these cases should be explained by collateral ventilation from interbronchial communications of intersegmental or interlobular type [24] . The air reaching the affected areas from the healthy lobules is trapped exactly as in obstructive emphysema . Krahl [31] experimentally produced pulmonary emphysema by passing a valve into the bronchus of the lower lobe of the right lung of rats, where it stayed for periods ranging from eighteen to seventy-one days . The pulmonary tissue of these rats showed a general increase in the diameter of the peripheral airways and degeneration of interalveolar septums . The altered tissue, stained selectively for elastics, revealed marked alteration in the AMERICAN JOURNAL OF MEDICINE



Unilateral Hyperlucent Lung-Rakower, Moran quantity and arrangement of the elastic fibers . As elastic and collageneous fibers are lost, the interalveolar capillary network becomes progressively more stretched, ruptures, retracts and disappears . The history of Case it in this report, and one of the cases of Margolin et al . [8] prove that a foreign body in one of the large bronchi can be the etiologic factor of unilateral hyperlucent lung . More frequently, however, as was shown by McLean [32], the seat of origin of the inflammation and air trapping leading to pulmonary emphysema lies peripheral to the bronchi, namely, in the bronchioles . The treatment for unilateral hyperlucent lung is guided by the extent of the symptoms . Antibiotic agents are used to control acute infections and minimize chronic ones . Prolonged antibiotic treatment in low doses should also be tried . A hyperlucent lung or lobe, when associated with definite symptoms such as cough, sputum, recurring episodes of infection, recurring hemoptysis, which interfere markedly with work and which do not react to conservative treatment, is an indication for surgery . SUMMARY

Five cases of unilateral hyperlucent lung are reported . The main roentgenologic features of this disorder are hyperlucency, oligemia, air trapping during expiration and an unusual bronchiectatic pattern . Unilateral hyperlucent lung should be considered the issue of an acquired inflammatory condition with damage of the peripheral bronchial passages . This damage results in a peripheral obstructive process with emphysema and bronchiolectasis, and functional insufficiency of the pulmonary arterial channels . This secondary insufficiency should not be mistaken for agenesis or congenital hypoplasia of the pulmonary arteries, conditions which are generally accompanied by major cardiovascular or pulmonary anomalies . The role of acquired systemic-pulmonary arterial shunts in the pathophysiology of the hyperlucent lung is discussed and their influence on the pulmonary angiographic pattern is explained . REFERENCES

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pulmonary arterial circulation . Report of two cases. Am . Rev . Tuberc . Pulm . Die, 79 : 641, 1959 . 18 . WIER, J . A . Congenital anomalies of the lung . Ann. Int . Mad., 52 : 330, 1960 . 19 . CARMAN, C . T . and MORROW, M . Chest conference.

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24, VAN ALLEN, C . M . and LINDSKOG, G . E . Collateral respiration in the lung . Role in bronchial obstruction to prevent atelectasis and to restore patency . Surg . Oynec. & Obst ., 53 : 16, 1931 . 25 . LEOPOLD, I . G. and SEAL, R. M . The bronchographic appearance of "peripheral pooling" attributed to the filling of centrilobural emphysematous spaces . Thorax, 16 : 70, 1961 . 26 . MAIER, H . C . Absence or hypoplasia of a pulmonary artery with anomalous systemic arteries to the lung . J. Thoracic Surg ., 28 : 145, 1954 . 27 . FLEMING, H . A. Absent left pulmonary artery and right sided aortic arch in Eisenmengcr's complex . Thorax, 13 : 272, 1958 . 28. ROSENBERG, S ., SCNwARTZ, A . and RAKOWER, J .

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