Document RpJxk7wqqG9q7r4YxmpXpq5pk

Pleural Asbestosis H. 3. EISENSTaDT, M.D. Medical Clinic, Port Arthur, Texas Asbestosis is a form of pneumoconiosis occa sionally encountered. The author points to the pleural reaction which may result with no gross or x-ray evidence of involvement of the parenchyma. The presence of asbestos was histologically proven in three of the reported cases. ASBESTOSIS is a respiratory disease causedby the inhalation of asbestos particles, ' mineral substances composed of mag nesium iron silicates that, form long flexible parallel fibers. These fibers possess a great ten sile strength, are resistant to heat, alkalies and acids, can be spun into yarn, and woven into textiles.1" Such properties make asbestos an important material for various industrial uses. Asbestos is needed in the manufacturing of blankets, clothing, threads, rope, tape, braided tubing, brake lining and brake blocks, wall paper, wailboard. shingles, firebricks, floor cov ering and plastics. Asbestos is mixed with ce ments and plasters. It is used as insulation material for houses, pipes, boilers, ranches, wire, heaters, ironing boards, heating pads, automo bile and machinery parts, etc.3-5- u-Due to the rapid expansion of its use, ait ever-increasing number of craftsmen and Laborers are exposed to this mineral. Recently, for instance, an aucomobile mechanic was reported to have acquired asbestosis while undercoating vehicles.3 In ad dition to personnel handling the material, other's not directly in contact may be exposed through air pollution.-'1 AMERICAN PRACTITIONER September 1962 Fortunately, not all workmen acquire this dis ease. It has been estimated from animal experi ments that13 at lease five million particles per cubic foot have to be present in the air to pro duce svmptoms. Onlv fibers ot a certain length hoc less than JO ami not more than 50 microns) seem to Ire dangerous." The exposure must be prolonged, and an individual sensitivity muse be present. Xevertheies.s, a greater number of pa tients suffering from asbestosis can be expected in the future. Manv of them may not obtain a correct diag nosis. The latter depends essentially on the history of exposure: in addition, the clinical pic ture of the disease will aid in its recognition. The discovery of the rod- and club-shaped as bestos bodies in tire sputum is of great signifi cance because it proves chat coucaet with asbestos dust has been made. Unfortunately, these bod ies which consist of mineral fibers covered by proteinaceous material are not expectoraced very often. The final proof of the disease depends on the demonstration ot chese particles inside the lung tissue (Fig. 1). This requires lung biopsy or autopsy.-5 The history of exposure to asbestos is often obscure because workmen are not aware that they are handling this material. In addition, it cakes five to ten years oE contact to develop symptomatology. Therefore, a pa tient may not realize that his ailment is con nected with his occupation. Furthermore, die svmDtoms appear graduailv and are nonspecific.11 Thev consist of tacieue. anorexia, weight loss, weakness, dvspnea. cough and expectoration. The physical examination may show a few basal rales, a mild evanosis and some clubbing of 573 sis can present itself as an idiopathic pleural dis ease without any obvious parenchymal manifesta tions. This pleurisy may be acute, subacute recurrent or chronic, ft may be unilateral or bi lateral.' It usually airects the lower lung fields, but mav involve an upper portion.6 The char acter of this pleurisy varies considerably. It rnav be a mild, self-limited disease; it may appear as a prolonged or recurrent disorder; or it mav be a primary malignancy of the pleura. Such pleural forms of asbestosis frequently es cape recognition as shown in the following three illustrative cases. Case 1. A 54-year-old white male had worked as an insulator for a number of years. In September, 1960, he suffered from a left-sided pleurisy. An x-ray film seemed to reveal a small pleural effusion. However, this diagnosis was not verified by thoracentesis because of the benign course of the disorder. The patient recovered completely from this episode. In March. 1961, a similar attack of pleurisv ap peared on the other side. At this time the symptoms were more severe, consisting of chest pain, nonpro ductive cough, anorexia and weight loss. A loud fingers.1,1 Initial chest x-rays will be negative.'-1 A defect ot pulmonary function, however, may already be present in the form of ;m nlveolarcapillarv diffusion block. Unfortunately, spe cial equipment is needed to demonstrate such a deficiency, and the customary spirometric tests for lung volume reduction and airway obstruc tion are usuailv non-revealing.--In the more advanced stages of asbestosis the chest film will show <ome abnormalities. There mav be bilateral basal fibrosis, groundglass clouding or lione\combing of the lower portion ot the lungs. Large noduiations similar to those ot silicosis are seldom seen, and localized areas of consolida tion--usuailv caused bv superimposed infectionare still more uncommoniv encountered." Ail investigators agree that pleural changes occur frequently in a-be^tosis. uarticuiarly oblit eration of the phrenicocostal sinuses, pieural "tents." plaques and calcifications as well as olcuromediastinal adhesions that are responsible for the so-called "shaggv heart." " However. it has not been sufficiently- emphasized that asbesto 574 Vol. 13 No. 9 AMERICAN PRACTITIONER iricticm nib could be heard over the right base.as well as 11:>c percussion note and suppression of breath sounds. An x-rav picture showed pleural effusion ,'Fis'. _). I'ulmonnrv abnormalities were minimal. The sputum contained streptococci and staphylococci but no asbestos bodies. The sedimentation rate was S3 nun. per hour (Westergrcn). The Latex agglutina tion was positive in a 1:80 dilution. L.E. ceils were absent in the peripheral blood smear: die tuberculin skin test was negative. A thoracentesis yielded 530 cc. of a sterile brown-colored fluid. It contaflSjd neither malignant cells nor acid-fast bacilli. The patient was placet! on a medical regimen consisting of bed rest, antituberculous medications and high caloric diet. About one month later, however, a sec ond pleural tap became necessary. The same thora centesis fluid was encountered. Soon afterwards a thoracotomy was carrietl out be cause of persistent symptomatology. The surgical exploration revealed pleural adhesions with partial obliteration of the pleural cavity. The visceral pleura was as thick as an orange peel: therefore, a decortica tion was performed in addition to a lung biopsy. All svmptoms disappeared after this operation, and the patient was restored to good health shortly hereafter. The pathologist i'Dr. Stuart Wallace. St. Mary's Hospital. Port Arthur) found "large amounts of dense connective tissue with infiltrates of lymphocytes and rtccsz 3 AMER1CAN PRACTITIONER September 1962 eosinophiles in tiie pleural sections. Along the pleu ral edge were giant cells surrounding small, tags of necrotic tissue (Fig. 31. The lung section resettled thickenmg of the alveolar walls with macrophages and asbestos bodies (Fig. 1)." Case 2. A 37-year-old refinerv foreman noticed a pleuritic tvpe of pain in his left side ior a number of venrs. His discomfort was attributed at first to roronarv artery disease and later to an irritabic bowel avndrotne. However, there wa never a typical an ginal pain nor a characteristic gastro-intestinal dvs- function. In addition, nitrogiveerin. anttsoasmociics. diet and bowel regulation brought no relief. On the torurarv. the pain became gradtsaiiv unbearable. One tiav. unexpected!'', a chest film showed a !?:': idee! pneumothorax widi effusion :'Fig. -} . No cause of this pleural complication could be elicited. Over a period of several months this aneumothorax was graduuih replaced b--' a nbrotitorax trig. eince '.he pain pefsi'ied a thoni oicim wa* undertaken ..itich revealed onjv connective tivue thickening. Howe'er, the patient continued to go downhill after the operation, and final!' destruction o: a rib was discovered during a follow up sunn. A biops' o: this region revealed pleural mesothelioma. The pa tient died short;' afterwards, but no aucopsv permit was granted. This case was originally reported bc- 575 ^Ipu VM\* :*$ Ficurf. 5 cause of die raritv of the malignant lesion and the difficulties of its diagnosis.5 However, in retrospect, the patient was exposed to asbestos work for many years and apparently suffered from asbesiosis. This disease had produced a partial symphysis of the pleura 10 which separated the cavity entered by the surgeon from the site of the malignant tumor. L'nfortunatelv, no lung biopsy was obtained in any of the explorations. Such a specimen would have been necessary 10 confirm die diagnosis. Case 3. In January. 1959. a 5S*year-oiti oil refinery foreman who had worked with asbestos insulation for manv vears suffered from an acute left-sided hemor rhagic oieurai effusion. Ten years earlier he had been hospitalized for a long time because of bilateral oieurisw He made a complete recovers-, however, ever since this episode, bilateral pleural calcifications `Fie. o -- were visible on x-ray picture'.. In 1959. increasing chest pains, progressinz weight loss and atvoica! ceils in the thoracentesis iiuid ieaci to an exoioruiorv thoracotomy.5 This procedure re vealed oicurai svmplnsis with piaoues and adhesions. Micro>cooic examination of tiie pieura! specimen showed onlv non-specific granulomas. Ten months :a:er. however. a rib destruction was .iemonstrated similar to that of the previous patient ;Fiz. fi --and a bioosv of this region as well as ar. 576 ;iuiO|J>y established the diagnosis of primary pieuril mesothelioma associated with piilmonars asbestosis Comment In these three cases asbesiosis presented itself as an "idiopathic pleural disease." The first patient suffered from a benign effusion. The second revealed a spontaneous pneumothorax changing gradually into a massive fibrochorax and terminating as a primary pleural mali*. nancy. The last patient had initially bilateral benign pleurisy healing with pleural calcifica tions anil died many years later of a unilateral malignant pleural disorder. This course of events is typical of asbestosis. At no time did these persons reveal any prominent clinical and roentgenological findings of parenchvmal Junodisease. Unfortunately, pulmonary function studies were not performed in these patients except in Case I after decortication. At that time normal results were encountered. Appar ently, pulmonary asbestosis does not manifest itself clinically without marked impairment of respiratory function while pleural disease mav F:cc:-:r S Voi. 13 No. 9 AMERICAN PRACTITIONER 1 i -u occur in the absence of respiratory insufficiency. The diagnosis of pleural asbestosis may be easily missed if only a pleural biopsy is performed be cause tire characteristic asbestos bodies are not present in the diseased pleura itself.10 Appar ently. thev -:;.xe too large to reach the pleura through the lymphatic channels. They usually remain in the small bronchial ducts2-0 and do not even enter the alveoli.'3-10 However, they seem to release some fibrogenic toxin responsible for the severe connective tissue reaction sur rounding them.'3-12 This pjeuro-pulmonarv fibrosis has been suspected to be an immuno logical response because it becomes apparent after many years of latency.6-10 The presence of many eosinophile cells in the peripheral blood as well as in the tissue section, the rapid sedi mentation rate and the positive Latex aggluti nation test of Case 1 seemed to be best explained by such a mechanism. Changes in serum protein and rapid sedimentation rates have been pre viously found in asbestosis.21 However, a posi tive Latex test has not been reported. This laboratory finding may represent a link to rheu matoid pleurisy20 and rheumatoid pneumonoconiosis.4 However, our patient never had any form of joint involvement that is so typical for the latter two disorders. In the light of modern experiences the old dictum "idiopathic pleurisy is due to tuber culosis unless proven otherwise'' must be modi fied. It is true that a considerable number of such instances will still.be caused by the tubercle bacillus. However, in recent years exploratory thoracotomy has revealed a great variety of other causes of idiopathic pleural disease. Asbestosis will have to be added to this group. Oniv a thorough surzicai exploration with pleural and parenchvmai biopsies will permit differentiation of these lesions, inch a procedure can alwavs be followed immediately by decortication and partial resection of the lung which are required to accomplish a cure in the majority of cases. However, in asbestosis even such aggressive theraov will not comoieteiv eliminate the danger reactivation oi the pleural disease on the ocher side nor the development of pulmonary fibrosis, respiraiorv insumciencw cor pulmonale and primarv puimonarv malignancvd-2-:: Thereiore, the best medical approach to asbestOsA still AMERICAN PRACTITIONER September 1962 consists of taking proper preventive measures in the form of pre-employment and oeriodic health examinations of workers, limitation of working periods, ventilation of work rooms, and safe protective respiratory devices. Summary The widespread use of asbestos makes asbes tosis an important occupational health problem. This type of pneumonoconiosis is not easily rec ognized. A history of exposure to such mineral dust is a significant clue: however, it may not be obtainable and, even if elicited, it may be misleading. Only a lung biopsy demonstrating asbestos bodies in die pulmonary parenchyma can clinch the diagnosis, particularly if this dis ease presents itself primarily as an idiopathic pleurisy. Acknowledgment The author expresses his appreciation to Dr. E. C. McRee, Port Arthur, for the permission to report his patient {Case I). Bibliography !. Anderson, John, and Francis A. Campagna: As- bestosis ami carcinoma of die lung. Arch. Env. Health, 1:39. 1960. 2. Bader, Mortimer E.. Richard A. Bader, and Irving J. Selikoff: Pulmonary function in asbestosis of the lung. Am. J. Med., 30:235, 196!. 3. Brugsch, Heinrich G., and Harold Bavlev: As bestosis in a worker engaged in automobile undercoating. New Eng. J. Med.. 265:379. 1961. 1. Caplan. A.: Certain unusual raciioioekui aooear- ances in the chest of coal-miners surierin; irom rheumatoid arthritis. Thorax. 3:29. 1953. 5. Casclemun. Benjamin, and Bcttv U. Kibbee: Case records of the Massachusetts Generai Hospital, weekly clinicopatbologicai exercises, case 73- i96I. New Er.e. J. Med.. 255:745. 1961. 6. Clinicooathological Conference: Computations of asbestosis. demonstrated at the Postgraduate Medical School of London. Brit. Mrd. J.. No. 5iS2:i345. 19-50. ' 7. Clinicouatholoeic Conference. I'. S. Naval Hos pital. Philadelphia. I'enn. t.'. S. Armed Forces Med. J.. 2:203'. I960. A E-senstadt. H. 3.: Malignant mesothelioma of the pleura. Div Chest. 30:549. 1936. 9. Eisenscadt. H. 3.: Prunarv maiienant mesotheli oma of the pleura. [ournal-Lancet. 30:511. I960. ` ' 577 T r 10. Merad, Brian E.. and Royer Williams: The pa thology of asbestosis with reference to lung function. Thorax, 16:204. 1961. ]]. Hurwitz. M.: Roentgenologic aspects of asbesto- sis. Am. (. Roenc. Radium Therapy and Nuc. Med.. 85:236. 1061. `' 12. Lvnch. Kenneth M.: Pathology of asbestosis. A. M. A. Arch. ind. Health. 11:1 S3, 1955. 13. McGrath. Margaret, and M. L. Thomson: Pul monary diffusion at small lung volumes in asbestosis and chronic bronchitis with emphvsema. Clin. Sci.. 21:13, 1961. 14. Mitchel. Jerry: Health progress in an asbestos textile works. Arch. Env. Health, 3:42. 1961. 15. Sanders. O. A.: Asbesiosis as differentiated from ocher pneumoconiosis. A. M. A. Arch. Ind. Health, 11:208, 1955. 16. Smith. Kenneth W.: Pulmonary disability in as* bestos workers. A. M. A. Arch. Ind. HeaHli 12:198. 1955. `' 17. Telischi. M.. and A. I. Rubcnstone: Pulmonary asbestosis. Arch. Path.. 72:234. 1961. ' !.S. Thomson. M. A.. Margaret McGrath. W. j Smither. and J. M. Shepherd: Some anomalies in die measurement of pulmonary diffusion asbestosis and chronic bronchitis with emob.v- senia. Clinical Science, 21:1, 1961. ' 19. Vorwald. Arthur J.. Thomas M. Durkan. and Philip C. Pratt: Experimental studies of -j,%. bestosis. Arch. Ind. Hygien. and Occud. Med.. 3:1. 1951. " *' 20. Ward, R.: Pleura! effusion in rheumatoid disease. Lancet. 2:1336. 1061. 21. Williams. Roger, and P. Hugh-Jones: The signifi. cance of lung function changes in asbesiosis. Thorax. 15:109. I960. The Author Dr. H. B. Eisenstadt is a native of Berlin. Germany. He formerly served as German specialist for internal diseases. Since 193S he has practiced Internal Medicine in Port Arthur. He is a Diplomate of the Ameri can Board of Internal Medicine and a Fel low of American College of Physicians, Chest Physicians, Cardiology and Gastro enterology. 578 Vol. 13 No. 9 AMERICAN PRACTITIONER