A system of practical medicine. By American authors. Vol. 3

by Unknown

⁴⁰ Dis. of Resp. Organs.

⁴¹ J. W. Hunt, Dub. Med. Journ., loc. cit.

⁴² S. C. Chew, case reported to Med. and Chi. Soc. of Md., 1883.

Displacement of Lung.—The lung in cases of effusion is drawn up by its own retractile energy. It has been demonstrated that this force is considerable. As the effusion advances the lung recedes to a certain point, when the fluid, having overcome the retractility of the lung and having a fixed point below, actually exerts positive pressure upon the lung (Garland), and compresses the air out of the alveoli and the compressible bronchi. This compression cannot take place until the diaphragm is no longer elevated into the thorax, but is bagged down by the excessive weight of the fluid. There can be no compression of lung until its elasticity has been exhausted. The gradual effect of the continued contraction of the lung is to straighten out the letter S curve. The force of lung necessarily diminishes gradually as it contracts in volume. On the other hand, the immediate effect of compression is to obliterate that curve. So long, therefore, as we are able to trace a well-marked letter S on the chest, we may be certain that the lung is well out of reach of compression (Garland). Peyrot⁴³ showed by plaster-of-Paris injections into the chests of cadavers, and then making cross-sections, that deformities of the chest are not due to a development of one side, the other remaining normal, but that they consist of a mutual adjustment of all parts. The simultaneous movement of the sternum toward the left in left-sided effusions makes the displacement of the heart appear greater than it actually is.

⁴³ Arch. gén., Juill., 1876.

The Diaphragm and Intercostal Spaces.—The diaphragm is not depressed below the edges of the ribs, nor do the intercostal spaces bulge until the weight of the fluid exceeds the lifting force of the lung. The admission of air into the pleural sac produces the same result. The depression of the diaphragm is due in part to the weight of the fluid, but chiefly to the diminished contractile energy of the retracted and diminished lung. The displacement of the mediastinum depends upon similar conditions. Since the traction of the lungs always affects both sides of the thorax, the movable mediastinum must follow the lung, which is still capable of contracting, and therefore with right-sided exudations the left lung will draw the parts over to itself. Only with excessive effusions in the pleural cavity does the pressure of the fluid come into activity.

The liver and spleen may be pushed below their normal position by excessive effusion after the diaphragm yields to the weight of the fluid. Woillez found the liver displaced downward in the abdominal cavity in one-fourth of the right pleurisies and only once in left-side pleurisies. The extent on the right side was from two or three centimeters to three fingers' breadth, even as far as the umbilicus.

The stomach, when the diaphragm sinks, may be pushed downward; thus the so-called semi-lunar space of Traube may be obliterated. Ferber noticed a peculiar displacement of the stomach in two cases where he had produced an artificial hydrothorax of the left side. The fundus was pushed to the right, and the stomach was folded over on itself to a certain extent. A second and marked folding-in of the greater curvature occurred near the pylorus. This condition of stomach, with left-sided pleural exudations, has been hitherto entirely neglected by authors. May not the vomiting which is often observed with excessive effusion, and which has been attributed to violent acts of coughing, be due to this doubling over of the stomach?

Auscultation.—At the commencement of acute pleurisy, when hyperæmia exists with dryness of the pleural surfaces, auscultation shows a respiratory murmur lessened in intensity and duration. There is also a jerking unevenness in the rhythm of respiration, and weakness or indistinctness of the vesicular murmur consequent upon the imperfect and irregular expansion of the lung. On the healthy side the respiratory murmur is hypervesicular, and becomes puerile and noisy in character. In from twelve to eighteen hours the plastic fibrinous deposit on one or both pleuræ causes us sometimes to hear, over circumscribed spots, at the end of inspiration and the beginning of expiration, a fine friction sound, which varies in intensity over the points of contact of the surfaces. This is especially the case in the infra-mammary, infra-axillary, and infra-scapula regions. Woillez heard friction sounds in 52 of his 82 cases. The pain in respiration makes it very jerking and irregular. The contact of the surfaces pushes aside the lymph, and thus we hear the sound at a given point at one inspiration and not at another. It is heard more distinctly during inspiration than expiration. The reason of our not hearing the friction sound at the early stage of pleurisy continuously, but with interruptions in inspiration and expiration, is because the opposed rough pleural surfaces do not continuously rub against one another, but remain adherent for a few moments, until a deeper inspiration tears them asunder. The effusive stage comes on so rapidly in acute pleurisy that often when patients are examined the friction sound of the first stage has disappeared. It has been generally taught that the cause of the disappearance of the friction sound, and its subsequent reappearance as convalescence commences, are owing to the fluid separating the surfaces and its reabsorption. We have seen, from Garland's experiments and from careful clinical percussion explorations, that the fluid does not come between the two surfaces unless in very great effusion, but that it occupies the cavity between the lung and diaphragm. Stokes long since showed that there was temporary paresis of respiratory muscles, and consequently loss of movement of the surfaces over each other, which movement was necessary to produce friction sound. The reappearance of friction sounds indicates recovery of this muscular power. When heard, the friction is of the grazing variety—the most delicate form. Walshe designates it as the attrition species, and says it is audible over a limited extent of surface, occurring with occasional respirations, dry, and limited strictly to inspiration. As the effusion appears, we find, beginning with the lower border, that the respiratory murmur disappears, becoming less distinct as the effusion advances in the pleural cavity. Ordinarily, we hear no breath sounds. The absence, however, of breath sounds as a sign of pleuritic effusion is by no means a constant one. When the fluid contains many fibrinous bands, binding the lung down to the costal pleura, or when the effusion is very large and forces the air nearly out of the pulmonary tissue, pressing it into a firm mass against the vertebral column (at a point corresponding to the spine of the scapula), or when the lung is solid simply from the residual air being pressed out of it, diffused bronchial tubular breathing is heard. The tubular sound is conveyed, not ordinarily through the fluid, but by the parietes of the chest and by the solid plastic linings and adhesions. The fluid, if in large quantity and filled with fibrinous bands, may also feebly conduct the sound, which, being produced on solid surfaces, is best conducted by solids. We hear, in fact, a respiratory sound of low pitch, but tubular in quality. It is bronchial, but it differs widely from the familiar bronchial respiration observed when the lung is consolidated in pneumonia. It is a diffused distant tubular sound unaccompanied by moist sounds, soft in its quality and muffled. It has not the brazen, harsh character of pneumonic bronchial respiration. In pneumonia this sound is immediately under the ear, the lung being in contact with the inner surface of the ribs, and rendered a good conductor by its solidity, and the sound rendered louder by the increased consonating properties of the walls of the bronchi; whereas, in pleurisy, the lung is contracted above the level of the fluid, or, when the effusion is excessive, is removed from the walls by an indifferent conductor of its sounds, and the sounds are conveyed from the compressed lungs at their base by the walls of the chest, and, in a degree, by the deposits on the pleural surfaces. The bronchial breath sound which we hear over the lung, compressed by fluid, near the vertebra continues sometimes a long time after the absorption of the fluid, because the lung, deprived of air, expands slowly. If the effusion be small, we do not hear bronchial respiration, because there is sufficient air in the alveoli to prevent the conduction of the sound, the air not being compressed out by the effusion, but the whole lung being lessened in volume. If, again, the mass of fluid be very large, it prevents the free transmission of the waves of sound, and we do not hear them.

The auscultatory phenomena necessarily vary according to the amount of fluid in the cavity, the extent of the adhesions, the retraction, and the compression of the lung-parenchyma. If the compression be sufficient to prevent the air from passing down the bronchi, we do not hear bronchial respiration, because where, as in health, it is not communicated to the ear (owing to its non-conduction by the lung-tissue), it cannot be produced. Douglass Powell⁴⁴ calls attention to another unusual pressure effect—altered quality of voice and cough, a husky voice, and a laryngeal quality of cough undistinguishable from that so often heard in cases of mediastinal tumor or aneurism. These disappear after paracentesis.