ETIOLOGY OF FIBRO-SEROUS PLEURISY.—The etiology of acute primary pleurisy is frequently obscure. It may be hæmatic in origin, or it may be secondary, arising from pathological causes or antecedent disease. It is difficult to state with certainty whether it occurs in perfectly healthy persons, because there may be occult pathological conditions which cannot be appreciated. However, individuals are attacked with acute pleurisy who to all appearance, both to themselves and to those around them, are healthy. Authors differ very widely as to the disease being ever caused in healthy persons by exposure to cold. The older writers bring many proofs that such is the case. Ziemssen states that he could not trace the disease to exposure to cold in a single instance in 54 cases. Anstie holds the same view. Loomis states that in all instances where it (pleuritis) has followed upon exposure he has been able to find some predisposing cause. It is undeniable that pleuritis very frequently indicates the existence of some constitutional cachexia. Vital statistics show that it is more frequent in winter and spring than at other seasons. The vicissitudes of the weather, of temperature, and other atmospheric conditions have unquestionably a marked influence on the prevalence of the disease. Drafts of air passing over the chest or over other parts of the body, particularly when the subject is surrounded in-doors with a warmer atmosphere, wet clothing, intensely cold or a raw, damp atmosphere inhaled by persons coming out of a comparatively high temperature, especially if they are improperly protected by clothing, appear to be direct causes of primary pleuritis. If individuals thus exposed are debilitated by fasting, by such medicines as mercury, iodine, iodide of potassium, by over-exertion, by free perspiration, or by previous disease, they will be still more liable to contract the disease. Overheated apartments, especially at night during the sleeping hours, frequently are the direct cause of acute pleurisies or of croupal pneumonias. These cases are of such frequency that we are obliged to differ from the high authorities who consider the pleura as free from acute idiopathic inflammations as is the peritoneum.
There are numerous predisposing causes which, when examined, are found to lessen the power of resistance of the organism. Senility is an important one; so is childhood. Formerly it was supposed that pleurisy rarely attacked children. This view was prevalent because the disease often escaped detection. Of all chest diseases in children, mistakes in diagnosis are most frequently made with pleuritis.
We might suppose that this disease would be frequently met with in children, because they are oftentimes ill protected against the vicissitudes of the weather; besides, their feebleness predisposes them to feel keenly such shocks to their powers of endurance. The disease may occur at any age, and is more common under two years than was formerly supposed (Eustace Smith). Empyema is the form most frequently found in children, the effusion soon becoming purulent in them. Ziemssen tabulates the ages of 54 children whom he treated for primary pleuritis: first year of life, 3; second, 1; third, 7; fourth, 4; the remaining 39 between the ages of five and sixteen years.
Pleurisies are more frequent in males than in females, in the proportion of 5 to 3, owing to the greater exposure of the former to the exciting causes, and notwithstanding their stronger organisms. Among the predisposing causes we must not fail to give due importance to the malhygienic conditions which so powerfully impair the forces of the body. Prominent among these are sedentary occupations, imperfect alimentation, city lives, overwork of mind and body, deficient sunlight, overcrowded houses, and dampness of soil. These and many others interfere with the formative forces and lessen the power of resistance to exciting causes of pleurisy.
Traumatic pleurisies are caused by injuries or other mechanical causes. Injuries to the walls of the chest, contusions, burns, scalds, and lacerations which are superficial, frequently give rise to primary traumatic pleurisies. If the ribs are fractured, or blood, air, or pus gets into the pleural cavity, we have what has been termed secondary traumatic pleurisies.
Secondary Pleurisies.—The exciting causes of secondary pleurisies are numerous. They are pathological, and more readily appreciated than the causes of primary pleurisies. Owing to the anatomical connection between the lungs and the pleura, diseases, acute and chronic, of the former frequently give rise to pleurisies.
Among acute affections of the lungs, the several forms of pneumonia are the most frequent causes of pleurisies. Fraentzel states that we always find fibroid pneumonia associated with pleurisy as pleuro-pneumonia, even when the inflammation of the lung-tissue itself does not reach the pulmonary pleura. There is an intimate connection also between caseous pneumonia and pleurisy. This is sometimes quite circumscribed, and leads to adhesion of the pleural layers at the affected spot; sometimes it is diffused over a great part of the pleura, and it is then not infrequently associated with a considerable outpouring of different kinds of effusions. Catarrhal pneumonia rarely occurs without secondary pleuritis (Fraentzel). Pleurisies may also be caused by violent bronchial catarrhs or by hemorrhagic infarctions.
There are cases where, from the presence of tubercles under the parietal pleura, inflammatory action is set up and pleuritis ensues. Vomicæ bursting into the pleural cavity or tubercular perforation in pulmonary phthisis gives rise to pleurisies. Inflammation of the liver, cellular abscesses, and pericarditis may cause secondary pleurisies. Diffuse peritonitis is often complicated with pleurisy, the inflammatory process extending from the peritoneum to the pleura, through the diaphragm, by means of the serous canaliculi. This frequently occurs in puerperal peritonitis, and is almost invariably fatal (Fraentzel). The author had a case of fatal peritonitis in a man sixty-five years of age, which originated from an empyema. There was no rupture nor perforation of the diaphragm, so that the inflammatory process must have extended from the pleura to the peritoneum by means of these canals. Malignant diseases of the mammæ, oesophagus, lungs, and hydatids produce secondary pleurisies. Eruptive fevers, especially scarlatina, variola, typhoid fevers, are among the most frequent pathological causes of secondary pleurisies. It is doubtful whether their germs pass through the circulation or through the lymph-canals, and produce local inflammation of the same nature as their own, or whether they render the pleura more sensitive to shocks of various kinds. Rheumatism, gout, and nephritic diseases are frequently followed by pleurisies. As we have rheumatic endocarditis and pericarditis, in like manner there are rheumatic and uræmic pleurisies. Alcoholism and pyæmia, septicæmia and the puerperal state, especially during the first month after parturition, are powerful predisposing causes of pleurisies, as are also any morbid conditions of the skin, kidneys, or intestinal canal which interfere with their eliminating or depurating functions. This includes all forms of blood-poisoning. Hutchinson says that children suffering from congenital syphilis are especially liable to serous inflammations, and that pleurisy is in them a not uncommon cause of death. Niemeyer denounces the impropriety of giving the name of secondary pleurisy to all cases of pleurisy occurring in subjects with broken-down constitutions or weakened by other diseases. We often meet with such cases when Bright's disease exists. Niemeyer holds that it is not dependent upon renal disease, but upon the increased predisposition for all kinds of inflammatory disease. A trifling cause will sometimes excite a pleurisy when the resistance of the organism is materially lessened by previous disease.
SYMPTOMATOLOGY.—Rational Symptoms.—These vary according to the severity of the disease. Ordinarily, attacks of acute pleurisy come on suddenly, and it rarely happens that there is any appreciable feeling of malaise. Usually the first symptom is an acute pain in the side, which alarms the patient. The significance of this severe stitch is generally appreciated, as the subject at once calls attention to his sufferings. The pain is sharp, cutting, stabbing, that causes him to hold his breath as long as possible. When he is forced to breathe, it is by the action of the superficial intercostal muscles. He endeavors to fix his diaphragm and hold it rigid in order to prevent the surfaces from coming in contact and thus increasing his agony. This causes him, necessarily, to breathe frequently in order to get sufficient air. The greater the intensity of the pain, the more frequent and shorter are the respiratory acts. The dyspnoea and the effort to lessen the pain give the patient an expression of great suffering. Usually, the pain is felt over a circumscribed spot under the nipple of the affected side. Sometimes it is experienced as low as the sixth or seventh intercostal space, but rarely posteriorly below or under the scapula or in the axilla. In children the seat of pain is not always in the chest. Their lower intercostal nerves are often affected, and the sensation being referred to the ends of these nerves where they ramify on the abdominal wall, the pain is often seated in the abdomen. Such being the case in children, care must be taken not to confound pleurisies in them with epigastric or hypochondriac irritations. In adults, the pain is rarely located in the abdomen when it is caused by pleuritis in the lower portion of the pleural surface or in that part covering the diaphragm. In children there is also much tenderness on pressure. In what has been termed subacute or latent pleurisy the stitch may be entirely absent. Valleix found pain in 40 cases out of 46. Sometimes it is absent in ordinary breathing, but is brought on by sneezing or violent coughing or strong percussion. In severe cases, the effusion coming on rapidly, the pain may subside by the second day. If the effusion comes on slowly, the pain may keep up for six or eight days. The continuance of the pain always shows that the inflammatory process in the pleura is continuing, although the pulse and the temperature may be normal. The renewal of the sensation of pain after the pleurisy has passed away justifies us in the conclusion that there is a return of the inflammation. When the pain is agonizing, with signs of collapse, it is indicative of a secondary pleuritis arising in the course of a chronic caseous pneumonia. Tubercular and purulent exudations are distinguished from the sero-fibrinous by the longer duration and the greater intensity of the pain—two circumstances which afford a reliable basis for the diagnosis of such cases. The severe pain in pleuritis is probably caused by the inflammation extending to the sheaths of the nerves and to the nerve-texture itself (neuritis), as well as by inflammation of the pleura itself.
Severe attacks of acute exudative pleurisy may commence with a severe initiatory chill, followed by high fever, but ordinarily there are in pleurisy slight rigors, initial in their character. Some authors question whether they are not caused by the limited points of pneumonia connected with the pleuritis. If the rigors occur at regular intervals for days, we have reason to suspect tubercular trouble or empyema. The temperature does not run any regular course in pleurisy, nor does it bear any fixed relation to the pulse and the respiration. It usually varies from 100° to 102° F. In violent, acute cases it may reach 105° F.