UNUSUAL PHYSICAL FINDINGS IN PLEURAL EFFUSION: INTRATHORACIC MANOMETRIC STUDIES *

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1 UNUSUAL PHYSICAL FINDINGS IN PLEURAL EFFUSION: INTRATHORACIC MANOMETRIC STUDIES * By ARTHUR BERNSTEIN, M.D., F.A.C.P., and FRED Z. WHITE, M.D., Chicago, Illinois THE diagnosis of pleural effusion on physical examination has been based on the classic findings of absent tactile fremitus, dullness or flatness to percussion, and absent breath sounds. That the presence of increased breath sounds to the point of bronchial breathing and increased voice sounds can be associated with pleural effusions is not well known. In an institution such as ours, with an active teaching program for four large medical schools, and interns and residents from many centers, it has been surprising to note the frequent lack of knowledge that pleural effusions can have protean findings. The fact that atypical findings may exist is not a new concept; it was described by Laennec in HISTORICAL Laennec, 1 in his "A Treatise on the Diseases of the Chest and on Mediate Auscultation," written in 1818, said, "When, however, the texture of the lungs becomes indurated or condensed from any cause, such as pleuritic effusion,... the vesicular respiration having then disappeared, or being much lessened, we can frequently perceive distinctly the bronchial respiration, not only in the large but even in the small ramifications of the bronchi.... The cause of this bronchial respiration appears to me very obvious; in fact, when the air is prevented from penetrating the cells, this is the only kind of respiration that can exist; and it is found to be louder and thereby most distinct in proportion as the lung is more condensed, and so becomes a better conductor of sound." He was also the first to describe and stress egophony as an important sign in pleural effusions. Charles J. B. Williams 2 in 1834, in "A Rational Exposition of the Physical Signs of the Diseases of the Lungs and Pleura," explained these physical findings on a more physical basis, but in context agreed with Laennec. The more modern texts used commonly in teaching today 8 * 4 ' 5 make only passing reference to these "unusual" phenomena, the emphasis being placed on the more typical signs. Deviations from the usual findings are quite apt to be confusing, as was demonstrated by two cases seen on a medical ward at about the same time. * Received for publication March 3, From the College of Medicine, University of Illinois, and Cook County Hospital. 733

2 734 ARTHUR BERNSTEIN AND FRED Z. WHITE CASE REPORTS Case 1. This S3 year old white female was admitted for the second time because of increasing ankle edema, dyspnea and orthopnea. She was known to have rheumatic heart disease. Physical examination revealed decreased tactile fremitus, amphoric breath sounds and whispered pectoriloquy over an area of dullness on the right below the fourth rib posteriorly. This was interpreted as pulmonary consolidation. However, because a thoracentesis had been done on her first admission, it was repeated, and yielded 1,800 c.c. of serous fluid with a specific gravity of The second case was strikingly similar. Case 2. A 54 year old white female had complained of orthopnea and increasing dyspnea for two years and of ankle edema for two months. Six months earlier she had a left midhumeral amputation because of an embolus and resulting gangrene. Physical examination revealed an extremely dyspneic, slightly cyanotic white female. Her heart was fibrillating with an apical rate of 114. Examination of the chest revealed dullness of the left chest below the fifth rib posteriorly, with bronchophony and tubular breathing over the area. Because of the previous history of an embolus, the auricular fibrillation and these physical findings, a diagnosis of pulmonary infarction was made. However, thoracentesis yielded 1,200 c.c. of serosanguineous fluid with a specific gravity of This was followed by immediate resolution of the physical findings. TABLE I No. Name Age Sex Etiology 1 2 W~ Physical Findings Pressure mm. of HsO Pleural Fluid Ins. Exp. Amt. Sp. Gr. 54 F Cardiac "Unusual" , F Pneumonia Usual M.I. 42 F Carcinoma "Unusual" , E. B. 50 M Carcinoma "Unusual" , E. D. R. 42 F Carcinoma "Unusual" , M. F. 73 M Cardiac "Unusual" , P. Y. 53 F Cardiac Usual , J.W. 61 M Cardiac Usual , M. W. 21 F Tbc. Usual J.W. 27 M Tbc. Usual S.W. 70 F Carcinoma Usual , G.N. 47 F Carcinoma Usual , L.J. 55 M Cardiac "Unusual" , R.J. 73 M Cardiac "Unusual" , G.G. 64 M Cardiac Usual , W.A. 58 M Cardiac Usual , L.W. 44 F Cardiac "Unusual" , "Unusual": Findings of pulmonary compression with dullness-bronchophony and/or whispered pectoriloquy. Usual: Absent or diminished breath sounds and dullness. Several other cases have since come to our attention (table 1). Further study was undertaken to determine why a pleural effusion should yield findings resembling other disease entities. It was postulated that the fluid exerted pressure in these cases and caused parenchymal compression.

3 UNUSUAL PHYSICAL FINDINGS IN PLEURAL EFFUSION 735 PHYSICS From the standpoint of the transmission of sound, the lung can be considered as composed of a system of tubes gradually decreasing in size, with the smallest tubes terminating in spongy tissue. The characteristic sounds, then, must be transmitted through this system and the chest wall to the examiner's ear. The spoken sound originates in the larynx and is passively transmitted through the lung. Breath sounds are produced by air moving through the trachea and bronchi. Vesicular sounds are produced by air moving in and out of the alveoli, and this gives a more or less constant background murmur of sound. In both health and disease, sounds from within the chest usually reach the chest surface with but a trifle of their former intensity, under even the most favorable conditions. Most of the loss is effected between media of different densities such as air and tissue, or air and fluid, and is due largely to the reflection of sounds. There is no appreciable loss between tissue and fluid. Air, fluid and tissue are each elastic media and good sound conductors. Fluid, however, will conduct sound better than air. 2 ' 6 Reflection of sound, with loss of intensity due to dispersion, is also caused by tense membranes containing air. This occurs in the normally expanded lung. As these tense membranes relax, sound loss is reduced. Sounds are also blocked by obstructions of an air passage, unless the area affected transmits sound directly across to the chest surface. This may be seen in an occlusion of a third division bronchus, with resultant segmental atelectasis. The same physical process would be presfent in a pneumonitis with consolidation, or in a pleural effusion externally compressing pulmonary parenchyma. Increased sound transmission also occurs under a variety of conditions. A collapsed but aerated lung loses less sound conduction by reflection than does a normal lung. Solidified lung is a better conductor than a normally aerated lung, because it is of the same media and sound loss through it is practically negligible. However, some of the energy of sound is lost in passage from within the air tube to the solid lung. In a compressed lung, the vesicular sound being absent, with the resultant loss of this background murmur, bronchial sounds when present will appear more pronounced. 7 ' 8 The caliber of the bronchi is also important in sound transmission, because when sound reaches bronchi of 5 mm. or less it is reduced in intensity because of friction. Nothing is conducted in tubes of 3 mm. or less. For typical breath sounds to be heard, there must be good conduction between the chest wall and bronchi of greater than 3 mm. bore. The sound will be of greater intensity if conducted from bronchi of greater size because less sound energy has been lost along the tubes. Sounds are fairly distinct, and pectoriloquy is produced when bronchi of 5 to 6 mm. are reached. 9 ' 10 It has been shown by anatomic dissection X1 that bronchi of 3 mm. bore

4 736 ARTHUR BERNSTEIN AND FRED Z. WHITE are about 3 cm. inward from the pleura in the upper portion of the lung; 3.5 to 5 cm. inward in the basal and axillary portions, and 1.2 cm. inward near the vertebral column. Less compression then will be necessary near the vertebral column to reach bronchi of significant size. Fluid between the lung and the chest wall is of itself a good conductor. In contact with the chest wall, however, it lessens or abolishes the normal tissue vibratability and causes some sound loss. Sound, once transmitted to the fluid, is carried to the chest wall unaltered because there is no loss due to sound reflection in the fluid. MANOMETRIC STUDIES Because of the above discussion and our findings of pleural effusion in those findings considered "unusual," we decided to determine by manometric studies whether the fluid was under pressure and causing parenchymal compression. The lung normally floats in a potential pleural space having a negative pressure. Fluid introduced into this potential space will be subject to certain forces, as it would be in any other closed space. Gravity will tend to pull the fluid to the bottom of the space and capillary action will pull some of the fluid up the chest wall. The fluid, if under pressure, will exert pressure in all directions equally, in accordance with Pascal's law. The amount of compression or displacement of the lung depends on the external force, pressure and amount of fluid. There are also many variable factors which resist displacements such as fibrosis and congestion within the lung, fixed mediastinum and adhesions preventing movement of the involved lung. Manometric readings were taken to determine the pressure contained in the fluid in effusions with usual and "unusual" findings. A spinal manometer connected to a three-way valve and a thoracentesis needle was used (figure 1, A). Since this could not demonstrate negative pressures, the "U" manometer of a pneumothorax apparatus was used in certain cases. Because the height in the fluid at which the needle was inserted could not be accurately predetermined, readings were taken at two levels in the effusion, one 10 cm. above the other, and were found to be approximately equal (cases 4 and 11). In an effusion, then, the fluid is in accord with Pascal's law, which states that pressure in a fluid is transmitted equally in all directions. In an enclosed system, such as would be had in the pleural space, the pressure is transmitted to lung, chest wall and manometer equally, regardless of where the manometer needle is inserted. The level of the manometer fluid will not be the same as that of the effusion, as would be expected in an open system (figure 1, B). In such a system, the only force would be that of gravity, while in the pleural space the fluid is under pressure and transmits that pressure to the manometer. Pressure readings taken above the fluid, at the vertebral border of the scapula, demonstrated that normal negative pleural pressure was maintained

5 UNUSUAL PHYSICAL FINDINGS IN PLEURAL EFFUSION 737 at that level (cases 15 and 16). This had earlier been demonstrated in dogs by Hewlett 12 with artificially induced hydrothorax. The results of these manometric studies (table 1) demonstrated that in those effusions with "unusual" findings the fluid was under positive pressure through all phases of the respiratory cycle. It is not the height of pressure that is important but only that it is elevated or positive. In this series of 17 cases eight had "unusual" findings on physical examination, and all eight had pressures that were positive throughout the cycle. All of these were in effusions due to cardiac decompensations (cases 1, 6, 13, 14, and 17) or carcinoma (cases 3, 4 and 5). This is probably because these effusions are more likely to have a fairly rapid onset and to contain more fluid. An FIG. 1. effusion due to an inflammatory process, however, could probably achieve the same results if acute and massive enough. All the remaining patients (cases 2, 7, 8, 9, 10, 11, 12, 15 and 16) had usual findings and showed negative pressure in the inspiratory phase. This was demonstrated by absence of fluid in the spinal manometer or negative reading on the "U" tube of the pneumothorax apparatus. It is also of interest to note that effusions that had "unusual" findings but did not appear to be "massive" on x-rays or percussion contained more fluid than an effusion of equal height with the usual findings. This is because the thickness of the fluid is difficult to determine by either x-ray or percussion, and the total fluid will depend on this dimension. A thick effusion will be more likely to cause compression and yield bronchophony and tubular breathing than will an equally high but thin effusion.

6 738 ARTHUR BERNSTEIN AND FRED Z. WHITE SUMMARY Manometric studies were performed on 17 cases of pleural effusion to determine the pressure contained in the fluid. An attempt was made to correlate the pressures with the physical findings. In all eight of those with constant positive pressures throughout all phases of the respiratory cycle, "unusual" findings of bronchophony, tubular or amphoric breath sounds and even whispered pectoriloquy were noted. The etiology of all the effusions in this series was either cardiac decompensation or carcinoma. However, this is probably because these are more apt to be larger effusions which have developed rapidly. Absolute pressure does not appear to be significant, but only that some degree of positive pressure is produced and held. This pressure must be sufficient to compress parenchymal tissue down to bronchi of sufficient size to produce these auscultatory findings. CONCLUSIONS 1. By more meticulous interpretation of physical signs, pleural effusions can be diagnosed in the presence of bronchophony, tubular or amphoric breath sounds and even whispered pectoriloquy over an area of dullness to percussion. 2. Manometric readings of pleural fluid have been presented in cases with usual and "unusual" findings. It is demonstrated that the "unusual" findings are caused by compression of lung parenchyma by fluid. 3. The absolute pressure is not important; only that the pressure is positive throughout the respiratory cycle. BIBLIOGRAPHY 1. Laennec, R. T. H.: A treatise on the disease of the chest and on mediate auscultation, 1835, DeSilver, Thomas and Co., Philadelphia. 2. Williams, C. J. B.: A rational exposition of the diseases of the lungs and pleura, 1834, Carey, Lee, and Blanchard, Philadelphia. 3. Cabot, R. C, and Adams, F. D.: Physical diagnosis, 1942, Williams and Wilkins Co., Baltimore. 4. Freilich, E. B., and Coe, G. C.: Manual of physical diagnosis, 1947, Year Book Publishers, Chicago. 5. Major, R. H.: Physical diagnosis, 1945, W. B. Saunders Co., Philadelphia. 6. Wood, A. B.: A textbook of sound, 1944, G. Bell and Sons, Ltd., London. 7. Montgomery, C. M.: Transmission of sounds through the chest, Chap. Ill of Norris and Landis: Diseases of the chest and principles of physical diagnosis, 1938, W. B. Saunders and Co., Philadelphia. 8. Bullar, J. F.: Experiments to determine the origin of the respiratory sounds, Proc. Roy. Soc., London, 5. B 37: 411, Fahr, G.: The acoustics of the bronchial breath sounds, Arch. Int. Med. 39: 286, Martini, P.: Die Schallubertragung des Stethoskops, Ztschr. f. Biol. 71: 117, Martini, P., and Miiller, H.: Studien ueber das Bronchialatman, Deutsches Arch. f. Win. Med. 143: 159, Hewlett, A. W.: Pathologic physiology of disease, 1917, Appleton, New York.

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