Chapter XXXIX: Part 39

Theory and observation show beyond a doubt that in all cases where {560} there exists a decided intra-pleural tension pleurotomy of the thorax modifies efficiently the circulatory and respiratory functions. Instead of causing suffocation, it diminishes almost always, and that instantly and remarkably, the dyspnoea. In 1868, Maisonneuve[175] made the startling announcement, which he claimed was nevertheless rigidly true, that of 100 patients who die after surgical operations, 95 are poisoned by organic substances absorbed. He claimed that the liquids exuded from the surface of wounds become corrupt when exposed to the external air, and that subsequently they undergo morbific changes and become formidable poisons. If, he said, we can prevent the dead liquids from putrefying, the gravest operations could be performed without danger. No one who studies the results of empyema in the past can question that the greatest danger is from the blood-poisoning known as septicæmia, caused by the absorption of the septic infection by the lymphatics.[176] No matter what may be the nature of septicæmia, it is sufficient that the vast surfaces of the pleura produce certain prurient secretions, which, when absorbed and carried into the circulation, cause hectic fever with its results. We claim that there is less danger from putrid absorption when free incisions are made than from those only large enough to introduce a drainage-tube. Rome[177] collected 49 cases, but of these 10 contained fetid pus; 9 of the number had been treated by one or many, even up to fifteen, aspirations. He concludes that the surgical interventions, other than pleurotomy, provoked in the purulent liquid of the pleura putrid fermentations in one-fifth of the cases. The products of this fermentation irritate actively the serous membrane, and cause an abundant suppuration intractable in its nature, and there is imminent danger of rapid exhaustion and hectic fever. One-third of Rome's cases contained solid pieces which could not be removed in any other way than by making free incisions. Although subserous cavities are not perfectly analogous to phlegmonous abscesses, yet they closely resemble each other. Histologically, the inflammatory process and its phases are the same, but there is this difference--absorption of the deleterious products is more active. Why allow a warm abscess to be transformed into a cold abscess, which will open later spontaneously after having caused grave disorders? We have seen how frequently large collections of pus sooner or later open either through the lung or through the chest-walls. If an opening has to be made, the more promptly the better. In the first stage, especially in acute purulent pleurisy, the slight neo-membranes and fibrinous deposits, barely solid, readily undergo granular fatty degeneration, and are absorbed if relieved of the pus. In this stage the two folds of the pleura are in their best condition for becoming adherent to each other, and by obliteration of the pleural cavity to end the disease. If acute empyema be treated early and gently before the lung is compressed or injured, with free opening and constant drainage, the patient being in a recumbent position on face or side, the pleura needs no washings. The orifices made spontaneously are frequently insufficient to completely empty and to keep up the current of pus as it forms. In bronchial fistula, unless the air is prevented from coming from the lung into the pleura by a valvular opening, we have frequently to resort to pleurotomy. If in empyema necessitatis the orifice partly closes or is not free enough, we must not hesitate to enlarge it or make a counter-opening to enable the matter to flow out. In tubercular pyo-pneumothorax, where the purulent fluid has been the primary lesion and has perforated the lung, the operation is not indicated. E. Moutard-Martin's treatise was founded upon 17 subjects, 5 of whom died and 12 were cured. Of the 12 cured, 2 had bronchial fistula in pneumothorax without any sign of tubercle; 5 had permanent fistulous openings and discharged {561} occasionally a few drops of pus; 7 were cured without fistula. Blake[178] reported 19 cases treated by permanent openings, with 15 "cured and much relieved." He operated by making incisions from one to two inches long, parallel with the ribs, between the seventh and eighth ribs, a little inside of the scapula. His practice was to keep the orifice open. He used either a spiral wire covered with gutta-percha or a gum-elastic catheter fastened to a shield and kept in position by adhesive plasters. Martin Oxley[179] by pressing open the incision with a pair of dressing forceps introduced a silver or india-rubber tracheotomy-tube to keep the orifice open. He related several instances where pieces of tubing fell into the cavity and remained there without injury for months, and in one case as long as several years. Dabney[180] urges with force the importance of our having a continuous discharge of pus as far preferable to its daily removal, "not only because it seems less liable to become fetid, but because, as the two surfaces of the pleura have to come together and heal by granulations, the retention of pus would delay this process by keeping the costal and pulmonary surfaces apart." Thorough drainage by two orifices or a wide incision kept open by two tubes is more effective than a simple drainage-tube. Antiseptic precautions are essential to ensure success at every stage of the operation.

[Footnote 175: _London Prac._, 1868.]

[Footnote 176: Ranney, _Annals of Anat. and Surgery_, 1881.]

[Footnote 177: _Thèse de Paris_, 1882.]

[Footnote 178: _Boston City Hospital Reports_, 2d series.]

[Footnote 179: _Liverpool Medico-Chirurg. Journal_, January, 1882; _N.Y. Medical Abstract_.]

[Footnote 180: _American Journal Med. Sciences_, Oct., 1882.]

Value of Injections and Washings.--The object of injections is to enable us thoroughly to wash out the cavity and to promote adhesions between the pleural surfaces. The chief danger being from septicæmia, it is of the greatest importance that the pus should not be allowed to remain in the cavity longer than can be avoided. The body-temperature, taken twice daily, is one of the best means of ascertaining the extent of the re-formation of pus. Stagnant pus, mingled with air, will undergo fermentation and cause putridity; hence the great value of incessant drainage through unobstructed tubes. When the pus is free from unpleasant odor and runs freely, it is not necessary to use washings or injections of any kind, for the cavity will purify itself. Washings and injections have sometimes been found very injurious and irritating, and sudden deaths have been attributed to them. If flocculi form, washings of tepid water with a very small percentage of alcohol or of salicylic acid (1 per cent.), used without force for fear of rupturing some of the recently-formed capillaries, are useful. When modifying injections are used, the patient ought to lie on the opposite side. In this way all the diseased parts are reached by the fluid. An ordinary syringe should not be used, but a Thudicum bottle or a fountain syringe: either of these can be raised sufficiently high to allow a gentle flow into the cavity. If the discharge becomes fetid, injections of solution of permanganate of potash (1 or 2 grains to ounce j) or of tinct. of iodine (1:4) in water ought to be used. The author has never seen any results of poisoning from the use of carbolic acid, but he has always used a feeble solution, 2 or 3 per cent. Dabney had symptoms of carbolic-acid poisoning in one of his cases where he used a 2 per cent. solution, notwithstanding the fact that he had taken every precaution to ensure its prompt return. A. T. Cabot[181] mentions a case of carbolic poisoning in a boy four years of age produced by a feeble solution of one part to thirty of water used only to cleanse the instruments, tubes, and hand of the operator. Kuster's[182] experiments show that anæmia and septic and pyæmic fevers predispose the system to carbolic-acid poisoning. He recommends an 8 per cent. solution of chloride of zinc. Chlorate of potassium drachm j to pint j has been used with benefit. The medical journals contain so many reports of the serious, and even fatal, results from absorption of carbolic acid when thrown into abscesses {562} that we are compelled to abandon it in favor of other injections. B. W. Richardson long since showed the great value of iodine as a disinfectant. It not only corrects the fetor of decomposed pus, but at the same time lessens the secretion from the walls. The first injections should be weak, gr. 4 or 5 of iodine and iodide of potassium to a pint of water. Liq. iodinii com., ounce ss to ounce iv, ought not to be used until the surfaces have become accustomed to the action of iodine. Injections of medicated fluid ought not to be used unless they are absolutely necessary, because in some instances they have produced fainting attacks and epileptiform seizures with alarming convulsions. These results have followed injections of different fluids--borax, carbolic acid, iodine, permanganate of potassium, and even warm water. Similar phenomena have followed the injection of the bladder, the uterus, and even from passing a catheter. The shock may have been too sudden or the injection too forcible or the fluid too cold. A. L. Mason[183] suggests that it is probably owing to sudden irritation of the lymphatics through the great splanchnic nerve, with anæmia of the brain. Paralysis of the limbs after convulsions makes the theory of embolic origin probable. These accidents must not make us underrate the great value of frequent washings with injections when rendered necessary by the approach of putrid infection. The number of these washings should depend upon the urgency of the symptoms, and antiseptic injections should not be employed unless we find evidences of fetor, because of one great objection: they do not favor the expansion of the lung.

[Footnote 181: _Loc. cit._]

[Footnote 182: Quoted by Dabney, _loc. cit._]

[Footnote 183: _Boston City Hospital Reports_, 2d Series.]

Cases of long-standing compression of the lung could hardly result in complete re-expansion, but the general health will be recovered and the chest, contracted by approximation of the pleural surfaces from the walls being pressed in or ribs resected, will cease to secrete pus. If fever persists, with diarrhoea, sweats, emaciation, and fetid suppuration, it shows that the washings are not sufficient in number. They can be repeated as often as every three or four hours, to be decreased in frequency as the patient improves. Under frequent washings Feyrot[184] reports favorable results in almost hopeless cases. Time is very precious when these symptoms of exhaustion or septicæmia set in, as it is of the utmost importance that we should endeavor to prevent promptly the absorption of the putrid products, the inevitable effects of which are to produce, before long, fatty and amyloid degeneration of the principal viscera. The most effective way of using detergent fluids is by syphons through two tubes perforated at their extremities and fastened with shields. A Thudicum douche-bottle or a fountain syringe can easily be used by patients themselves as often as is required. The orifice and the tubes should be protected by thorough and rigid antisepticism. As the case improves the cavity gradually gets smaller, the two pleuræ become adherent, and the quantity of fluid lessens until only a small amount flows out. Every eight or ten days we carefully draw out the tubes by degrees, until we have only a little canal beneath the walls. We can thus let the orifice heal slowly, for the sac is obliterated and the patient cured.

[Footnote 184: _Thèse de Paris_, 1876.]

In the hands of Boyer, Delpech, Dupuytren, and Sir Astley Cooper the bistoury gave bad results, but as now used, with all modern appliances and antiseptic precautions, it affords infinite relief and many cures. We claim that by early pleurotomy, with Listerism scrupulously used at every stage of the operation, and if necessary with detergent washings, the mortality from this extremely grave disease can be very materially lessened.

Double Pleurisy.

Pleurisy may occur on both sides at the same time. Double pleurisies are secondary, not primary, and result from rheumatism, or still more frequently, {563} according to Louis, from tuberculosis. In 150 cases of pleurisy quoted by him, there were no bilateral cases which were not produced by rheumatism, gangrene, or tuberculosis. A double pleurisy in a previously healthy person creates a strong suspicion of tubercular origin. There is generally an interval of some days before the attack of one side is followed by that of the other. When effusion takes place the dyspnoea is very great. Death is imminent unless the fluid is withdrawn by aspiration. Maintenon[185] states that the inflammation may be so intense and the fever so high as to destroy life before the effusion is thrown out. The physical signs are the same as in unilateral cases. The effusion is never so great on one side as on the other. The progress of disease is rapid, and the result is almost always fatal.

[Footnote 185: _Thèse de Paris_, 1873.]

Diaphragmatic Pleurisy.

The serous lining of the upper surface of the diaphragm may be involved in an ordinary pleurisy, or inflammation may be limited to it without involving either the pulmonary or the parietal membrane. In this latter case we have modifications of the characteristic symptoms and physical signs. Functional disturbances and special symptoms enable us to diagnose it. There is a febrile movement with occasional delirium, and some of the prominent symptoms, but without the physical signs to indicate the exact locality. The pain is intense, and dyspnoea exists even to the extent of orthopnoea and respiratory anguish, the respiration jerky and convulsive. The pain comes on suddenly in one of the hypochondriac regions, extending up to the attachments of the diaphragm to the costal surfaces. The pain is intense, and increased by full inspirations, by physical efforts, by vomiting, and even by the eructations of wind. The position of the patient attracts attention: as he sits with the trunk inclined forward, he has an anxious and distressed expression of countenance, sometimes accompanied by nausea and vomiting with singultus. Pressure elicits a characteristic tenderness; if applied under the false ribs, it causes suffering. The phrenic nerve is painful on pressure practised over the accessible points of its course, between the two inferior bands of the sterno-cleido-mastoid at the base of the neck. There are also painful irradiations in the cervical plexus above the clavicle and in the scapular region. Pressure over a circumscribed spot of the epigastric region causes a sharp agony of pain. This point is at the intersection of two lines--one, the external border of the sternum; the other, at the osseous portion of the second rib. Guéneau de Mussey[186] has named this the diaphragmatic bottom. This pain extends sometimes to the vertebra and upward to the first intercostal space. Auscultation and percussion at the base of the lung give us some results: impaired expansion of the lung at the base and dulness on percussion; the diaphragm is in a great degree immobile, owing partly to the pressure upon it, and partly to a paresis from inflammation of its upper serous covering (Stokes[187]). When the inflammation is on the right side, we may find an icteroid tint, with vomiting, delirium, etc., with the liver pushed below its normal position in the abdomen. The inflammation of the pleural covering of the diaphragm may be caused by sero-hepatitis extending through the diaphragm (Copeland[188]).

[Footnote 186: _Archiv. de Méd._, 1879, vol. ii.]

[Footnote 187: _Dis. of Chest_, 1837.]

[Footnote 188: _Dict. Med._, vol. iii., edited by Lee.]

If the effusion is confined to the space between the lung and diaphragm, the diagnosis is obscure. There may indeed be cases where we have but few of the symptoms already mentioned. If the fluid is not confined to this portion, but flows into the pleural cavity, it gives great relief, and the result is favorable. Diaphragmatic pleurisy may, however, end in death, either by its discharge into the peritoneal cavity or by constitutional disturbances.

{564} Interlobular and Mediastinal Pleurisies.

The effusion is sometimes confined by adhesions between two lobes. The mediastinal variety is situated between the pleural boundary of the mediastinum and the adjacent portion of the pulmonary serous membrane. It is but rarely met with, and may be diagnosed by local symptoms. The flatness on percussion in the interlobular variety is very circumscribed. Both forms cause local pains, but in the mediastinal variety the pain is very deep and perceptible at the middle of the sternum, and is increased by the respiratory movements. In both varieties there is more or less fever. If either variety exist on the left side, the condition of the pericardium must be carefully examined, as pericarditis may be confounded with it. These limited collections of fluid may burst into a bronchus and be expectorated.

Multilocular Areolar Pleurisies.

Multilocular encysted collections of fluid in the pleural cavity are due to the partitions made by pseudo-membranes which divide the pleura into subcavities. These occur generally in subjects who have had previously dry or adhesive pleurisies. They are more serious than ordinary pleurisies. We meet with them in aspirating, when, after draining off the fluid from the base of the pleural cavity, we find the lung expanding, but above that point there is absence of respiratory murmur and of other physical signs indicating the presence of fluid. Reybard[189] divides multilocular pleurisy into three varieties, with varying symptoms and physical signs, according to whether it exists at the upper, middle, or lower portion, right or left side. Owing to the thickness and distribution of neo-membranes, it is frequently difficult to localize the points of collections of fluid. Aspiration is the most accurate means of ascertaining the exact point and extension of the effusion.

[Footnote 189: _Bullétin Acad. Méd._, 1879.]

Rheumatic Pleurisy.

HISTORY.--The recognition of the fact that we can have local manifestations of rheumatism in the texture of the lung itself, of the bronchi, and of the pleura is of comparatively recent date. There had been indefinite, loose statements, or rather suggestions, in some of the writers in the early part of the century, such as Chomel and Andral, as to the possibility of rheumatism appearing in the pulmonary textures; but we believe that the first definite description of the disease was made by T. H. Buckler of Baltimore in 1865.[190] He claimed that the white fibrous tissue of the bronchi could be the seat of rheumatism, as well as similar textures about the joints. He illustrated his views by cases observed and reported by himself. He showed how, as a result, there were symptomatic engorgements, more or less solid, of the pulmonary parenchyma or rheumatic pneumonia. In 1854, Black[191] found crystalline particles of uric acid and of urate of soda deeply imbedded in the thin white fibrous tissue of bronchi. Buckler showed the metastatic character of rheumatic inflammation in the bronchi and lungs as elsewhere. Buckler's subsequent papers[192] published in connection with this subject, show remarkable success in treatment of fibro-bronchitis and rheumatic pneumonia based upon his views of their pathology.

[Footnote 190: _Fibro-Bronchitis and Rheumatic Pneumonia_.]

[Footnote 191: _Edin. Med. Journal_, 1854.]

[Footnote 192: _Boston Med. Journal_, 1882, and _Amer. Med. Journal_, Oct., 1882.]

SYMPTOMS.--We find rheumatic pleurisy coming on in the course of {565} rheumatic fever with the characteristic mobility of the points of inflammatory action. Laseque[193] gives the symptom with accurate details--the acute pain in the side of the chest without cough or expectoration. He describes the pain as differing from that of ordinary pleurisy, in that the extent of pain is greater and not so limited, due to the fact that the rheumatism invades the aponeurotic tissue which forms the covering to the intercostal muscles. It persists longer and is wider spread. The dyspnoea is caused by the inability to move the respiratory muscles and by the disease invading the aponeurotic centre of the diaphragm.

[Footnote 193: "Pleurésie rheumatismale," _Arch. Gén. de Méd._, 1873.]

The rapidity of the inflammation causes the sudden pain and the accompanying effusion in even a few hours. In a well-defined case recently seen by the writer in a lady forty-seven years of age the rheumatism literally jumped from a large joint to the pleura, giving rise to a severe pain, without cough or expectoration, with an increase of 2° of temperature and 20 beats of pulse. There was a moderate effusion. In forty-eight hours, under the influence of an initiatory dose of quinine (20 grains), followed by free doses of salicylate of sodium, the attack subsided and the friction sound at the base of the lung disappeared. This case did not follow the rule mentioned by Senx,[194] that the disease, upon leaving the pleura of one side, appears in the same manner on the other. It sometimes goes to the pericardium and endocardium from the pleura. Chomel[195] insisted upon the frequent examination of the heart to ascertain whether this had occurred.

[Footnote 194: _De la Pleurésie rheumatismale_, Paris, 1878.]

[Footnote 195: _Art. Pleurésie Dict._, in 30 vols., 1842.]

Rheumatism of the pleura does not always appear and disappear suddenly. It sometimes is gradual in progress and slow in recovery. It usually occurs when we have manifestations elsewhere, but the pleura may be the point first attacked, as is more frequently the case in pericarditis.

DIAGNOSIS.--The diagnostic signs are hereditary or personal tendency to the disease, the character of the local pain, the mobility of the disease, violence of pain and its rapid disappearance, and the existence of profuse sweats. Suppuration rarely occurs.

PROGNOSIS is in its nature serious, not from the intensity of the disease, but from its being a visceral rheumatic affection. It is, moreover, frequently double, and may recur often in the same subject.

TREATMENT is that of rheumatism elsewhere--salicylic acid and its salts, alkalies with opiates. Thoracentesis is rarely indicated, because mechanically the effusion does not seriously impede respiration: if the pericardium be involved, it may be necessary in order to relieve the pleura or the pericardium.

Hemorrhagic Pleurisy.

DEFINITION.--Pleurisy complicated by hemorrhage. Hemorrhagic pleurisy is the union of an ordinarily slight hemorrhage in the pleura with inflammation of that membrane (Laennec).

ETIOLOGY AND PATHOLOGY.--These must be studied together, because the pathology of the disease explains its etiology. While hæmothorax designates hemorrhage into the pleural cavity without inflammation, hemorrhagic pleuritis involves necessarily the idea of inflammation accompanied by effusion of blood, whether this occurs before, during, or subsequently to the inflammation. We cannot assign the name hemorrhagic pleurisy simply because there may be slight red coloration of the effusion. Microscopic researches have shown that all effusions, even the simplest, contain more or less white and red blood-corpuscles. The presence of a certain number of the red discs no more justifies us in calling the pleurisy hemorrhagic than the presence of {566} the leucocytes would entitle us to call it purulent pleurisy. Dieulafoy[196] states that there can be from 500 to 4000 red globules to the cubic millimeter without producing any coloration. They must reach 5000 before they will really attract attention. He says, however, that when the number of red corpuscles reaches 2000 the effusion is "histologically hemorrhagic," because the presence of blood is analogous to the state of engorgement or congestion of the first stage of pneumonia or other phlegmasia, and constitutes a particular phase of pleurisy which must produce purulent matter. The name hemorrhagic pleurisy ought to be used when the number of red blood-corpuscles is sufficient to enable us, by the unaided vision, to detect the presence of blood. We may, however, find a fluid in the pleural sac which is red and yet does not contain blood-discs, but their coloring principle, the dissolved hæmatin. Jaccoud[197] designates this condition pseudo-hemorrhagic pleurisy. Vulpian and Charcot explain the slight discoloration by the presence of hæmatin crystals, which, having been imbedded in the false membranes, escape into the flow of the chest. Nolais[198] included both of these discolored effusions among the varieties of hemorrhagic pleurisies: "Hemorrhagic pleurisies include all those of which the liquid borrows the red coloring matter of the blood." Moutard-Martin (R.)[199] divides hemorrhagic pleurisy into three varieties: simple, as produced in simple, acute, or subacute pleurisy; tubercular; and cancerous. Trousseau[200] considered all hemorrhagic pleurisies as caused by cancer. Beigel[201] states positively that in cancerous pleurisy the effusion is limpid with a yellowish tinge. Walshe[202] held the same views. Nolais, Moutard-Martin (R.), and Fernet satisfactorily demonstrated that such is not the case, but that the hemorrhagic effusion may be simple and independent of any organic disease. It may be produced by acute inflammations of the pleura as well as by cancer of the lung or pleura. It may be connected with pleuro-pneumonia or miliary tubercle. It comes, although more rarely, from fevers, such as measles, and from certain dyscrasiæ due to renal, hepatic, or even splenic lesions. When hemorrhagic pleurisy follows hæmothorax, the blood, after remaining liquid at least one or two hours, initiates the inflammatory action which has, according to Ch. Nélaton,[203] for its object the encystment of the clot. Cornil and Ranvier[204] claim that the cyst is caused by the retracted clot, and that after absorption of the serosity this cyst may become organized. The presence of air causes fetidity of the blood and purulent pleurisy.

[Footnote 196: _De la Thoracentèse par Aspiration dans la Pleurésie aigue_.]

[Footnote 197: "De l'Humorisme ancien comparé à l'Humorisme moderne," _Thèse de Concours_, 1863; _Gazette Méd._, 1860, quoted by Nolais.]

[Footnote 198: _Thèse de Paris_.]

[Footnote 199: _Thèse de Paris_, 1878.]

[Footnote 200: _Clin. Méd._]

[Footnote 201: _Reynolds's Syst. of Med._, 1871.]

[Footnote 202: _Dis. of the Chest_.]

[Footnote 203: _Thèse de Paris_, 1880.]

[Footnote 204: _Path. Anatomy_.]

We may have hemorrhagic effusions occurring simultaneously with acute pleurisy, with pulmonary congestions, pneumonias, and apoplexy of the lung. They are caused by the violence of the inflammation with local plethora, producing a sanguinary stasis--a mechanical result of intense congestion. Moutard-Martin (R.) states that in these cases the red globules come through the walls of the blood-vessels, as do the leucocytes, by diapedesis. Jaccoud[205] admits that the blood-vessels are altered by the inflammation, perhaps also by the derangement in the vaso-motor innervation. The tissue of the pleura is penetrated by both red and white blood-corpuscles, and the blood-vessels and lymphatics are dilated, red corpuscles being found in lymphatics. By far the greatest number of hemorrhagic pleurisies are secondary to pleural inflammations, either resulting from acute causes or from cancerous or tubercular disease, or from diseases causing a dyscrasia of the blood, such as nephritic diseases, hepatic, cardiac, scorbutic affections, or alcoholic excesses. The secondary result of these pleurisies is the formation of neo-membranes, fibrous {567} in their nature, which pathological anatomy shows contain, as they become organized, abundant blood-vessels with thin and brittle walls. A slight exciting cause is all that is necessary to produce their rupture. The primary cause is the false membrane, and, in some cases, vascular granulations, which have rapidly formed, perhaps in twenty-four hours--conditions eminently favorable to the production of hemorrhage. In cancerous, tubercular, and dyscrasial conditions of the blood, the blood-vessels are especially weak and easily give way, owing to the defective nutritive properties of the blood itself, just as, in typhoid fever, we have nasal and intestinal hemorrhage, and in typhus, petechiæ. In 200 cases collected by Moutard-Martin[206] there was found intra-pleural effusion in three-eighths of the cases. Only one-third of that number were hemorrhagic. In 42 cancers observed between 1872 and 1876, 35 were without pleural effusion, 1 only was hemorrhagic. M. Moutard-Martin reports 34 observations of hemorrhagic pleurisy produced by cancer, 19 by tubercle, and 31 following simple pleurisy. Of these last there were 7 cases of effusion complicated with a pneumonia, 3 with a cirrhosis, 6 with a cardiac affection: all except 12 of these cases had some complication. Most of these (12) recovered, so he had not the autopsies to verify his diagnosis. Rayer[207] cites 4 cases of bloody effusion in the pleura occurring in the course of a nephritis. Poutin[208] reports 1 in renal sclerosis. M. Natalis-Guyon[209] reports an epidemic of measles where many infants died of hemorrhagic pleurisy. Marguerite cites 13 cases complicating pneumonia, granulations, chronic pleurisy, small-pox, etc.

[Footnote 205: _Clin. Méd._]

[Footnote 206: _Loc. cit._]

[Footnote 207: _Traité des Mal. des Reins_.]

[Footnote 208: _Soc. Clin. de Paris_, 1879.]

[Footnote 209: _Soc. Méd. des Hôpitaux_.]

Rilliet and Barthez[210] say that it is common to find in infants considerable discoloration of effused serum in variolic and other organic poisons. It seems fair to conclude that hemorrhagic pleurisy may occur in a large number of cases where the blood has undergone alterations, but to produce it, it is necessary that the pleura should have been rendered vulnerable by pre-existing causes, because it ordinarily resists, better than many other membranes, the hemorrhagic tendency. If we admit the existence of tubercular or cancerous hemorrhagic pleurisies, we ought not to consider those as simple which are produced under the influence of the other causes that we have mentioned. The tubercular granulations are deposited either on the pleural surface or in the parenchyma of the lung near the surface, the most frequent locality being in the thickest parts of the organized false membranes. The rupture of their blood-vessels causes the escape of blood into the pleural cavity. The effusion, more or less discolored, rarely exceeds a liter in quantity. Effused blood from cancerous origin may either come from rupture of the vessels in the growths themselves by ulceration, or from the neo-membranes in their vicinity.

[Footnote 210: _Traité des Mal. des Enfants_, t. iii.]

The primitive seat of the cancer is rarely in the pleura, but most frequently in the lung, the cancer being of secondary formation arising primarily from ganglions of the mediastinum. Hemorrhagic pleurisy may be caused by laceration of the newly-formed blood-vessels in the neoplasms by aspiration or by the lung expanding too suddenly. We conclude that hemorrhagic pleurisy is generally owing, directly or indirectly, to vascular neo-membranes which are produced in simple, in tubercular, and cancerous pleurisies.

SYMPTOMS.--The symptomatology of this form of pleurisy does not differ materially from that of other varieties. We cannot attach much importance to the initiatory symptoms nor to the march of the disease. If the quantity of blood be great, we must expect general weakness, pallor, and even fainting. We may have oedema of the walls, as in purulent pleurisy, and exceptionally in serous pleurisy. Ordinarily, however, hemorrhagic pleurisy is more extensive, and limited to the inferior part of the chest, owing to the interference with the venous circulation. If cancerous in its origin, we shall have dyspnoea {568} and violent intercostal neuralgia from pressure of the tumor. When the effusion is formed in the pleural sac, the physical signs already enumerated indicate its presence. Some authors, especially Fernet, Moutard-Martin, Alcoud, and Guéneau de Mussey, attach considerable significance to Bacelli's whisper-pectoriloquy as showing that the effusion is not serous in character. Nolais questions this view, and says that this sound ought to be heard whenever there is blood, whereas they state it is heard only at the base or summit of fluid. When hemorrhagic pleurisy results from tuberculosis, it is never from the ordinary ulceration form, but always from the acute miliary, non-ulcerating variety. We must not, therefore, expect to be aided in our diagnosis by the progress and symptoms of pulmonary phthisis. We may, however, detect uncertain, indefinite symptoms which are hard to interpret as indicative of tuberculosis. The effusion is rarely excessive in this variety, whereas when resulting from cancer it is often very abundant and is rapidly reproduced.

DIAGNOSIS.--We may suspect the presence of hemorrhagic effusions, but only by exploratory punctures can we arrive at certainty of diagnosis. We must bear in mind that we may withdraw with the aspirator-needle some drops of blood at its insertion and at the close of the exploration from the highly vascular neo-membranes or from the lung itself. Having ascertained the nature of the fluid, the differential diagnosis must be made as to the cause, simple, tuberculous, or cancerous. We must study the manner of access of the disease, and especially ascertain if its invasion was violent, with a quantity of blood (d'emblée), or whether it came from the neo-membranes. In the simple variety there are the ordinary acute or subacute symptoms of pleurisy, without any preceding symptoms. In cases of tubercular origin we have to aid us a small quantity of fluid effused and the insidious character of symptoms. In cancerous cases we must expect to find traces of hereditary or of personal taint which may have affected the general health. We must look for cancer elsewhere, and examine carefully to see if there be any tumor of the mediastinum or intra-thoracic pressure, or any infiltration of the lymphatic glands, especially above the clavicle. The fluid drawn in the exploration ought to be examined microscopically, for we may detect evidences of cancer. Walshe[211] cites a case where encephaloid débris was thus discovered. Other authors also give similar cases.

[Footnote 211: _Diseases of the Chest_.]

PROGNOSIS.--This depends upon the nature of the disease producing it. When caused by the newly-formed membranes connected with simple serous pleurisy it is ordinarily not serious, for the mere presence of blood in the pleura has no bad influence over the restoration of health. It is more the intensity of inflammation, with the quantity of blood effused, that indicates gravity of prognosis. Dieulafoy[212] considers the prognosis as unfavorable in the hémorrhagie d'emblée form, drawing the distinction between this and the histologically hemorrhagic. He thinks that every purulent pleurisy was at first hemorrhagic, and the presence of pus shows greater intensity of inflammation. Homolle[213] also states that the pleurisies rich in red globules are ordinarily very acute, and, in consequence of that fact, predisposed to purulence. Purulency is not the sole cause of danger. We fear compression of the lungs, and still more septicæmia. In the tubercular and cancerous forms the prognosis must be very serious. When the hemorrhagic pleurisies arise in the course of organic diseases of the heart, kidney, and liver, they are of grave import.

[Footnote 212: _Loc. cit._]

[Footnote 213: _Rev. des Sci. Méd._, 1880.]

TREATMENT.--If the quantity is excessive, local applications and ergot ought to be employed to arrest the flow. If the dyspnoea and oppression are great, it is best to draw off at least some of the fluid. If the quantity be not large enough to embarrass respiration, we must expect nature to absorb {569} it, or by local inflammation to encyst it. Lacaze[214] reports a case where a fistula was established, and the case was cured. Dieulafoy gives another case where six punctures were made, and no less than 6 liters, in all, were withdrawn. He injected afterward a solution of 4 grammes of sulphate of zinc to 400 grammes of water, and the patient was cured. In the first stage of the disease we use palliatives--morphia hypodermically, bromides, and chloral--if indicated. During febrile symptoms of acute cases we refrain from withdrawal of fluid unless it is excessive. The question of thoracentesis has been discussed in regard to simple pleurisies. The same rules apply, a fortiori, when the nature of the fluid is hemorrhagic. Ordinarily, the abundance of fluid, and the dyspnoea which results therefrom, indicate the operation. We prefer not to draw off the fluid completely--only enough to relieve the embarrassment of respiration--because we destroy the equilibrium of pressure on one side against the neo-membranes and the compressed lungs on the other. Congestion of the lung may thus be produced with albuminoid expectoration. Moutard-Martin (R.) coincides with Dieulafoy in limiting the amount to be withdrawn to one liter. Of course the fluid is slowly aspirated. After part of the fluid is withdrawn, what remains is absorbed, remains stationary, or increases in quantity. We repeat the operation, and slowly draw off greater quantities of fluid if it returns; especially in cancerous cases, where the effusion is often very large, the operation gives great relief. It is rarely large enough in tubercular cases to justify thoracentesis.

[Footnote 214: _Thèse de Paris_, 1851.]

Tubercular Pleurisy.

Tubercular pleurisy may be acute or chronic. It may occur during the course of ordinary tubercular disease of the lung, by extension of the disease from the lung to its serous covering, or it may proceed from tubercular deposit on the pleura independently of any previous disease of the lung. Acute tubercular pleurisy may be dry and situated at the summit of the chest, or may be what is called accidental pleurisy. Dry pleurisy is almost constant in tuberculosis of the lung. Its existence is, in itself, a powerful presumption of pulmonary phthisis, especially when it is situated at the apex. In tuberculosis pleuritic inflammation is lighted up by slight and scarcely appreciable causes. Its commencement is insidious, with little or no pain or fever: indeed, it is with subacute symptoms that the disease slowly advances. The first intimation the patient has of the disease is the impairment of his breathing-power by the presence of fluid. The fluid is not generally in large quantities, and is serous or sero-fibrinous, and sometimes sero-purulent. Latent pleurisy of the older writers was frequently tuberculous in its origin. This form of tuberculosis may precede or follow the deposit of tubercles in the lung-tissue. The tubercles may be deposited to a slight extent in the tissue of the lung, and their presence is shown by an irritating cough only when the pleurisy approaches insidiously. The tubercular granulations over the visceral pleura are extended to the parietal surface also, and notably to the circumference of the fibrous leaflet of the diaphragm--an especial point of elevation for the secondary products.

This disposition of tubercular lesions of the pleura is one of the most striking examples of what is called infection from contiguity, and is a powerful proof of the infective property of tubercular products which from an initial nucleus is propagated from point to point. Acute tuberculosis of the pleura is one of the most common manifestations of acute phthisis. It more frequently causes acute than subacute pleurisy. Chronic tuberculosis almost always produces purulent pleural effusions. It is much {570} more common in infants than in adults, and is sometimes met with in children from three to ten years of age (Barthez et Rilliet[215]). Tubercles may be developed in the intra- or extra-serous membrane. Among old people the tubercle sometimes appears first in the recent false membranes produced by pleuritis (as associated with caseous pneumonia, or genuine tuberculous processes in the lungs), or in connection with tubercles of other organs (Fraentzel[216]). The advance of this disease is habitually slow, or at least not accelerated by the development of other tubercular diseases. The diagnosis is often accompanied with great difficulties, for the disease may be confounded with chronic or with purulent pleurisy, especially if these are developed in a tuberculous subject. In both cases we have hectic, night-sweats, emaciation, etc. Thoracentesis alone can give definite results when the effusion is in considerable quantity. When suppurative pleurisy supervenes in tuberculous subjects, the prognosis is very grave. Should the pus be sufficient in quantity to embarrass respiration, it can be drawn off cautiously by aspiration. The open method of drainage and free incisions should not be used, for experience has shown that they injure instead of benefiting the patients.

[Footnote 215: _Mal. des Enfants_.]

[Footnote 216: _Ziemssen's Cyc._, vol. iv.]

Hydrothorax.

From [Greek: hydôr], water, and [Greek: thôrax], the chest.

DEFINITION.--Dropsy of the chest. The accumulated fluid in the pleural cavity which resembles the serum of the blood is not the product of inflammation, but is caused by mechanical obstruction to the circulation or by blood-poisoning. Hydrothorax is never idiopathic, but invariably secondary, resulting from disease, not of the pleura, but of the circulatory system or of the blood itself.

HISTORY.--Before pathological anatomy had been accurately studied, effusions resulting from inflammatory processes in the pleura were confounded with simple hydrothorax, which is not a variety of pleurisy. Royer[217] and Laennec[218] divided hydrothorax into idiopathic and symptomatic; Darwell[219] adopted in a great measure their views. They did not draw the distinction between the passive transudation of serum, constituting the condition known as hydrothorax, and exudations resulting from idiopathic pleurisy. Before physical modes of exploring the chest were used there was great uncertainty in the diagnosis of collections of fluid in the pleural cavity.

[Footnote 217: _Dict. de Méd._, 1832.]

[Footnote 218: _Dis. of Chest_, Forbes's edition.]

[Footnote 219: _Cyc. Pract. Med._]

ETIOLOGY.--Dropsical effusion in the thorax is produced by the same causes which give rise to collections of watery fluid in other serous cavities and in the connective tissue, constituting general anasarca. Primary among the causes is obstruction of the venous circulation in the walls of the chest or in the lungs. Mitral disease, especially insufficiency with dilatation, deranges the normal circulation in the lung and its serous coverings, producing hyperæmia, oedema of the lung, and finally serous effusions into the pleural sac. General dropsy results. According to Fernet,[220] in dropsies resulting from mitral disease oedema of the lungs and hydrothorax always precede all other oedemas. Fraentzel,[221] on the contrary, states that it does not occur until there is no longer any room for the transuded fluid in the deeper portions of the subcutaneous tissues. Other diseases of the heart produce hydrothorax. Whenever there is abnormally high venous pressure, which invariably follows dilatation of the right side after compensatory hypertrophy has reached its limit, and the heart literally yields to the backed current of blood, we must expect dropsical results. Intra-thoracic tumors, aneurisms, emphysema, and sclerosis of the {571} lung cause hydrothorax by pressing upon the venous trunks and upon the thoracic duct without producing general dropsy. Chronic diseases, such as cancerous disease, chronic malaria, etc., produce great exhaustion and give rise to general hydræmia. Especially is this the case in chronic disease of the kidneys, such as the several varieties of nephritis and amyloid degeneration, where there has been a loss of albumen for a long time and the blood-serum has been rendered poorer in solid constituents. Hydrothorax is not a disease, but a symptom resulting from a variety of causes which produce physical exosmosis of the serum of the blood.

[Footnote 220: _Nouveau Dict. Méd._, vol. xxviii.]

[Footnote 221: _Ziemssen's Cyc._, Amer. trans., vol. iv.]

PATHOLOGICAL ANATOMY.--Hydrothorax being merely dropsy of the thoracic cavity, there is no lesion of the pleura. There is a collection varying from 100 grammes to many liters of fluid in the cavity. It differs from the effusion in subacute pleurisy in its small quantity of fibrin, in having far less of albuminoid material, and no white blood-corpuscles. The water collects almost always in both sides of the chest, more on the side on which the patient lies in bed. In the recumbent position the fluid gravitates posteriorly more than the effusions of pleurisy. In the upright position it will follow Ellis's curved line more regularly than in effusions resulting from pleurisy, for there are no adhesion-bands interfering with its doing so. The fluid is limpid, of a light-yellow or citron color. Its composition resembles that of the plasma of the blood, but it contains more water and less of the constituent elements. Alex. James[222] found that the amount of mineral matter was the same in dropsical fluids in all parts of the body, and that the organic albuminoid substances were larger in quantity in the pleura than in any other cavity. The amount of organic substances varied directly in accordance to the degree of pressure on the different capillary vessels. The anatomical changes in the pleura and the subpleural connective tissue are similar to those found in other collections of dropsical fluid. They are swollen and thickened by maceration with water. They become opalescent and less firm of texture. The lungs retract as the fluid increases in quantity. As the filtrates collect in both pleural sacs, the lungs do not forcibly collapse. The patient would sink at once were this the case. The arch-tension of the diaphragm is but rarely overcome, and consequently we must not expect to find the liver and spleen pushed down, especially when there is fluid in the peritoneal cavity. The position of the heart, unless there is a marked difference in the collections of the two sides, is but little altered, the retractive force of both lungs being impaired.

[Footnote 222: _Med. Times and Gazette_, Jan., 1880.]

SYMPTOMS.--The general accumulation of watery fluid is not attended by any pronounced symptom until it has reached the point of interfering mechanically with the normal play of the lungs. At first dyspnoea is only perceptible on increased physical exercise. When the quantity is excessive, the individual suffers when perfectly quiet. The patient, until the fluid is excessive, lies on his back as the most comfortable position, but as the quantity increases he is often obliged to sit up in bed.

The dyspnoea is ordinarily much more oppressive than in pleuritic effusions, because both lungs are compressed. There is no rise of temperature, no pain in the side, no tenderness on pressure, no acceleration of the pulse, and but rarely any cough, as there is in pleurisy. The dyspnoea often becomes very painful, and may even produce orthopnoea, being accompanied by short and frequent acts of breathing. Where there are very large amounts of fluid the mechanical interference with the breathing is so great that cold sweats, cyanosis, and asphyxia follow, the pulse becoming smaller and more feeble until the patient dies.

The physical signs are, in general, the same as those of pleuritic effusions, especially the subacute form, with some slight variation. Inspection {572} and mensuration do not aid us as in pleurisy, for in hydrothorax the accumulation of fluid is bilateral instead of unilateral. The tension is not sufficient to dilate the walls of the chest. Palpation shows absence of vocal resonance, but not invariably, for we are unable to compare the two sides. We must remember that we have oedema of the walls of the chest, which would partially prevent the thoracic vibrations from being felt. Percussion flatness is not as absolute as it is in pleurisy, unless the fluid is in excessive quantity, for the tension of the fluid is feebler and the lung contains more air. The lung is never completely compressed, as in pleurisy, there being no fibrinous bands to constrict it. The percussion vibrations, unless very lightly made, are communicated to the lung; and so there is dulness instead of flatness. The absence of fibrinous bands permits the fluid to change its position with the varying postures of the patient. This rarely occurs in pleuritic effusions after the first few days. Finally, Skodaic tympanic resonance at the apex is but seldom met with in simple hydrothorax.

Auscultation.--The presence of fluid between the lung and parietes prevents us from hearing the vesicular murmur. The distant bronchial respiration is rarely heard in hydrothorax, as it is in pleurisy, because the lungs are not completely deprived of air, and when present is less intense. Ægophony is frequently heard over the upper limit of the fluid, the whispering voice being transmitted through the fluid. Owing to pulmonary oedema there are subcrepitant râles, but never pleuritical friction sounds.

DIAGNOSIS.--Ordinarily, the diagnosis ought to be made without difficulty. The only disease with which there can be any danger of confounding it is subacute pleurisy. The principal points of differential diagnosis have been enumerated above. In subacute pleurisy (latent pleurisy) we have, in less intensity, the ordinary pleuritic symptoms. The pleuritic friction murmur is present, and a fluid containing the products of inflammation. Very exceptionally is subacute pleurisy double, whereas hydrothorax is almost invariably so.

The history of the case enables us to arrive at an accurate diagnosis. The withdrawal of a small quantity of fluid with a fine perforated needle, and its chemical and microscopical examination, will complete the diagnosis in doubtful cases.

Oedema of the lung can scarcely be confounded with hydrothorax. The absence of the physical evidences of water in the cavity, and the crackling sound heard in auscultation, are distinctive of oedema.

PROGNOSIS.--The prognosis is always serious, but it depends upon the nature of the disease producing the dropsy. If this can be removed, the collection of water may disappear. But, unfortunately, the circulatory diseases which produce it are generally chronic and incurable. The fluid can, by general treatment and mechanical means, be reduced, and the life of the patient prolonged and made comparatively comfortable. Sooner or later a large number of cases must succumb.

TREATMENT.--The treatment should first be directed to the primary disease causing the dropsy. If heart disease be the promoting cause, we must, by means of digitalis, endeavor to promote compensating hypertrophy, and by arsenic and iron improve the quality of the blood. If Bright's disease be the cause, the skimmed-milk diet, with iron and manganese, must be given with remedies which lessen the hydræmic condition of the blood. Digitalis, diuretics, jaborandi, and drastic purgatives give decided results. Of all purgatives, elaterium in decided doses (¼ grain), guarded by conium or hyoscyamus, causes most relief by producing free watery stools. Mechanical means must be resorted to without hesitation. It is best first to remove the fluid from the lower extremities by the insertion of Southey's capillary canula with caoutchouc tubing attached. Large quantities of water may {573} thus be drawn off without local irritation, erysipelatous in its nature, being produced. Thoracentesis by aspiration averts death very often, and gives the greatest possible relief when the effusion is large enough to produce dyspnoea. In a case under the author's care life was prolonged many months and large quantities of fluid were removed. Altogether, there were twenty-two operations and 1563½ ounces of water removed. As often as every week one or other side had to be emptied, the quantity removed each time varying from 49 ounces to 112 ounces. For two months previous to death filtrates collected in the abdominal cavity also, and had to be frequently withdrawn.

Pneumothorax.

DEFINITION.--A collection of atmospheric air or of gas in the pleural cavity. Pneumothorax ([Greek: pneuma] and [Greek: thôrax]).

In ancient times gaseous collections were frequently noticed in serous cavities, especially on opening the chest for empyema and at post-mortem examinations. The presence of air resulting from laceration of the lungs by fractured ribs was known and designated as emphysema thoracis. Air in the pleura was considered as an accidental complication which occurred with empyema or as formed after death. Morgagni and others mentioned the presence of gas as formed in the pleural cavity. Itard[223] was the first to speak of it as a disease and to name it pneumothorax. Owing to the imperfect knowledge of pathology at that period, he attributed the production of the air to the decay of the lung from chronic suppuration, and to the decomposition of the long-retained pus. Laennec was the first to give an accurate anatomical and clinical account of the disease.

[Footnote 223: _Thèse de Paris_, 1803.]

HISTORY.--Pure pneumothorax--that is, pneumothorax caused by the presence of air alone in the pleura--is but rarely met with, except for a short time, when it has been introduced from without by traumatic injuries. The irritating effects of gas, unless it comes in small quantities through the ribs from wounds in the chest-walls, are very frequently followed in a short time by the production of a quantity of serosity or of pus. If air is introduced into the pleural cavity from perforation of the lung, there is also liquid matter from the lungs of such a character as at once to provoke inflammatory action. Such a condition is then denominated hydro-pneumothorax or pyo-pneumothorax. The latter was, in fact, recognized by Hippocrates by the sign of succussion, though not so designated.

ETIOLOGY.--Laennec divided pneumothorax into three distinct varieties: 1st, essential pneumothorax, resulting from the spontaneous formation of gas in the pleural cavity; 2d, pneumothorax from putrid decomposition of liquids effused into the pleura; 3d, pneumothorax by perforation, due to rupture into the pleura or to an accidental opening by which atmospheric air or gas from the lungs is introduced into the pleural cavity. This division, having Laennec's high authority, was for a long time generally received. It has now been established that the pleuræ cannot secrete air.

Proust[224] collected 25 cases of so-called spontaneous pneumothorax, and showed that they could all be otherwise satisfactorily explained. In some cases errors of diagnosis had been made by mistaking tympanitic sonority at the anterior-superior portion of the chest, or the existence of the amphoric breathing found in pleurisy, for pneumothorax. Some were cases of pneumonia in which tympanitic percussion resonance deceived observers. Then, again, there was found, among the cases cited, pneumothorax resulting from rupture of a tubercular cavity or of a hydatid. In tubercular cases Proust found that the orifices made were so small--no larger, as Gairdner of {574} Edinburgh had stated, than a pin's point--that they could not be detected, or that they had cicatrized before the post-mortem examination, or perhaps closed by adhesive false membranes. Other investigations by Ewald[225] and Jaccoud[226] have confirmed Proust's views that essential pneumothorax does not occur. Researches in pathological physiology disprove the possibility of a serous membrane producing a secretion of gas or of its passing from the blood through the capillary walls. We therefore conclude that pneumothorax from secretion of air within the pleura is contrary to physiological facts generally accepted, and is disproved by pathological investigations.

[Footnote 224: _Ibid._, 1862.]

[Footnote 225: Quoted by Fraentzel, _Ziemssen_, vol. iv.]

[Footnote 226: _Gaz. hébd._, 2^{ème} serie, 1864.]