Document 82oop7MJXKOGQDOxZ9BjOKQ2d

J: Electrocarterization. Bus I: Induction of uring electro10-65. in the cardiac Ventilatory Failure Due to Asbestos Pleurisy hythmias. Am on catheter h . 975; 55-. 50V' i.s; catheter. IncL erence to venf on. Anesthesia _ es prophylactic^' associated with' ^esiology 1982; albert miller, m.d. ALVIN S. TEIRSTEIN, M.D. IRVING J. SELIKOFF, M.D. New York, New York DP: Therapeutic j Janesthesia for,, Med 1979; 301; | Seven patients are described who had a distinctive syndrome of chest wall restriction caused by asbestos-induced pleural fibrosis. All had severe dyspnea and predominant pieurai disease on radio graphic examination, with pulmonary function findings of reduced vital capacity, total lung capacity (measured in five patients), and maxima! voluntary ventilation. Five patients had ventilatory failure with carbon dioxide retention; four of these have died and one is ! close to death. Examination of the thoracic organs in five patients showed minimal or no parenchymal fibrosis in three and less severe involvement of the parenchyma than of the pleura in the remaining two. Neoplasms were suspected in three patients because of ex tension of the pieurai fibrosis into the lung. Two of these patients had pieurai uptake of 67-gallium citrate attributable to the inflammatory reaction. With the increasing duration since onset of exposure in the nine million workers who have been exposed to asbestos, as well as in other exposed persons, it is expected that additional cases of ' ventilatory failure caused by asbestos-induced pleural fibrosis will be encountered. from the Pulmonary Division, Department of Heec*jcine (AM, AST), and the Environmental Ser ies Laboratory (US), Mount Sinai School of ""Seine of the City University of New York, New New York. This investigation was supported part by NlEHS Center Grant ES-00928 and by **Jack Mar.;:, fund. Requests for reprints should *Siressed to Dr. Albert Miller, Pulmonary J*oraiory, Artnenberg 24-26, Mount Sinai Hos- Y* t Gustave l. Levy Place, New York, New ^ 10029. Manuscript accepted June 13, It has not been recognized that ventilatory failure, cor pulmonale, and death may result from extensive pleural fibrosis caused by exposure to asbestos, even though little or no parenchymal disease is present. Benign pleural effusions, pleural fibrosis presenting as localized plaques or diffuse thickening, and pleural calcification are well-known complications of asbestos exposure. The recognition of these lesions has been emphasized, but their functional impact has received little attention and has generally been described as minor. We herein describe five patients who met the following criteria for ventilatory failure due to asbestos-induced pleural fibrosis: (1) exposure to asbestos in the absence of other pleuropulmonary disease; (2) severe dyspnea (grade 3 on the British Medical Research Council three-point scale [1]); (3) vital capacity and total Jung capacity (measured in four patients) of less than 50 percent of predicted; (4) maximal voluntary ventilation of less than 80 percent of predicted; (5) carbon dioxide retention (Paco2 of 52 torr or more); (6) absence of airway obstruction: ratio of one-second forced expiratory volume to forced vital capacity of more than 0.75; (7) predominant pleural disease evident radiographically (all five patients) and on examination of the thoracic organs at surgery (three patients) or autopsy {one patient). In addition to these five patients with carbon dioxide retention, we have encountered others with a similar but less severe pattern of functional impairment. We report two representative cases without carbon dioxide retention to illustrate the range of physiologic find ings. ' December 1983 The American Journal of Medicine Volume 75 911 ASBESTOS PLEURISY--MILLER ET AL TABLE I Clinical Findings in Seven Patients with Asbestos Pleural Fibrosis Palienl 1 2 Asbestos Exposure insulation Insulation 3 Insulation 4 Aboard ship 5 Shipyard 6 Insulation 7 Insulation Lung Tissue Necropsy Bilateral thoracotomy Thoracotomy Thoracotomy None Thoracotomy None Significant Pulmonary Fibrosis* No No Yes No No Yes No Observed Pleural Effusion NA No No Bilateral Recurrent Yes Yes Pleural Uptake of Gallium Outcome NA Negative Positive Negative NA Positive NA Cardiorespiratory failure, death Cardiorespiratory failure, improvement after first decortication, death Cardiorespiratory failure, suspected neoplasm, death Cardiorespiratory failure, suspected neoplasm Cardiorespiratory failure, death Cardiorespiratory insufficiency, suspected neoplasm Dyspnea on exertion NA = information not available. Three of the total of seven patients described were suspected of having neoplasms of the pleura or lung because of extension of pleural fibrosis into the lung. The seven cases reported herein, together with others recently described [2], exhibit a distinctive picture of restrictive ventilatory impairment with en trapment of the lung due to asbestos-induced pleurai fibrosis. This is to be differentiated from the betterknown restrictive impairment due to asbestotic inter stitial fibrosis. Asbestos pleural fibrosis is another cause of chest bellows dysfunction that has been reported with post-traumatic or postempyematous fibrothorax. With many patients from the huge pool of asbestos-exposed workers (estimated to number more than nine million) [3] now presenting with asbestos-induced disease, resulting ventilatory insufficiency will be increasingly common. It is important, for legal and financial con siderations, to recognize asbestos exposure as the cause and, for clinical considerations, to separate pleural from parenchymal fibrosis as the mechanism for ventilatory failure, because management and the role of surgery differ. PATIENTS AND METHODS A prospective study was begun when Patient 2 had the same relation between asbestos pleural fibrosis and ventilatory failure that we had noted previously in Patient 1. All patients were hospitalized at the Mount Sinai Medical Center in New York City. Conventional pulmonary function tests were performed by standard techniques [4]. Predicted spirometric values were those of Morris, etal [5], as confirmed by our laboratory in an investigation of 229 normal nonsmoking adults [6]. For maximal voluntary ventilation, values were those of Baldwin et al [7], and for total lung capacity were those of Goldman and Becklake [8]. The single-breath diffusing capacity for carbon monoxide was not corrected for venous carbon monoxide or anatomic dead space. Prediction equations were those of Bates et al [9], as well as those derived by our lab oratory form a survey of 511 subjects randomly selected from the general population [10]. For the single-breath diffusing capacity for carbon monoxide/alveolar volume, alveolar volume was the single-breath helium-diiutional total lung capacity; predicted values were those from our survey [10]. Static pulmonary compliance was measured in three patients by the technique of Mead and Whittenberger [11] using an esophageal balloon pressure sensor. Spirometric values, maximal voluntary ventilation, and arterial gas values were obtained in ail patients. Patient 1 was studied before other techniques were available, Patient 5 could not tolerate the body plethysmograph, and Patients 4 and 5 were unable to hold their breath long enough to allow determination of the single-breath diffusing capacity for carbon monoxide. RESULTS AND SELECTED CASE REPORTS Clinical findings are summarized in Table I. All seven patients had progressive, severe shortness of breath. Additional symptoms were pleuritic pain or chest tightness and nonproductive cough. Pleural effusions were noted during the course in fotr of the seven patients described. These were recurrent or bilateral in two patients. Pleural thickening described at thoracotomy was predominantly parietal. When decortication was performed (in four patients), the pleural was described by the surgeon as a thick `'rind/ often 2 cm in thickness. This is illustrated in Figure 1 from Patient 3 and Figure 2 from Patient 6. !n all patients except one (Patient 5), the pleural fr. brosis was bilateral. This exceptional patient, who had dense fibrosis and calcification of the lower half of the left pleura on radiographic examination, died of cartx*. dioxide retention. ." The extensive pleural disease with the development of mass-like shadows on roentgenographic examination suggested mesothelioma or lung cancer in three of th seven patients. These were evaluated by scanning with 67-gallium citrate, which revealed uptake of the isotoP| in two patients who were shown to have pro!iferjj*S pleuritis but no malignancy at thoracotomy. Positiv? 912 December 1983 The American Journal of Medicine Volume 75 ASBESTOS PLEURISY--MILLER ET AL come >ry failure, death j )ry failure, improvement after ft i, death j >ry failure, suspected neoplasn, Dry failure, suspected neoplasrr Dry failure, death Dry insufficiency, suspected ne< '.ertion 1. Surgical view of the right >rax in Patient 3. The chest wall is id; the thickened parietal pleura is a clamp. The pleural space and retie visceral pleural are visible. dpi [10]. For the single-breath monoxide/alveolar volume, gle-breath helium-dilutional tl aiues were those from our surj ipliance was measured in threr tead and Whittenberger [1 l]i jressure sensor. j s, maximal voluntary ventilaj re obtained in all patients. Path techniques were available, j 5 body plethysmograph, and Ft i hnfW their breath long enougf! 3 e-breath diffusing cad LECTED CASE REPORTS e summarized in Tabfe f. A essive, severe shortness o >ms were pleuritic pain < productive cough. > were noted during the cour: nts described. These werer oatients. Pleural thickening^ vas predominantly parieta > performed (in four patie bed by the surgeon as a thic kness. This is illustrated in j Figure 2 from Patient 6. except one (Patient 5), the f al. This exceptional patient, J calcification of the lower h sographic examination, died< pleural disease with the dev Top, the surgical fieldcfur. ows on roentgenographic exj xacotomy in Patient 6. The park nelioma or lung cancer in th[ Irnsfan.o f w'ell demonstrated, the v nese were evaluated by scan from ,-dorlying lung. B , which revealed uptake of tjj removed parietal pleura. Its /h >re shown to have pro i thickness are well seen in m. ^,iancy at thoracotomy Hon. December 1983 The American Journal of Medicine Volume 75 913 . ASBESTOS PLEURISY--MILLER ET AL TABLE II Pulmonary Function in Seven Patients with Asbestos Pleural Fibrosis .`-X Patient Date Lung Compli MW ance VC TLC* (liters per (liters/cm DlCOsb Paco2 (ml) (ml) FEV1/FVC minute) H20) (ml/torr per minute) dlco/va (torr) pv? (torr) 1 1965 1,420 0.86 76 52-* 64 Sat 81% : (47) 2 10/72 1,420 2,440 He 0.97 (78) 60 - i* 41 70 preop 8/75 (33) 1,820 (41) 3,170 0.70 (59) 58 ' 9.2 3.5 39 85 ^ (43) (48) (55) (41 versus 36)T (89) 2/80 1,500 0.80 49 10.2 4.1 44 -- 70 55 ---y; 37 (51) (51 versus 40) (102) 3 1/75 2,200 3,760 0.84 . . . 9.9 3.1 75 8/78 (44) 1,030 (49) 2,810 0.98 68 0.03 (46 versus 31) (76) ' v&tei; 48 -- 70 63 '%&" preop (20) (36) (65) 4 10/77 1,370 3,650 0.96 74 51 77.:*(pr preop (28) (48) (74) 7/79 1,190 3,460 0.92 5 4/78 (25) 1,720 (39) (46) 0.89 50 (44) 66 >70 56 <45 X ' >r-> 6 2/78 1,940 4,080 0.87 79 0.05 17.1 5.6 41 77 Si* preop (34) (47) (54) (48 versus 55) (137) 12/80 1,780 3,530 0.65 60 34 71 ,e-:- (32) (43) (42) 7 5/77 2,720 4,150 0.86 78 0.07 20.7 5.9 34 88 (63) (66) (70) (85 versus 72) (122) Values in parentheses are percent predicted. . * Results are plethysmographic unless indicated (He = multiple breath helium dilution). T The first value is from reference 10, the second from reference 11. DlCO/VA -- ratio of carbon monoxide diffusing capacity to alveolar volume; DlCO$b - single-breath diffusing capacity for carbon monoxwe; FEV,/FVC = ratio of one-second forced expiratory volume to forced vital capacity; MVV = maximal voluntary ventilation; TLC = total lung capacity; VC = vital capacity. ^ findings on gallium scanning have been described in benign asbestos pleural disease [12]. In five of the seven patients (including four of the five with ventilatory failure), there was little or no radio graphic evidence of interstitial fibrosis. On examination of the thoracic organs at thoracotomy (four patients) or autopsy (one patient), palpable fibrosis of the lungs was absent in three and less prominent than the pleural fi brosis in the other two. Thoracotomy with decortication was undertaken in four patients. This was done to rule out a neoplasm in the three mentioned earlier and did not improve their clinical status, in part because the less involved side was surgically treated in two of them. In one patient (Patient 2), decortication of the more involved side was performed to improve respiratory function and resulted in a substantial increase in exercise tolerance and im provement in measured lung function. Decortication of the opposite side was recommended but refused by the patient until his condition was nearly terminal, at which time the procedure stabilized his condition and allowed withdrawal of mechanical ventilation. In all cases, the lung expanded well after decortication. ;.{ip# Results of pulmonary function tests are summarized in Table II. Of the five patients who had respiratory failure with carbon dioxide retention (Patients 1 to.5), four have died and one is severely disabled. The vital capacity was less than 50 percent of predicted in all five^ patients, ranging as low as 20 percent (1.03 liters)... Average was 33 percent of predicted. The maximal ; voluntary ventilation was reduced in all five (average ^, ; lowest value 44 percent of predicted) in the absence^ of airway obstruction. Indeed, the ratios of one-second^ forced expiratory volume to forced vital capacity were.. high (average 0.93, range 0.86 to 0.98), and flow rates = such as maximal mid-expiratory flow were reduce.dto : a lesser extent than the vital capacity, consistentjjjth* restrictive impairment. Full lung volumes were rag?.-?; sured in three patients; total lung capacity was reduG^' (less than 50 percent of predicted) in all. The singjgjsl breath diffusing capacity for carbon monoxide {$ sured in two patients) was reduced; the ratio of sing 914 December 1983 The American Journal of Medicine Volume 75 ASBESTOS PLEURISY--MILLER ET AL :o2 w) (forr) : 64 Sat 81%#*.. r '^r<-4 70 70 70 56 <45 m, vWW\ :Hi#ZT 71 <* mB:-i ;arbon monox^^-iS TLC - total luij}t^ all cases;* a e sumrrtanz' ad respirato itients l.toj Died. The^,^ licted In aijfivg t (1.03 liters The maxin e (average^ i the absegc of one-seccfig, capacity^ and flowra *re redti onsistent IS / Vvc.^ ( I. The* noxide^i atio of si breath diffusing capacity for carbon monoxide to al veolar volume was normal. Patient 6, who did not have carbon dioxide retention, had equally severe reductions in vital capacity, total lung capacity, and maximal voluntary ventilation. Although single-breath diffusing capacity for carbon monoxide was low, the ratio of carbon monoxide diffusing capacity to alveolar volume was increased. Patient 7 had a similar pattern but less severe reductions in forced vital capacity, total lung capacity, and maximal voluntary ventilation. In this patient, the ratios of one-second forced expiratory volume to forced vital capacity and sing'e-breath diffusing capacity for carbon monoxide to alveolar volume were increased. Pulmonary compliance was measured jn three pa tients, with (Patient 3) and without (Patients 6 and 7) carbon dioxide retention; it was markedly reduced in all three. Patient 1. Born 1912 and a nonsmoker, the patient had been an insulation worker from 1929 to 1946 and again from 1959 to 1961, with lesser exposure in intervening years. In 1963, routine chest radiography revealed bilateral infiltrates with extensive pleural thickening and pleuropericardial ad hesions. Clubbing and rales were noted on physical exami nation. The vital capacity was slightly reduced (72 percent of predicted). Over the next two years, dyspnea and signs of right heart failure developed. On his first admission to the Mount Sinai Medical Center on November 12,1965, the vital capacity was 1,425 ml (47.5 percent of predicted). Arterial oxygen saturation was 81 percent at rest and 68 percent on one minute of step-up exercise; Paco2 was 52 torr. The pa tient was readmitted in April and in October 1966, at which time Paco2 was 64 torr. The patient's condition continued to deteriorate; tracheostomy was performed, and the patient died on December 11. Postmortem examination revealed marked thickening of the parietal and lesser thickening of the visceral pleura. The lung parenchyma showed only minimal fibrosis. Right ventricular hypertrophy was observed. Patient 2. Born 1916, this patient had been an insulation Worker from 1939 to 1956. In 1963, he was found to have radiographic changes consistent with asbestos exposure; spirometric results were normal. He had smoked two pack*9$ of cigarettes per day beginning at age 14 but stopped smoking at this time. In 1972, he noted increasing shortness of breath and a 35-pound weight loss. Chest film (Figure 3, top) now showed massive bilateral pleural thickening, greater 00 the left than on the right. Pulmonary function tests revealed severe restrictive impairment (vital capacity 33 percent and total lung capacity 41 percent of predicted) with maximal voluntary ventilation 59 percent of predicted. Left pleurectooiy was performed to improve pulmonary function. The Pteura showed dense fibrosis, chronic inflammation, and .areas of neovascularization and hemorrhage. Hyperplastic ^osothelial cells, neutrophils, and fibrin on the pleural surface fro noted histologically. Postoperatively, the patient had Pn<ed improvement in exercise tolerance. Previously unable across the room, he was now doing household chores 5 . shopping. The vital capacity increased 400 ml (31 per- s <* - .....................' Figure 3. Top, Chest roentgenogram of Patient 2 in 1972 showing massive bilateralpleural thickening greater on the left and involving the lower two thirds of the thorax. Bottom, Patient 2 in 1980, eightyears after left decortication showing extension of pleural thickening at the right base. cent) compared with the preoperative value. This improve ment was maintained until 1979, when he noted increasing dyspnea and limitation in activities. The pleural thickening on the right side had progressed, as seen in Figure 3, bottom. Decortication was advised but deferred by the patient. By August 1980, vital capacity had decreased 320 ml (18 per cent) and maximal voluntary ventilation 9 liters per minute (16 percent) from their values in 1975. The patient required permanent mechanical ventilation through a tracheostomy. December 1983 The American Journal of Medicine Volume 75 915 ASBESTOS PLEURISY--MILLER ET AL Figure 4. Chest roentgenogram of Patient 6 showing bi lateral pleural thickening greater on the left. On the right side, the short fissure is thickened and depressed, and there is a density medial to this that had not previously been noted. He had upper gastrointestinal hemorrhage in January 1981. In April, right pleurectomy was performed. Pulmonary artery and right heart pressures were increased, although pulmonary capillary wedge pressure was normal. The parietal and vis ceral pleura were markedly thickened. The lung, which was described by the surgeon as "trapped," expanded well at the 'end of the procedure. Postoperatively, the patient's condition improved enough to allow him to perform the activities of daily living with a permanent tracheostomy but without me chanical ventilation. He died one year later at home. Patient 6. Born 1935, this patient had been an insulation worker from 1955 to 1977. He had smoked two packages of cigarettes a day from 1953 until 1967, when chest radiog raphy showed progressive bilateral pleural thickening, greater on the left side. From 1973 to 1977, the patient noted in creasing shortness of breath. In 1977, a new density was seen in the right mid-lung field (Figure 4). The vital capacity was 34 percent and the maximal voluntary ventilation 54 percent of predicted. Transbronchial as well as percutaneous lung biopsy performed because of suspicion of bronchogenic carcinoma revealed pulmonary fibrosis and ferruginous bodies. Gallium scanning demonstrated increased activity in the right mid-lung field, corresponding to the abnormality seen on chest roentgenography. Thoracentesis showed a markedly thickened pleura. Protein concentration of the pleural fluid was increased. No abnormal cells were seen. Needle biopsy of the pleura revealed dense fibrosis with areas of inflammation and hemorrhage. Computed tomographic scanning revealed extensive pleural thickening on the left and pleural thickening on the right, continuous with a mass-like density intruding anteriorly into the lung (Figure 5). Because mesothelioma or lung cancer could not be ruled out, right thoracotomy was performed in March 1978 (Figure 2, top) even though pleural involvement was greater on the left side. The parietal pleura was thick and rigid, described in the surgical report to be "like shoe leather" (Figure 2, bottom). The mass density seen on computed tomographic scanning proved to be a projection of visceral pleura into the middle lobe. The pleura was densely hyalinized, showing areas of neovascularization, chronic inflammation, and necrosis of collagen with neutrophils. An acute fibrinous exudate was seen on the surface. After parietal and visceral pleurectomy the lung expanded well. The patient still had dyspnea on minimal exertion when last seen 18 months after pleurec tomy. The vital capacity was now 32 percent of predicted, similar to the previous value, but the maximal voluntary ventilation had decreased further to 42 percent of predicted. The left hemithorax showed progression of the pleural iiv volvement, and decortication was advised but refused by the patient. . 'SZii Comment: This patient resembles the first five:jte degree of dyspnea, the pleural findings on radiography) computed tomographic scanning, and thoracotomy, and _ the reduction in pulmonary function were of similar severity. He differs only in the absence thus far of car bon dioxide retention. . Patient 7. Born 1937, this patient had been employed as an insulation worker from 1952 to 1969. He had smoked more than two packs of cigarettes per day from 1954 to 1975, at which time he presented to the Mount Sinai Medical Center with dyspnea on exertion of one year's duration. Six months previously, he had been hospitalized elsewhere for pleural effusions. Chest radiography revealed bilateral pleural thickening more extensive on the right, with calcification. Pulmonary function tests showed moderate restrictive im pairment. Despite the reduction in total lung capacity, the single-breath diffusing capacity for carbon monoxide was well preserved. Arterial gases were normal except for a slightly 916 December 1983 The American Journal of Medicine Volume 75 ASBESTOS PLEURISY--MILLER ET AL 3 i tire left side? increased alveolar-arterial gradient for P02 (18 torr). The J, ^scribed in patient declined further evaluation. (Figure 2, bottoiffis - Comment: This patient has a pattern of ventilatory lographic scanning impairment similar to, but less severe than, that in the iura into the midSi^j other six. l, showing areas' m, and necrosis11 COMMENTS inous exudate'll scerai pleurectc iil had dyspnea5 nths after pleurl Hyaline and calcific plaques, diffuse thickening, and obliteration of the costophrenic angles are recognized . pleural consequences of exposure to asbestos. They ;rcent of predicte maximal volunt srcent of predi'c are specifically coded by the Internationa! Labor Office , [oentgenographic classification [13]. Pleura! findings >on radiographic examination are more common In n of the pleura? "(certain cohorts than is interstitial fibrosis. Minor re- d but refused byj .ductions in lung function have been reported in asbestos ?s the first five^ igs on radiograg d thoracotomy?! ^workers with these pleural abnormalities [14--16]. Diffuse pleural thickening was associated with venti- tlatory impairment on submaximal exercise testing J[17]. ' - >n were of sirm >ce thus far'of! - virj ^ Pleural fibrosis so severe as to result in ventilatory ` failure has not been reported. Wright et al [2] described been employe ie had smoked! m 1954 to 197.' inai Medical1 uration. Six m. 5ewhcre for'^le d leral v six cases with marked pleural thickening that resulted {)r\ entrapped lungs. These patients had grade 1 dyspnea v on the British Medical Research Council scale (walking > stairs or hurrying on level ground) and had no evidence Sfor respiratory failure as did the first five patients de li scribed herein. The pattern of physiologic impairment -(was otherwise quite similar. The vital capacity was , Wiu i calcificafi irate restrict^ lung capacit i monoxide was] r decreased, although much less so than inour first five patients (mean 69 versus 33 percent of predicted), but i the ratio of one-second forced expiratory volume to ^forced vital capacity was high. The authors emphasized except for a sIh iyhat although single-breath diffusing capacity for carbon J,monoxide was decreased, the ratio of carbon monoxide 4#ffusing capacity to alveolar volume was high. Sterling Herbert [18] reported six cases similar to those of `iWright et al. |;.Jhe dyspnea, which was so prominent a symptom |jn all our patients, and the carbon dioxide retention, pWch supervened in five, can be explained on the basis increased work of breathing and dead space ventiJffion secondary to decreased lung volumes and chest II compliance. Relative preservation of gas transfer despite re- Sroion in lung volumes (high ratio of carbon monoxide ;ing capacity to alveolar volume) fits the pattern v'entrapped lung" that may be seen in musculo|5jetal disorders (for example, kyphoscoliosis) or Agjffal disease (such as, fibrothorax resulting from old |S?Pyema or asbestos-induced pleurisy). The reduction journal voluntary ventilation, present in all seven of n of the, a/ *k!okenk % T?/ou>tf IodS^ patients, Is consistent with impairment of the chest L'$Ws- Reduction in maximal voluntary ventilation is 'scteristic of kyphoscoliosis [19]; its absence has jH.stressed in asbestotic interstitial fibrosis [20]. Recently, Britton [21] demonstrated a significant decrease in vital capacity in asbestos workers that correlated with increasing pleural abnormality. When subjects with different degrees of pleural involvement were analyzed by holding constant the degree of in terstitial fibrosis (profusion rating), the vital capacity decreased with increasing pleural involvement in each category of interstitial fibrosis. The investigator con cluded that pleural involvement alone can result in disability. Measurement of pulmonary compliance does not separate pleural from interstitial fibrosis. The usefulness of esophageal pressure recordings in the presence of gross pleural disease is questionable [2]. Pulmonary compliance was markedly reduced both in our series (three patients) and in others' [2,18]. In the seven patients we describe, four had one or more known episodes of pleural effusion. Benign pleural effusions due to asbestos inhalation have been de scribed by several investigators [22-30], although a few of these cases resulted in mesothelioma after a period of time [23,30]. The latent period for benign pleural effusions is shorter than for all other compli cations of asbestos exposure. It is the only manifesta tion seen within 10 years of onset of exposure and the most common abnormality within the first 20 years. Epier et al [30] reviewed serial roentgenograms of 1,135 workers and noted 34 cases with effusion. Inci dence was related to intensity of exposure and was 9.2 cases per 1,000 person-years for heavily exposed workers. Prevalance was 7 percent in this group. Fewer than 10 percent of the workers with effusions had sig nificant parenchymal fibrosis. In follow-up study, vir tually all subjects with effusion showed blunted costo phrenic angles and 54 percent showed diffuse pleural thickening. Diffuse pleural thickening was generally a sequela of acute effusion. By contrast, in the more numerous workers with pleural plaques, there was no relation to effusion. Review of cases in the literature as well as of the patients presented herein suggests that the intense pleural inflammation secondary to asbestos, which often manifests itself as an effusion, eventuates in the extensive pleural fibrosis we observed. The effusions are exudative and often bilateral and/or recurrent. Since they may be small and asymptomatic [30], they may go undetected and their relation to consequent pleural thickening remain unrecognized. Herbert and Sterling [31] described granulation tis sue organizing a pleural exudate. Dense fibrosis ex tended into the interlobular septa. The series of 12 patients with asbestos effusions described by Gaensler and Kaplan [23] included four who underwent decort ication (one patient had bilateral procedures) "to es tablish the diagnosis, to restore pulmonary function, and December 1983 . The American Journal of Medicine Volume 75 917 ASBESTOS PLEURISY--MILLER ET AL to prevent recurrence.' ' Many findings at thoracotomy were similar to those in our patients. The pleura was vascular and thickened (up to 2 cm). There were areas of fibrinous exudation, vascularization, and proliferative mesothelium. The lung was partially atelectatic but in flated readily after decortication. Physiologic studies when no effusion or the least residual was present re vealed restrictive changes in three patients. In one of these, the maximal voluntary ventilation was also re duced. Navratil and Dobias [32] described seven patients in Czechoslovakia with "pleura! hyaiinosis complicata" whose courses were marked by acute inflammation with effusion. This was followed by diffuse pleural thickening and restrictive impairment. Unfortunately, no lung function or arterial gas data were reported. Some degree of interstitial fibrosis is likely in all patients with pleural changes induced by asbestos, since the offending fibers are thought to reach the pleura by way of the parenchyma and lymphatics. Nevertheless, in five of the seven patients we describe, there was little radiographic evidence of interstitial fi brosis. Even when the thoracic organs were examined, in three of these five patients, palpable fibrosis of the lungs was absent and the jungs expanded well after decortication. We cannot state whether microscopic evidence of interstitial fibrosis was present in these three patients. Biopsy specimens of grossly normal lung were not obtained because surgery was undertaken to improve severely limited lung function and/or to rule out neoplasia. , Two patients had radiographic evidence of interstitial fibrosis and are indicated as having "significant pul monary fibrosis" in Table I. Their interstitial fibrosis was less prominent at thoracotomy than was their extensive pleural involvement. In these two, and in the other five patients, the physiologic pattern was more consistent with entrapped lung rather than with interstitial pulmcH nary disease. . Progressive weight loss, bloody pleural effusions, and extensive pleural thickening with mass-like shadows on radiographic examination strongly suggested mesothelioma or bronchogenic carcinoma in three patients. Differentiation couid not be established by gallium scanning. Of the malignant mesotheliomas scanned at this institution, 12 percent failed to take up 67-gallium citrate [12]; however, uptake was demon-' strated in two of our three patients who had extensive/ nonmalignant pleura! disease. Because closed pleural' biopsy was believed to be unreliable, the diagnosis in these three patients was established by careful exam ination of the large amount of tissue removedJit decortication. The need for diagnosis impelled surgical' intervention on the less encased side in two of the three patients. . Similar "pseudotumors" secondary to asbestos havd - been reported by Hillerdal and Hemmingsson [33]. These were localized fibrotic thickenings of the visceral pleura and underlying lung parenchyma. Based on our experience in Patient 6 and Hiilerdal's experience in three cases, computed tomographic scanning is valin able in recognizing pseudotumors but may not obviate the need to establish a histologic diagnosis. This can be accomplished by thoracotomy, as in pur cases, or by thoracoscopy [34]. ,c-^3h When pleurectomy was performed (in four of pur patients), the underlying lung was noted to expand well.Since the functional impairment is due to entrapment' of lung by fibrocalcific pleura, pleurectomy may irfh' prove ventilatory function. Our experience (one patient) with this procedure for this purpose rather than for di- agriosis is insufficient to allow any generalization':^ 'ViTfV'V REFERENCES 1. MRC Committee on the Aetiology of Chronic Bronchitis: Standardized questionnaires on respiratory symptoms. Br Med J 1960; 2; 1666. 2. 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