Document gDMYKEnE3OZObkz0ed5D0v9xG

FILE NAME: Smoking (SMOK) DATE: 1947 DOC#: SMOK014 DOCUMENT DESCRIPTION: Book Excerpt - Diseases of the Lungs and Bronchi D ISEA SES of the CHEST With Emphasis on X-ray Diagnosis By ELI H. RUBIN, M.D., F.A.G.P., F.G.G.P. Clinical Professor of Medicine, New York Medical College, New York; Director of Medicine, Seton Hospital, New York; Visiting Physician in Chest Diseases, Morrisania City Hospital, New York; Attending Physician. Division of Pulmonary Diseases, Montefiore Hospital and Country Sanatorium, New York: Associate Physician in Chest Diseases, Lebanon Hospital, New York. The Principles of Surgical Treatment By MORRIS RUBIN, M.D., D.S., F.A.C.S. Clinical Instructor in Surgery. Mew York Medical College, New York; Active Consultant in Thoracic Surgery, Fordham Hospital, New York; Visiting Surgeon, Seton Hospital, New York; Associate Visiting Thoracic Surgeon, Morrisania City and Triboro Hospitals. New York; Adjunct Thoracic Surgeon, Montefiore Hospital, New York. 355 ILLU STRA TIO N S WITH U PLA TES IN COLOR W. B. S A U N D E R S COMPANY PHILADELPHIA & LONDON Copyright, 1947, by W. B. Saunders Company Copyright under the International Union \ll Rights Reserved This book is protected by copyright. No part of it m ay be duplicated or reproduced, in any manner without written permission from the publisher Reprinted O ctober. 1947. M ay, 1948, and M arch, 1950 MADE IN U . S . A. PR ESS OF W. B. SA U N D ERS COMPANY PH ILAD ELPH IA Fig. 178.--Silicotuberculosis showing grayish-black appearance of lung due to associated anthracosis; ulcerative tuberculosis in the upper lobe. Roentgenogram reveals nodular silicosis and increased hilar densities. A, Silicotic nodules consisting of dense cores of fibrous tissue surrounded by laminated whorls of hyaline fibers. B , Spindle-shaped structures (asbestos bodies) which give a prussian blue reaction for iron. (Copyright, Ciba Pharmaceutical Products, Inc., Summit, N. J.) 346 DISEASES OF THE LUNGS AND BRONCHI ized extension into adjacent lung fields often directs the physician's attention to the pos sible existence of a dust disease. Pendergrass has suggested the term " modified silicosis" to cover such instances where abnormal shadows are noted in the roentgenogram in the absence of a definite history of exposure to a silicious atmosphere or where exposure has been to a mixture of dusts. A presumptive diagnosis of "modified silicosis" is justified on the basis of the roentgen findings, to be confirmed or dis proved by additional studies. Several physicians have drawn attention to peculiar eggshell calcifications occasionally encountered in the roentgenogram of silicotic lungs. These nodules are spheroid in shape, having an apparently calcified casing around them. They may occur within the parenchyma or in the hilar glands. A number of explana tions have been offered to explain their pecu liar configuration. It has been postulated that they represent calcified areas of tuberculosis infection or silicotic nodules or calcified de generation in or around silicotic nodules. Riemer suggests that the shadows result from direct inhalation of calcium along with silica particles. As additional evidence for his belief he cites studies on calcium dust inhalation showing analagous roentgen shadows. Clinical Features.--A diagnosis of silicosis cannot be made on the basis of symptoms and physical findings alone, although the presence of the condition may be suspected in commu nities where silicosis is prevalent. A detailed occupational history and a roentgenogram are indispensable. What may seem to an individ ual a trivial occupation, particularly if he was engaged in it many years before, may prove to be important as a possible source of lung injury. On the other hand, a man who has spent many years in a mining industry may not have contracted a dust disease. A recent experience was quite illuminating. A man of twenty-nine came to me for a routine chest examination because his wife was found to have advanced pulmonary tuberculosis. The roentgenogram revealed moderate accen tuation of the hilar markings and linear, in places nodular, densities in the midportions of both lungs, chiefly the right (Fig. 185). The appearance of the roentgenogram did not suggest tuberculosis. The patient's occupation at the moment was that of a fruit merchant. On closer questioning, however, it was found that for almost three years, during the war, he had worked on ships as an electric arc welder of steel plates. Part of the time he used galva nized steel with a coating of zinc and the rest of the time black iron without a coating. Although he had some protection against the fumes, it seemed likely that the roentgen changes were due to inhalation of metal fumes, a recognized source of pulmonary injury. The past history may reveal increased sus ceptibility to infections of the upper respira tory tract, pleurisy, recurring pneumonias or "asthma." The initial stages of simple silicosis seldom cause significant symptoms except for unaccountable dyspnea which is out of propor tion to the extent of the disease. With greater lung involvement, the dyspnea becomes in creasingly severe and is soon associated with cough, at first dry, later productive, the spu tum often mixed with blood. The individual may have a feeling of tightness in the chest, at times of a painful nature. Increasing weakness and vague abdominal complaints are frequent. Silicosis with infection is characterized, in addition, by abundant expectoration, at times frank hemoptysis, fever, sweating and marked loss of weight. Although dyspnea and cyanosis may be evident even when the individual is at rest, orthopnea is not seen unless there is also cardiac insufficiency caused by increasing in terference with the lesser circulation. Engorge ment of the veins in the neck, enlargement of the liver and spreading edema appear later. The few who escape tuberculosis or cardiac failure are apt to succumb to intercurrent pneumonia. Several observers have found a greater in cidence of carcinoma of the lung in silicotics than among nonsilicotics. The role played by silicosis in carcinogenesis is obscure. Many doubt that a relationship exists between the two, their presence in the same lung being ascribed to age, sex and other factors which favor the development of carcinoma. The physical findings are not illuminating. Silicosis of advanced degree may be present in an individual who appears well nourished and in the best of health. Examination of the chest reveals evidence of emphysema. There is diminished costal and diaphragmatic excur sion, the expiratory phase especially being prolonged. The finger tips may show clubbing. There is usually hyperresonance on percussion 348 DISEASES OF THE LUSOS AND BRONCHI roentgen examinations facilitate the detection of incipient stages of the disease. ASBESTOSIS Asbestos is a hydrated silicate of magnesium in combination with traces of iron, nickel, calcium and aluminum. The substance is mined in many parts of the world, including Canada, where most of the American supply (chrysotile) is obtained. Mined asbestos comes in long, thin, fibrous strands which can be spun or woven. Its pliable texture and high resistance to heat and chemicals make asbestos an important industrial product in the manu facture of mattresses, brake-lining, fire-proof ing material, electrical insulation, in jacketing boilers and steam pipes, and in a variety of building fixtures. Although the dust hazard associated with the asbestos industry does not nearly compare in prevalence with that of the silica industry, the rapid growth of the former puts asbestosis among the important forms of dust diseases. Inhaled asbestos fibers range in size from 10 to 200 microns or more. Their action on the lungs is mechanical rather than chemical. The large particles, unable to enter the alveoli, lodge in the lumen and obstruct the respira tory bronchioles. Atelectasis of the distal alve oli is followed by a fibrotic reaction in the collapsed tissue. Xonobstructed alveoli under go compensatory emphysema. Contrary to that seen in silicosis, there is practically no nodulation unless silica is mixed with the asbestos dust. The hilar lymph nodes are not much enlarged for the reason that the lym phatics are not actively engaged in the patho logic process. The gross appearance of the lung is charac terized by scattered areas of diffuse fibrosis, affecting chiefly the lower lobes, emphysema of the uninvolved parts and intense pleuritis. Depending on the extent of coexisting anthracosis and silicosis, there are associated changes and pigmentation of the lungs and lymph nodes. Infection with pyogenic organisms and tubercle bacilli modify the pathology. Tuber culosis has been found in about one-third of the autopsied cases, but there is some doubt as to whether asbestosis per se favors the development of tuberculosis, or whether vul nerability to tuberculosis is primarily due to poor working conditions and incidental factors. A striking feature of the pathology is the presence of " asbestos bodies" seen on histo logic examination of lung tissue. These golden yellow or brown bodies have been shown by Gloyne to be composed of a central c o re of asbestos fibers, covered by a layer of ironcontaining material which is believed to be de rived from blood pigment of the tissues. Asbes tos bodies may be found in the sputum of asbestos workers, but their presence does not necessarily indicate lung disease. The roentgen appearance of early asbestosis is not revealing. Advanced disease often shows distinguishing characteristics. The fine pulmo nary fibrosis, patchy areas of interspersed em physema and overlying pleuritis are reflected roentgenologically in a " ground-glass" appear ance of a uniform quality, in places showing denser opacities which, however, seldom as sume the nodulation of silicosis (Figs. 183, 184). The lower portions of the lungs are chiefly involved. A marked pleural reac tion manifests itself in obliteration of the costophrenic sinuses, an unevenness of the diaphragm and a felted or " porcupine" appear ance at the periphery of the cardiac silhou ette, the last caused by pleuropericardial adhesions. The onset of the disease is insidious with gradual increase in cough, expectoration, dyspnea, loss of weight and, in time, inability to work. The physical examination is not re vealing. Wood and Gloyne draw attention to a peculiar earthy complexion of the face and a slight, violet tinge in the cheeks and lips of some individuals. Occasionally, asbestos corns occur in the skin pf the hands caused by the penetration of asbestos fibers into the superfi cial epidermis. It takes, on the average, be tween five to ten years for asbestosis to de velop. Whether the disease can progress after contact is broken with asbestos dust is still unsettled. Death results from tuberculous or nontuberculous infection, congestive heart disease or other intercurrent diseases. The measures listed for the prevention of silicosis apply also to asbestosis. Several other silicates have been reported to cause pneumonoconiosis. Fullers' earth, which is used extensively in bleaching fats and oils, has been found to cause pathologic changes in the lungs with symptoms similar to those seen in silicosis. Beryllium dust, a sili cate compound, used in the manufacture of OCCUPATIONAL HAZARDS INVOLVING THE LUNGS 349 Fig. 183.--Asbestosis in a man of 31 exposed to asbestos dust for five years. Roentgenogram reveals fine reticular infiltrations affecting chiefiy the lower portions of the lungs. (Courtesy, Dr. E. P. Pendergrass, Hospital of the Univer sity of Pennsylvania. Philadelphia, Pa.) Fig. 184.--Asbestosis in a man of .53 who worked for an asbestos company part time for eight years and full time for thirty years. Fourteen fellow workers died of asbestosis. Roentgenogram reveals nodular and dense, diffuse linear infiltrations involving both lungs with intervening emphysema. (Courtesy, Dr. E. P. Pendergrass, Hospital of the University of Pennsylvania, Philadelphia, Pa.)