[Diaphragmatic pleurisy may be mis taken for plcurodynia or a tender point of neuralgia. Both sides are affected alike frequently. The determining cause is a microbic infection. The exudate may be purulent or subfibrinous. The pleurisy may be primary or secondary. A very constant and characteristic sign is the so-called diaphragmatic button: a tender spot two fingers' length from the linea alba at the level of the tenth rib. It can be found even when there is no spontaneous pain. There is also tenderness along the attachment of the diaphragm, and another very tender spot on this line near the spinal column, as well as along the course of the phrenic nerve. Physical signs are: depression of the tenth rib, enlargement of that side of the chest at the same level, de crease of vocal fremitus, and absence of respiratory murmur. Other symptoms are those of ordinary pleurisy. J. T. WHITTAKER, Assoc. Ed., Annual, '94.] Chronic Pleurisy.
There are two forms of this affection: one with and one without effusion.
1. Chronic Pleurisy with Effusion.— This may follow acute sero-fibrinous pleurisy. Paracentesis may be performed from time to time, but the fluid reaccu niulates. The exudate continues to be serous, with, in some cases, a large de posit of gelatinous material on the pleu ral surfaces. After some months or even years some retraction of the chest may take place, showing that the fluid has been partly absorbed. There may have been no symptoms beyond some dysp nom on exertion, but lighter occupations may be pursued with comfort.
In other cases the affection is latent from the beginning. The onset is not marked by any symptoms that attract at tention. With the accumulation of fluid, dyspncea appears on severe exertion and becomes more easily provoked as the fluid increases. Inquiry into the history usu ally discovers more symptoms than the patient was aware of. He was content to attribute his failing strength to tem porary causes without making an analy sis of his symptoms. Clubbing of the fingers and toes may be marked.
Probably the great majority of these cases are of tubercular origin. analogous to cases of peritonitis with similar patho logical changes and a similar history.
Aspiration should be resorted to in these cases and repeated as often as the fluid reaccumulates, as much of the fluid being removed as will flow without dis tress to the patient. Later, when it seems useless to repeat the aspiration, active counter-irritation to the chest may be continued and short courses of altera tives given. Every means possible to improve the general health should be adopted, as an out-of-door life, pulmo nary gymnastics, nutritious diet, and change of residence. A sojourn in high altitudes does good in some cases, being followed by re-expansion of the lung.
If the exudation becomes purulent, it should be drained, ribs being resected if necessary, unless free incision is contra indicated by the existence of pneumo thorax.
2. Chronic Dry Pleurisy.—This condi tion may be preceded by pleural effusion )r develop gradually as a dry pleurisy. (a) In the first class after the absorption of the fluid there remains on the pleural surfaces more or less fibrinous deposit, some of which is gradually absorbed and the remainder becomes organized into connective tissue. This restricts the respiratory movement to seine degree, causes some dullness on percussion, and feebleness or absence of respiratory sounds and, it may be, some retraction of the chest-wall. These results are more marked in the purulent cases, especially in those in which there has been long persistence of discharge. The pleura in these cases is a thick mass of connective tissue surrounding an airless carnified !ung. In less marked cases there may he bronchiectasis.
(b) PRIMITIVE DRI PLEURISY.— Pleural adhesions very often occur with out any history indicating pleurisy. It is rare not to find some adhesions at a oost-mortem examination. They may be local or general and be due to so slight a degree of exudation as to yield no signs on examination except Litten's diaphragm phenomenon. There may be no interference with respiratory func tion. Such adhesions may be due to acute or subacute pleurisy. In more considerable thickening there will be in spiratory retraction of the interspaces, loss of resonance on percussion, and fee bleness or absence of the respiratory sounds.
The late Sir Andrew Clark was of the opinion that chronic dry pleurisy may lead not only to great thickening of the pleura, but to extension of the inflam matory process to the lung, causing marked fibroid changes in it: pleuro genic cirrhosis. Great thickening of the pleura and fibrosis of the lung often co exist; but that the latter results from the former is open to question.
Similar changes occur in cases of chronic pulmonary tuberculosis, and for the production of the pleural thickening Fowler offers the following explanation: "Whenever a retracting lesion is present in the lung and is situated sufficiently near the surface, one or other of two events always happens: either the pleura becomes thickened or emphysematous bulhe are formed on the surface of the lung. If there is no lung-tissue between the retracting lesion and the pleura capable of undergoing distension, the former change occurs; if there is, the latter lesion is produced." This applies to the non-tubercular cirrhosis of the lung, as well as to the extreme thickening of the pleura in chronic pulmonary tuberculosis.