Chapter XL: Part 40

The second variety in Laennec's division--namely, where the gas results from decomposition of fluid in the pleural cavity--has been supported by such high authorities as Hughes Bennett, Townsend, Wunderlich, and Jaccoud. Yet it is difficult to understand how it could occur. The contact of air appears to be necessary for the decomposition of serum and pus in the pleural cavity. While shut up in a cavity coated with neo-membrane, a fluid may certainly remain undecomposed for a long time, and undergo decomposition as soon as taken out of the cavity. Recent researches in regard to putrid fermentations appear to confirm the view that the presence of air is absolutely necessary to produce that effect.

We believe, therefore, that perforation, with rupture of the visceral or parietal layer of the serous membrane, causing the introduction of air into the pleural cavity, is the invariable cause of pneumothorax and of hydro-pneumothorax. The causes of the rupture are in the lung, in the pleura, or in the adjoining organs. They may be traumatic or non-traumatic: the latter may be perfectly designated pathological causes, because the pneumothorax is always secondary, following upon a pre-existing pathological condition.

Traumatic pneumothorax may take place in consequence of an injury to the thoracic walls, of an exterior injury, or of a penetrating wound. The parts may be so bruised that pleural necrosis gives rise to sloughs and resulting openings. Fracture of ribs may tear the lungs, and allow air to enter the connective tissue and produce local emphysema. Violent contusions, as in a case recently observed by the author, produce laceration of the lung without the rib or costal pleura being injured.

Non-traumatic or Pathological Causes.--Laennec taught that pulmonary tuberculosis was the most frequent cause of pneumothorax; and further observation has demonstrated the correctness of this view. Walshe states that such is the case in 90 per cent. of the cases of perforation of the lung. In 131 observations reported by Saussier,[227] 81 were from pulmonary phthisis, principally from caseous pneumonia. Fraentzel[228] says, from his own observation, that 90 out of 96 cases of pneumothorax are produced by vomicæ on the surface of the lungs in the course of caseous pneumonia. Grisolle states that nine-tenths of the cases result from rupture of a lung-cavity. Fuller[229] reports 22 cases, in 18 of which the disease was produced by tubercular ulceration. Chambers,[230] at St. George's Hospital, reports that 21 out of 23 were tubercular. Fernet[231] states that pneumothorax results in nine-tenths of the cases from some of the forms of pulmonary phthisis.

[Footnote 227: _Thèse de Paris_, 1841.]

[Footnote 228: _Ziem. Cyc._, vol. iv.]

[Footnote 229: _Dis. of the Chest_, p. 226.]

[Footnote 230: _Dec. Pathologicum_, cap. v. sec. v.]

[Footnote 231: _Nouveau Dict._, vol. xxviii.]

Ordinarily, pneumothorax is unilateral; only exceptionally is it met with on both sides. In tubercular cases it is twice as common on the left side as on the right (Condrin[232]). In the total of 146 cases reported by Louis, Walshe, and Powell, 94 were on the left side; whereas when it is consecutive to a pleuritic effusion it is almost always on the right side--17 out of 18 (Saussier[233]).

[Footnote 232: _Thèse de Paris_, 1882.]

[Footnote 233: _Ibid._, 1841.]

{575} In tubercular cases perforation of the lung may occur at any period of the disease; the most frequent time, however, is that of the softening or while excavations are being formed, where adhesions have not yet protected the two sides by binding them together with neo-membranes. It may come from a small cavity. Andral met with cases where only a few tubercles existed. Townsend reported a case where one tubercle burst immediately under the pleura. The superior lobe of the lung is where the perforation generally occurs, because it is there that the tubercular lesion ordinarily commences and is most advanced (Louis). It is least frequent in chronic fibroid phthisis and most often met with in acute pneumonic phthisis. Douglass Powell[234] reports cases where sinuses extended from cavities, and finally burst into the pleura. Sometimes the rupture occurs at the base of the superior lobe, about the third or fourth rib; it may happen, however, at any point of the lung; it has even occurred at the base of the lung lying on the diaphragm (Houghton[235]).

[Footnote 234: _Med. Times and Gaz._, Jan. and Feb., 1869.]

[Footnote 235: _Cyc. Pract. Med._, vol. iii.]

Saussier[236] shows by the following table the relative frequency of the principal causes of pneumothorax in 131 cases:

Pneumothorax with phthisis . . . . . 81
" " empyema . . . . . 29
" " gangrene . . . . . 7
" " pulmonary emphysema 5
" " apoplexy . . . . . 3
" " hepatic fistula . 2
" " hydatids . . . . . 1
" " hæmothorax . . . . 1

[Footnote 236: _Thèse de Paris_, 1841.]

Empyema ranks second as a producing cause of pneumothorax. Ordinarily, by direct necrosis of the parietal pleura, an orifice is made through which the pus is evacuated through the bronchi, and air in inspiration enters the pleural cavity by the bronchial fistula. Pyothorax is converted into pyo-pneumothorax. The valvular opening may, however, be closed by inspiration so that air cannot enter, or adhesions may limit a portion of the pleura, and then we have a circumscribed pneumothorax. Empyema, by producing ulceration of the thoracic walls and pointing exteriorly (emphysema necessitatis), leaves fistulæ through which air enters the pleural cavity.

Gangrene of the lung by sloughs allows air to penetrate. Bronchiectasic cavities sometimes become the seat of putrefactive changes and ulcerations through the lungs into the pleura. Infective emboli being arrested in the smaller peripheral branches of pulmonary arteries, air enters the cavity; it is thus that pneumothorax arises in various kinds of surgical diseases when infective emboli pass into the circulation (Fraentzel). Flint[237] reports a well-marked case of pneumothorax, lasting less than one month, where there was every reason to suppose that it had been caused by rupture from interstitial emphysema. W. T. Gardner had previously reported a similar case. Saussier found emphysema was a cause in only 5 out of 131 cases. Fraentzel speaks of emphysema as rarely being a cause. Perforation of the oesophagus, ulcerative, cancerous, or traumatic from the use of bougies, produces pneumothorax. Suppurating bronchial glands--a case of which was met with by the author--bursting into the cavity produce pneumothorax. Hydatids of the lungs, abscesses of the abdomen, sometimes coming even from the cæcum and from the liver, burst into the pleural cavity and introduce air. Echinococcus cysts of the liver are occasionally emptied into the pleural cavity.

[Footnote 237: _Practice of Medicine_, ed. 1881; _Series of Amer. Clin. Lectures_, article "Pneumothorax," 1875.]

{576} Pneumothorax is more than four times as frequent in men as in women. One-third of the whole number of cases occurs in persons between the ages of twenty and thirty years; one-tenth between the ages of ten and twenty; one-twelfth between thirty and forty (Saussier[238]). Although pneumothorax has a number of exciting causes, yet they are all comparatively rare except pulmonary tuberculosis and purulent pleurisy.

[Footnote 238: _Thèse de Paris_, 1841.]

PATHOLOGICAL ANATOMY.--In traumatic pneumothorax and simple cases, such as from the bursting of emphysematous alveoli, the presence of air is the only pathological product. If the pleura and adjoining organs are not diseased, the rupture or tearing cicatrizes rapidly, and the air disappears in a few days by absorption. If a quantity of air be admitted, the pneumothorax may last for months; yet if the pleura is healthy, the air itself will not produce local changes. If blood or morbid products flow in with the air, then inflammatory changes occur, and we have deleterious products effused. Demarquay and Leconte[239] demonstrated the innocuousness of introducing air into healthy pleural sacs of dogs, having injected it repeatedly into the same dogs without any unpleasant result. These observers analyzed the air after it had remained in the chest, and confirm Davy's[240] researches as to the changes in its condition. The oxygen diminished gradually, and finally disappeared, while carbonic acid replaced it to nearly the same amount. This air from the pleura approximated in composition to the air of expiration. When blood and bronchial secretions with pus are thrown into the pleura, they promptly produce more serious results, especially intense suppurative pleurisy. Duncan[241] found in a case of pyo-pneumothorax a fetid gas to contain 26 parts of sulphuretted hydrogen and carbonic acid and 74 parts of nitrogen. Secondarily, lesions are produced--hydro-pneumothorax and pyo-pneumothorax. In other cases, the pleura having been previously the seat of chronic disease with purulent effusion, this latter undergoes fetid changes and septicæmia results. Under these circumstances the pathological changes are similar to those we have described as found in empyema. We find like increase of tissue-formation, of pus, and of the development of the gases, sulphuretted hydrogen and sulphydrate of ammonia, which give rise to a horrible fetidity. The quantity of air varies very much, as does the amount of fluid: there may be a small quantity of air and much fluid, or the reverse.

[Footnote 239: _Gaz. Méd._, 1864.]

[Footnote 240: _Phil. Trans._, 1823.]

[Footnote 241: _Edin. Med. and Surg. Journal_, 1827.]

The opening into the pleural cavity may be direct or oblique: if direct, it remains open; if oblique, it is generally more or less valvular. The symptoms, prognosis, and treatment vary accordingly. Through a patent orifice the air enters in inspiration, and goes out with the expired air from the lungs. As it cannot accumulate, there can be no positive air-pressure within the pleura. If, however, the orifice be valvular, although the air enters it does not escape, for it presses upon the valve and closes it. If the valvular fold be perfect, the air soon becomes excessive in quantity, and exerts dangerous pressure upon the lung and adjacent organs. By means of a trocar, attached by tubing to a water-pressure gauge, Douglass Powell[242] ascertained post-mortem the degree of intra-pleural pressure present in 16 cases of pneumothorax. In 4 out of these cases the pressure was nil. In 12 there was more or less intra-pleural pressure present, varying in degree from 1¾ to 7 inches of water.

[Footnote 242: _Medico-Chir. Trans._, 1876.]

Unless the lung be mechanically prevented, the entrance of air into the pleural cavity at once produces a retraction of the lung, owing to its elasticity. There is no compression of the lung unless the air is increased in quantity by each inspiration, and, having no exit, accumulates; then the lung may be forced against the spinal column and the residual air actually {577} forced out of the alveoli. Powell[243] questions whether the intra-thoracic pressure excited in pneumothorax is ever equal to what is sometimes the case in pleurisy: the highest he had ever met with in pneumothorax was 7 inches of water. Garland,[244] in repeating Damoiseau's experiments in testing the effects of the introduction of air into the pleural cavity, found that the air did not penetrate between the lung and the lateral chest-walls until the lower border of the lung had retracted upward the distance of several ribs.

[Footnote 243: _Loc. cit._]

[Footnote 244: _Loc. cit._]

One of the most pronounced effects constantly observed in pneumothorax is the immediate displacement of the heart to a greater extent than in pleurisy. Gaidy,[245] as far back as 1828, described displacement of the heart as an important sign of pneumothorax. He related a case where, at the moment of the perforation, the woman was conscious of the heart's beat having been transferred to the right of the sternum. Powell[246] out of 17 cases found the heart displaced in 16: in the seventeenth the unruptured lung was so consolidated that it could not collapse. In pneumothorax of the right side a careful examination is sometimes required to detect the displacement of the heart. The apex can be discovered at a considerable distance to the left of the nipple, with the right ventricle drawn to the left edge of the sternum. It has been generally believed that the cause of this displacement was the intra-pleural pressure of the air, but this does not satisfactorily explain it, for there can be no pressure until the elasticity of the lung has been overcome. In 13 of Powell's cases there was great displacement of the heart with different degrees of intra-pleural pressure. In 3 cases there was great displacement of the heart with no intra-pleural pressure. The same author[247] showed, experimentally, that the elastic tension of one lung, when unopposed by that of the other, was sufficient to draw aside the mediastinum, and with it the heart. He thus demonstrated that these displacements are by no means necessarily a sign of intra-pleural pressure, since they may occur to the right of the sternum without there being any pressure. Clinically, we know that the admission of air into the pleural cavity immediately and constantly displaces the heart, unless the opposite lung be consolidated or otherwise injured in its resiliency. This occurs even when the patent orifice of the perforation prevents the accumulation of any quantity of air. There is not enough air to produce direct pressure, but there is enough to impair the elastic traction of the lung, and thus to destroy the equilibrium of traction which keeps the heart in its normal position. The healthy lung by its unimpaired tractile force immediately draws over the heart. Skoda[248] maintains that "air does not enter the pleural cavity simply at the cost of the torn and retracted lung, but the sound lung also retracts to such a degree as to move the mediastinum." Garland's experiments[249] conclusively demonstrate that the air in pneumothorax is powerless to exert an appreciable lateral displacing force until the lung has completely collapsed; and this does not ordinarily occur. There can be, he says, but one cause of constant and early displacement of the heart--the elastic force of the opposing lung, which draws it over to itself. He adds that "the explanation of the greater displacement of the heart in pneumothorax is that the air, having practically no weight, cannot exert upon the heart the negative pressure which an effusion evidently would."

[Footnote 245: _Arch. Gén. de Méd._, tome xvii., 1828.]

[Footnote 246: _Medico-Chirurg. Trans._, vol. lix.]

[Footnote 247: _British Med. Journal_ and _Med. Times and Gazette_, July, 1869.]

[Footnote 248: _Auscultation and Percussion_, Eng. trans.]

[Footnote 249: _Loc. cit._]

The fluid in hydro-pneumothorax is very rarely of a serous character. Saussier found but 1 such example in 169 cases. It is almost always purulent pneumothorax, and frequently it has a very offensive fetid odor from putrid decomposition. Mixed with pus there are sometimes found masses of {578} pseudo-membranes, débris of lung, and gangrenous patches, as in purulent pleurisies. The fistulous orifice through which the air has entered is not always easily found, being often hid away among false membranes. It is small and tortuous, and can only be discovered by placing the lung under water and blowing air through the bronchial tubes. Sometimes the orifices close and the air becomes encysted, interlobular, or diaphragmatic. There is sometimes only one opening; again, there may be several. Nolais reports a case where there were six openings. Orifices with lacerated edges are met with, varying in length from one to ten or twelve centimeters. It must be borne in mind that perforation can take place without producing pneumothorax. Saussier found this occurred in 2 out of 74 cases, and in 8 out of 29 resulting from pleurisy. Fériol and Guéneau de Mussey give similar cases.

SYMPTOMS.--The initiatory symptoms of pneumothorax vary according to the cause which produces it. When the effusion of air into the pleural cavity is from perforation of a diseased lung (most frequently tuberculous, more rarely gangrenous or from an abscess), the first symptom is a sudden agonizing pain in the side, accompanied with dyspnoea amounting almost to suffocation. In rare instances, where strong old adhesions limit the pneumothorax, there may be only slight pain, without dyspnoea. The rush of a moderate quantity of air into the cavity causes the lung to collapse; but should the amount of air be excessive, it will render the symptoms of oppression most intense, for it will compress the lung and heart and obstruct the capillary circulation in the lung. Such must be the case, for there is no aspiration of blood from the large veins, and no aëration of blood in the lung. The patient often feels as if the chest were being torn away, and the expression of his countenance betrays distress and alarm. If the orifice be large and valvular, preventing the escape of the air, the air accumulates rapidly and completely forces the air out of the lungs, and death shortly follows, sometimes in a few hours. There is no rise of temperature or fever. On the contrary, the temperature very frequently falls one or two degrees below the normal in consequence of the sudden collapse, the pulse from exhaustion being very frequent and feeble, accompanied by cold sweats. The voice becomes exceedingly feeble and whispering. In many cases the patient does not sink at once from the shock of the perforation, but becomes less oppressed, although he suffers considerably, being unable to lie flat in his bed. Respiration is not only frequent (sometimes 60 per minute), but the dyspnoea is oppressive and distressing to witness. Fever follows invariably, and sometimes with great rapidity, caused by pleuritis. When this occurs, the patient again suffers from dyspnoea as the purulent fluid accumulates in the pleura and gradually dropsy comes on. These cause dyspnoea and cyanosis. The position of the patient, leaning forward, supporting his elbows on his knees, indicates his agony and difficulty in breathing; the pain appears to go through and produce local hyperæsthesia, and the patient dies from the empyema with hectic and oedema of the lungs. The pleurisy excited may be simply serous in its products, even when it is tuberculous in origin. Usually, however, it is purulent, and we must then expect to find the grave symptoms we have enumerated in speaking of empyema with hectic and septicæmia.

PHYSICAL SIGNS.--These are well distinguished and marked, and lead easily to its diagnosis. Inspection shows the side to be immovable and the dilatation permanent; the spaces between the ribs are obliterated and the shoulder raised. There is no rhythmical expansion and contraction of the walls of the chest, the diaphragm is not elevated, and the liver and stomach are kept down. Air continues to enter the cavity, until the quantity is so great that its tension is equal to the atmospheric pressure. The contrast between this condition and that of the healthy side is very great. In the former the breathing is labored, with painful muscular contraction in the walls and whole side. {579} Percussion over the chest gives a hyper-resonant sound, with a graver-pitched tympanitic resonance. There is but little sense of resistance to the finger, owing to the elasticity of the contained air. When fluid is secreted in the second stage we have absolute flatness at the base over a horizontal level, and tympanitic resonance above. The pitch of this last sound varies according to the tension of the gas contained in the chest and the correlative tension of the thoracic walls. If this tension be feeble, the pitch is higher; if it be extreme, the tone will be drum-like, muffled, acute, and the tympanitic character will be less easily perceptible. It may happen that the pitch will be so high that we may be misled and think there is flatness. It is not true flatness, but a clean and high-pitched sound, very different from the tympanitic sound usually found; it is sometimes remarkably metallic in character. With auscultatory percussion, using a solid pleximeter, we have the prolonged metallic resonance which Trousseau appropriately named the bruit d'airain.

The area of hyper-resonance and flatness on percussion is changed with the altered position of the patient. The fluid, obeying the law of gravitation, takes its hydrostatic level, and when the patient's chest is upright is horizontal. Hyper-resonance is often pronounced over the sternum, and sometimes infringes upon the healthy side. When the disease is on the left side it obliterates the normal dulness over the cardiac area.

Palpation.--Thoracic vibrations of the voice are not felt over the portion of the chest containing air, nor over that containing fluid. This absence of vocal fremitus is very characteristic. The hand detects that the heart has been displaced toward the sound side and that the abdominal viscera are pushed down.

Auscultation.--The auscultatory phenomena vary according to the cause of the pneumothorax and the size and direction of the orifice. In tubercular cases, where perforation has produced a large, free opening, as the air passes in and out of this large pleural cavity with firm walls (the lung having collapsed perhaps to one-third or less of its normal size), we have the physical conditions which give marked amphoric and metallic respiratory sounds, with absence of respiratory murmur. The amphoric breathing is of greatest intensity near the point of perforation, which ordinarily is at the mammary or upper scapular region, and is found in both inspiration and expiration. The cough and the whispered voice give the characteristic metallic quality. There is also metallic tinkling produced by droppings of fluid in the cavity, by the shaking of the body, or by vocalization. Even when the orifice in the lung is closed we may have amphoric echo, from sounds produced in the bronchi, and passing through a cavity filled with air. The intensity of these sounds varies in different cases. Sometimes they are very loud; in other cases they are feeble and seem distant from the ear. The fine metallic tinkling may be heard at one moment and disappear at the next. These amphoric and metallic sounds, heard at different points, are characteristic of pneumothorax with free openings. When, however, the orifice from tubercular perforation is small, oblique, or valvular, the respiratory murmur is inaudible, except perhaps at the very apex of the lung, and we cannot perceive any adventitious auscultatory phenomena beyond a faint, distant, hollow sound.

There is, in both kinds of orifices, the well-known splashing Hippocratian succussion sound on shaking the chest. The latter is pathognomonic of hydro-pneumothorax, and is sometimes heard when no other sign is present. The hands applied over the surface of the chest feel the fluctuations of the fluid striking against the interior walls. When pneumothorax follows purulent pleurisy we do not find immediately the pronounced symptoms nor the physical phenomena heretofore described as occurring when it is produced by rupture from the lung into the pleural cavity. The condition {580} of the parts is very different. Pus is present in considerable quantity in the cavity, and the ulceration of the costal pleura and the soft walls of the chest allows the fluid to flow outward and air to enter the cavity. Or there may be necrosis of parietal pleura into a bronchus and consequent discharge of pus through the mouth. The lung is already disabled. The violent pain in the side and the dyspnoea are no longer found. Indeed, the exact time of the rupture and commencement of the discharge is frequently unknown to the patient himself. The symptoms of entrance of air into the pleural cavity may not occur for some time. The patient who has had empyema is made more uncomfortable; the discharge through the mouth is offensive, and its quantity and its character call attention to the chest, in which percussion shows the presence of air; auscultation gives amphoric breathing, and succussion demonstrates the presence of air and fluid in the pleural cavity. Very soon, however, the presence of air produces putridity of the secretion, with loss of appetite, fever, diarrhoea, and the other alarming symptoms of pyo-pneumothorax. In some instances the pleura discharges its contents and heals over. There is another variety of pneumothorax, which is ordinarily attended with only temporary inconvenience, and which may soon disappear, leaving the patient no worse than before the attack. This variety of pyo-pneumothorax may be produced by the sudden rupture of emphysematous vesicles, by coughing, or even without any unusual force in the expiratory effort, the alveoli having become extremely thin and brittle by degeneration of their walls. For the minute the pain is violent and the dyspnoea great, but it soon subsides, and in a few days the gas may be all absorbed, unless it is in large quantity. If the pleura is healthy and the lung not otherwise diseased, the rupture may not cause any inflammatory action, fever, or effusion. The rupture may heal over entirely, or if some inflammatory effusion is produced it will probably be rapidly absorbed. In exceptional cases pleurisy may be excited and the case become prolonged. While the air remains in the pleura we have the physical signs characteristic of pneumothorax--displaced heart, as shown by palpation and auscultation, tympanitic percussion resonance, amphoric breathing, and succussion.

DIAGNOSIS.--Ordinarily, there should be no difficulty in diagnosing pneumothorax, no matter how it is produced. We have simply to consider well the already-mentioned modes of the commencement of the disease, and give due value to the characteristic physical signs, especially displacement of the heart, hyper-resonance on percussion, absence of vocal fremitus, amphoric respiration, succussion, and decided shifting of flatness and resonance on change of position. When all these signs are present, each being in itself almost characteristic, there can be but little question. Obstruction of a large bronchus would be followed by absence of health sounds and intense dyspnoea, but we should not have the other physical signs of pneumothorax. Extensive emphysema would produce some of the signs--exaggerated resonance on percussion and enlargement of the side. Emphysema, however, is bilateral, and the resonance over an emphysematous lung has not the same pronounced tympanitic quality as in pneumothorax. The enlargement in emphysema is more under the clavicle; the breathing not amphoric; the normal murmur, although enfeebled, is never completely annulled; and the heart is not displaced. Large superficial pulmonary cavities with firm but thin walls give us several of the physical signs of localized pneumothorax, such as amphoric respiration and metallic tinkling; but the succussion sound is never heard over them. The tympanitic percussion is rarely so pronounced in a cavity as in pneumothorax, and in the latter there is never the cracked-jar sound. In phthisical cavities of large size there probably would be depression instead of enlargement of the chest. The situation will ordinarily enable us to make the differential diagnosis, for localized pneumothorax is almost always low {581} down in the thorax, and the pulmonary cavities but rarely below its middle third. The progress of the case and clinical history would clear up the diagnosis. If a circumscribed pneumothorax was present with phthisis, the diagnosis might be difficult. Powell calls attention to the similarity of some of the signs of acute congestion rapidly supervening at the base of a comparatively sound lung to those of pneumothorax. But in the former the resonance, although high-pitched, is not truly tympanitic, and the heart is not displaced. There is no other disease of the chest where we find in such close proximity the two extremes of percussion sounds--flatness from the secondary effused fluid, and the tympanitic resonance above. If delicate, slight percussion is used, the line of demarcation can be clearly defined; if, however, the force of the percussion stroke be even of moderate intensity, the flatness is mingled with the tympanitic quality, as it is in percussing from the left lobe of the liver to the stomach.

PROGNOSIS.--The prognosis is unfavorable and always uncertain. During the first few days after the rupture of the pleura it is especially bad, though it becomes less so as time goes by. There are cases where the perforation and its results appear to prolong life. "If the opposite lung be healthy, we may hope that arrest of the pulmonary disease may convert the case into one of chronic empyema" (Powell). But, unfortunately, the rupture often occurs when the patient is emaciated and dying of chronic lung ulceration. Cases of pyo-pneumothorax produced in advanced phthisis or by gangrene of the lung are almost invariably fatal. The most unpromising cases at first sometimes prove the least serious, and, again, those that appear at the commencement slight, contrary to expectation, die. Much depends upon the condition of the other lung and the position of the perforation. If the other lung be healthy and the perforation low down, the chances of recovery are better. The progress is most favorable in the cases where the rupture occurs from emphysema. When from purulent pleurisy the discharge passes through a bronchus, the orifice may heal and in due time plastic material be thrown over it, and the air and fluid be left in the pleura. Cases are reported where the orifice remains open and pneumothorax lasts for a long time. Laennec reported one case where the patient lived six years. Fuller[250] reports another where the orifice was open at the end of eleven months, another nineteen months, and another twenty-seven months. We have mentioned Demarquay and Marotte's experiments of the innocuousness of air injected into the pleura. Air is harmless, as they have shown, in the pleura, unless sulphuretted hydrogen or sulphite of ammonia be developed. Fuller says the prognosis is very unfavorable when the effusion is large, with great displacement of the organs. Flint considers pneumothorax occurring as a complication of phthisis as almost hopeless. It is important to ascertain promptly the nature and direction of the opening, whether it be free or valvular.

[Footnote 250: _Diseases of Chest._]

TREATMENT.--This is in a great measure palliative. Hypodermics of morphia or opiates relieve the agony and lessen the shock caused by the perforation. Alcoholic and diffusible stimulants may sustain the heart in its struggle against the effects of dislocation and impaired circulation. Care must be taken not to depress the powers of reaction by too much morphia. Hot water in india-rubber bags applied to the chest gives great relief. Alcoholic stimulants must be given to prevent sinking from exhaustion. When the distension from air is excessive, paracentesis gives marked relief, the lives of patients having been prolonged for days by it. If the opening is valvular, to prevent the air from accumulating in excessive quantity Reybard's protected gold-beater's skin trocar may be used and kept in the chest. Otherwise fine aspirators may be employed, which would seem to be harmless, and the {582} operation be repeated whenever necessary. Larger points and the trocar should never be used, as there is danger of making a permanent fistulous orifice, as well as of injuring some blood-vessels or the lung itself. After the excess of air has been removed by aspiration the affected side should be strapped to control the inspiratory movements on renewal of positive pressure. Anstie[251] recommends drachm ss doses of ether every three or four hours. Fernet[252] recommends inhalation of oxygen. If fluid should compress the chest, some of it must be removed by aspiration, but care must be exercised, for the presence of fluid is conservative in its effects. Its pressure stops up the orifice and promotes its healing. If it becomes fetid, pleurotomy, with detersive washes, ought to be resorted to. Food should be frequently administered, with quinine and cod-liver oil, and good hygienic surroundings prescribed.

[Footnote 251: _Reynolds's System of Medicine_, vol. iv.]

[Footnote 252: _Nouveau Dict. Méd._, vol. xxviii.]

Hæmothorax.

DEFINITION.--Accumulation of blood in the thoracic cavity unconnected with inflammation of the pleuræ.

ETIOLOGY.--Hæmothorax may be caused by traumatic injuries, by the bursting of an aneurism, from ulceration through the walls of the aorta of the vena cava, or from the veins of the pleura. It may be caused by laceration of the intercostal arteries in penetrating wounds. In very rare cases a profuse bleeding takes place in caseous pneumonia or in gangrene of the lungs, and bursts into the pleural cavity (Fraentzel). Cancer of the lung or pleura may, by pressure, produce absorption and destruction of the walls of the blood-vessels, and cause discharge of their contents into the pleural cavity. Sir Thomas Watson[253] reports a case where enormous hæmothorax caused enlargement of the left side, pushing the heart to the right of the sternum from caries of two ribs with ulceration through an intercostal artery. The blood never escapes from the lung into the pleura when there is considerable pulmonary apoplexy.

[Footnote 253: _Practice of Medicine_, vol. ii.]

PATHOLOGICAL ANATOMY.--Blood is found coagulated to a greater or less degree in the pleural cavity, and the lesion producing the hæmothorax can generally be found; the remains of blood may be found even after it has been some time effused. If the hemorrhage does not prove fatal, it may all be absorbed, or it may by its presence cause local inflammation of the pleural membrane.

SYMPTOMS.--The symptoms are those of perforation into the chest--sudden intense pain on the diseased side, with internal hemorrhage, great pallor, feeble circulation, cold extremities, and syncope. Patients often die in a few minutes. If the hemorrhage is moderate in quantity, they revive and the circulation returns, but they complain of feelings of suffocation and oppression. Slowly the general strength returns and the patient recovers.

SEQUELÆ.--Most modern surgeons admit that serious hemorrhages into the pleura come from the thoracic walls, or from the blood-vessels in the neighborhood of the hilum, or from those which accompany the bronchial diseases of the second or third order. Hæmothorax is always consecutive to some primary lesion. Where it is caused by penetrating wounds or by the bursting of blood-vessels in the lungs, air enters the cavity and becomes mixed with the blood, producing a complication in the form of hæmato-pneumothorax. This frequently gives rise to pyo-pneumothorax with a collection of purulent and ichorous fluid.

DIAGNOSIS.--The previous history of the case, together with the characteristic symptoms we have mentioned, enables us to diagnose hæmothorax from {583} pneumothorax, which commences in a similar way. The only other condition likely to be confounded with it is effusion in pleurisy, the physical signs of which are somewhat the same. If the blood remains uncoagulated we shall have absence of vesicular murmur, with dulness on percussion, absence of fremitus, and no friction sound. The introduction of a fine hypodermic needle enables us to be certain of the nature of the fluid.

The PROGNOSIS is always serious. If the cause of the hemorrhage is the bursting of an aneurism, death supervenes in a short time. Hæmothorax, when caused by penetrating wounds, unless they produce hemorrhage, is not necessarily serious. The blood may entirely disappear in a few weeks. Entrance of air with the blood renders the prognosis more serious. Secondary pleurisy is not ordinarily severe unless pus forms.

TREATMENT.--If time is allowed, every effort must be made by local and general treatment to arrest the hemorrhage--ice-bags and hot-water bags ought alternately to be applied to the chest and between the scapula; the patient to be kept in the horizontal position and made to rest quietly; ice taken by mouth; small doses of morphia and large doses of ergotin must be given promptly hypodermically, as the stomach is in no condition to absorb remedies readily. If the accumulation be excessive and continues to embarrass the respiration very much, we recommend free incisions to take out sufficient blood to relieve the pressure and great dyspnoea. Unless danger is imminent, this is a hazardous experiment, as letting in atmospheric air among blood-clots may seriously complicate the condition. Should pleuritis or other complications occur, they must be rationally treated.

Growths in the Pleural Cavity.

Some authors mention various tumors which are rarely met with in the pleural cavity, and which are not peculiar to the serous membrane of the pleura. Among them may be placed sarcomas, fibro-sarcomas, and epithelioma. Their presence in other organs may assist in the diagnosis. Other varieties exist more or less connected with chronic pleurisies. Among these are fibromas, cartilaginous and osseous formations. Rokitansky speaks of lipomas as deposited on the costal pleura. The only varieties which we think it necessary to call attention to are cancer and hydatids.

CANCER OF THE PLEURA.--Cancer of the pleura is not a very rare disease, but ordinarily it is a secondary formation, coming from cancerous disease of the mediastinum, of the lung, or of some abdominal organ. Some authors doubt whether it is primary even in the lungs and mediastinum. It certainly is not often met with as a primary disease of those organs. Lebert[254] had only seen 6 observations, in 447 cases of cancer, involving the mediastinum, the pleura, and the lungs. Walshe[255] reported 29 cases of primitive cancer of the respiratory organs; in 18 cases one lung was diseased with its pleura, and in 13 the right lung. Lépine[256] in 1869 communicated a very curious case of primary cancer of the pleura in a child ten years of age. The right pleural cavity was filled by a white scirrhous tumor. Darolles[257] (1874) reported another example of primary cancer of the pleura, which afterward spread to the lung. Andral, Vidal, and Lebert reported cases where the tumors appeared to develop simultaneously in the pleura and other organs. Primary cancer of the pleura may exceptionally occur, but ordinarily the disease results from its extension step by step, or else distant propagation, from lungs, breast, mediastinum, or the abdominal organs. Most frequently the secondary {584} cancer appears more or less independently of the primitive tumor, and is seen in the form of disseminated points on the surface of one or both folds of the pleura. This propagation of cancer is now generally admitted to be through the intermediary of the lymphatic system; in fact, the lymphatics are themselves attacked by the degeneration, and they are seen, particularly on the surface of the pleura, in the form of white small cords. Some modern pathologists consider that the serous cavities are lymphatic cavities, which can, just as the vessels themselves, serve as ways of generalizing the disease (Cornil and Ranvier, Charcot, Lépine, and Virchow).

[Footnote 254: _Traité Prac. Mal. des Cancereuses_, Paris, 1851.]

[Footnote 255: _Nature and Treatment of Cancer_, London, 1846.]

[Footnote 256: _Bull. de la Soc. Anat._, 1869.]

[Footnote 257: Quoted by Fernet, _Nouveau Dict. Méd._, vol. xxviii.]

PATHOLOGICAL ANATOMY.--Primary cancer of the pleura is ordinarily encephaloid and multiple. Extended infiltration is very rarely found. Lebert reports one case in an infant of seven months. The multiple masses are ordinarily soft and pulpy, varying in volume from the size of a grain of millet-seed to that of a small nut. The aspect is yellowish-white. The juice is rarely pressed out of them. Under the microscope we see large cells and multiple cells with their nuclei. The small granulations or the lenticular masses are flat, resembling drops of wax. We may have solid bodies possessing all the characters of scirrhous, encephaloid, and colloid, grayish, or gelatinous structure. These cancerous productions are generally vascular, especially in the encephaloid variety. Their rupture frequently produces hæmothorax and hemorrhagic pleurisies. The bronchial glands, and finally the cervical glands, often become involved.

SYMPTOMS.--The symptoms of pleural cancer, especially of the smaller and secondary deposits, are often obscure and indefinite. They are not sufficiently definite to attract attention during life. If the masses are scirrhous and large, they press upon the lungs, impede respiration, and give rise to dyspnoea. If the disease is propagated from the lungs or breast, we may suspect cancer where we have a dull pain with some cough. Pain, indeed, is constant, but not violent, unless the nodules excite local inflammation. When scirrhous tumors press upon the intercostal nerves, the pain is very persistent. External pressure over the points gives rise to pain. The dyspnoea increases as the size of the tumor increases. The expectoration is occasionally bloody. The physical signs are sometimes characteristic--dulness on percussion, absence of respiratory murmurs, friction sounds, no vocal fremitus.

DIAGNOSIS.--Generally very difficult. The progress of the disease is ordinarily slow, and follows its development in other portions of the body. Cancerous cachexia, degeneration of the glands above the clavicle, hæmothorax, and hemorrhagic pleurisy, together with dry cough and persistent intercostal neuralgia, are, when present, valuable aids to diagnosis. Extensive caseous pneumonia and pleuritic effusions may be confounded with cancer of the pleura. These tumors may not be at the base, but in the middle of the thorax; dulness may not exist at the base as is invariably the case in pleurisy. The position of the body does not affect the limit of dulness in cancer.

The PROGNOSIS is always very serious, the disease being invariably fatal. In Walshe's cases the duration of the disease was from three and one-half months to twenty-seven months; average duration, thirteen and one-fifth months. One-fourth of his cases occurred between the ages of fifty and sixty years.

The TREATMENT is palliative--opium and other narcotics, and locally chloroform and aconite for the intercostal pains. When effusion results from cancerous inflammation the aspirator may be used to relieve the great oppression caused by the quantity of fluid.

{585} Hydatids of the Pleura.

Trousseau[258] considered hydatids of the pleura a comparatively rare disease. He believed that when found in the cavity it was frequently caused by cysts of the lung which had fallen into the pleural cavity. Vigla[259] mentions 3 cases. Davaine[260] met with 25 cases of hydatids, only 1 of which he believed originated in the pleural cavity. The acknowledged greater frequency of these hydatids in the right inferior lobe of the lung, gives probability to Dolbeau's[261] view that "they frequently proceed from cysts on the convex surface of the liver." Hearn[262] reports 75 cases collected from various observers as intra-thoracic, 15 of which were in the pleura, in the subserous tissue, between the parietal pleura and thoracic wall.

[Footnote 258: _Clin. Med._, vol. i., Philada. ed.]

[Footnote 259: "Des Hydàtides intrathor.," _Arch. gén._, 1855.]

[Footnote 260: _Traité des Entozoaires, etc._, Paris, 1860.]

[Footnote 261: _Thèse de Paris_, 1856.]

[Footnote 262: _Thèse de Paris_, 1875.]

PATHOLOGICAL ANATOMY.--In the greater number of cases, as examined at autopsies in Hearn's reports, the tumor was formed by a voluminous pocket occupying a large part or the whole of the cavity of the pleura. The walls of the envelope were formed of a transparent or slightly opaline and whitish membrane composed of numerous thin layers, containing on its interior surface the echinococci. In the interior of the cyst there was a limpid hyaline liquid with living parasites. Nothing different was noticed in cysts from those found elsewhere, except the absence of the usual adventitious membrane--a fact previously noticed by Davaine. When the cysts are very large they press upon the lung and adjoining organs just as is the case with large effusions in the pleural cavity. The heart, moreover, is pushed to one side, out of its normal position; the lung is compressed and diaphragm depressed.

SYMPTOMS.--The first appearance of cysts of the pleura causes but little disturbance of the functions of the lung. It is scarcely appreciable until it interferes with the play of the other organs. The three prominent symptoms are the pain, the dyspnoea, and the cough. The pain occupies the exact point where the tumor is situated, and radiates from that point. Once developed, it persists with tenacity throughout the duration of the disease. This persistence of the pain is indeed an important characteristic of the disease, and is a sign of value in the diagnosis between hydatids and pleuritic effusions. The dyspnoea increases progressively with the volume of the tumor. The cough is not heard as frequently as when the cysts occur in the lungs. It is dry, and does not cause hæmoptysis.

DIAGNOSIS.--Physical signs must be marked to enable us to distinguish fluid cysts of the pleura from cysts in the lung or effusions in the pleural cavity. When the hydatid tumor has attained sufficient size to cause pain and dyspnoea it generally presses outward the walls of the chest after the lung has been compressed. It does not occupy the base of the cavity, as the effusions do, and the dilatation has a globular form. Trousseau[263] has given several examples in which this shape determined the diagnosis. With this arching of the chest the immobility of the chest is an important sign. Vocal fremitus is diminished or totally abolished, and percussion elicits absolute flatness. These two physical signs assist us in making the diagnosis between hydatids and pleurisy. The auscultatory phenomena, from similar physical conditions, closely resemble those of pleuritic effusions. It must be borne in mind that sometimes hydatid cysts are complicated by pleuritic inflammations, caused by their presence. The diagnosis is unquestionably complicated by difficulties that are not removed unless the cysts burst through a bronchial tube and discharge a transparent and clear fluid in which the microscope shows the presence of echinococci. Such hydatid expectoration is a pathognomonic {586} sign of the existence of an intra-thoracic cyst. Hydatids of the liver may press the diaphragm far up into the pleural cavity without bursting through it. Trousseau maintained that without bursting they may make a passage for themselves through the distended, attenuated fibres of the muscular portion of the diaphragm, for the progress of these cysts is necessarily slow. We must not hesitate to make an exploratory aspiration to determine with certainty the nature of the fluid.

[Footnote 263: _Loc. cit._]

PROGNOSIS.--The prognosis is certainly very serious, but not so bad as when cysts of the same nature are situated in the lungs. Their spontaneous cure may be effected by bursting through a bronchus or even through the walls of the chest. The patient may, however, die from asphyxia during the discharge through the lungs. When not evacuated they may produce death by compression of the lungs.

TREATMENT.--If the disease is recognized previous to its making an opening through a bronchus, it can be treated safely and effectively by aspiration. Bird[264] reports a number of cures by this operation in Australia. Trousseau advises extreme caution, even in regard to exploratory punctures, unless adhesions have taken place between the tumor and the walls of the chest, for he fears the escape of fluid into the cavity of the chest and consequent purulent pleurisy. It is well to remember that this great practitioner was not aware of the innocuousness of capillary punctures and aspiration. If the bronchus has been perforated, we must hope for spontaneous cure. If empyema be caused by the tumor pleurotomy must be used as recommended by Moutard-Martin[265] and Vigla,[266] and constant washing of the pleuræ must be used. This treatment gives us reasonable assurance of success.

[Footnote 264: Quoted by Hearn.]

[Footnote 265: _Purulent Pleurisy_.]

[Footnote 266: _Loc. cit._]

History of Thoracentesis.

Thoracentesis ([Greek: thôrax], chest, and [Greek: chentein], to pierce) is the operation for the evacuation of collections of fluid, serum, pus, or blood from the pleural cavity.

Among the ancients, dating back to the time of Hippocrates, it was practised, and was known as the operatio empyematis. Hippocrates uses the word [Greek: empyon], signifying, literally, an internal collection of pus just above the cavity of the peritoneum, above the diaphragm. Subsequently he speaks of empyema of blood, empyema of serum, empyema of gas, but not of pus, applying the term to the operation, which he employed principally for empyema necessitatis. Subsequently the name empyema was used, as now, to designate a purulent collection in the pleural cavity.

If we may credit the story which has descended from mythological times, the operation for empyema had its origin in an accident. It is related that a certain Phalereus, who was attacked with what was denominated an ulcer on the lungs, was pronounced by all his physicians to have an incurable disease. In his despair he exposed himself in battle so that he might be slain; the enemy's weapon, however, pierced his side, making an opening through which the pus escaped, and he recovered.[267]

[Footnote 267: Cicero, _De Naturâ Deorum_, lib. iii. cap. 28.]

It is certain that from the most remote periods the chest was opened when collections of pus were formed. Galen states that the ancients employed actual cautery for that purpose. He reports that Euryphon de Cinde by this means saved the life of Cinesias, son of Evagoras.[268] The details into which Hippocrates and his school entered in regard to the operation show that it was frequently performed in their day. It is very remarkable that many of the more important precautions in the operation were observed by {587} Hippocrates. We find from the _Aphorisms_ that the operation was considered the only means of cure,[269] and that when these precautions were observed, and the fluid was white and of good quality, the patients recovered.[270] The principal precautions were not to delay the operation after the existence of pus was recognized, and to draw off the liquid. He further states that if the serous fluid in dropsy of the chest or pus in empyema should be drawn off too rapidly the patient would die. So impressed were the disciples of Hippocrates by this view that they adopted the operation of perforating a rib instead of cutting through the intercostal space, because they could with more ease stop up the orifice and regulate the outward flow of the fluid. The later Hippocratians preferred cutting instruments to actual cautery. Hippocrates, if unable to discover the locality of the fluid in the thorax by succussion, applied over the walls of the chest a linen compress which he soaked in earth of Eretria and warm water, and concluded that the collection existed at the points where the earth commenced to dry!

[Footnote 268: _Comm. in Aphor. Hipp._, lib. vii.]

[Footnote 269: _Aphorisms_, lib. vii., Aph. 44.]

[Footnote 270: _Ibid._, lib. vi., Aph. 27.]

When these signs failed, he cut through the most prominent rib at the base of the chest and toward the back. He made a large incision through the rib, but only a small one the size of a thumb-nail through the tissue beneath the rib. After allowing a small quantity of pus to escape, he introduced a tent of undressed flax, with a piece of thread attached to it. This he withdrew twice daily, to allow the pus to flow. At the end of two days he permitted the remaining pus to be discharged, and inserted a tent of linen. To prevent the lung, habituated to the presence of fluid, from drying too rapidly he injected wine and oil through a canula. When the excavated fluid was thin (serous?) he replaced the tent by a tube of tin, and when it ceased to secrete fluid he shortened each day the length of the tube, so that the cicatrization of the wound extended from the inner end of the orifice.[271] The genius of Hippocrates cannot but excite our admiration, as it did Laennec's, who selected as the subject of his thesis "The Doctrines of Hippocrates as applicable to the Practice of Medicine." Can it have been Hippocrates's modes of physical explanation that suggested to Laennec the idea that led to his great discovery of auscultation?

[Footnote 271: _De Morbis_, lib. i. p. 448.]

Hippocrates's operations were made by boring through the rib or with a red-hot iron or a bistoury cutting through the intercostal space. Galen (A.D. 150) had his pyulcon with which to draw out the fluid. Galen and Roger of Parma bored through the sternum. Many of the ancient surgeons, such as Eumphon of Cnidos, Paul of Ægina, Celsus, Solinger, divided the soft parts by caustics and the knife after laying bare the pleura. Blunt instruments were sometimes used, such as sounds. Celsus in his latter years lost confidence in the operation, and it fell into discredit among the Greeks and the Romans, by whom it seems to have been nearly abandoned. In the Middle Ages the question was discussed whether it was better to open the chest by steel or by fire in traumatic pleurisies. Trousseau states that about the sixteenth century the operation of trepanning the ribs was revived. About the same time the detersive injections which had been recommended by Galen were again advocated, especially by Fabrice d'Aquapendente. The operation was unpopular among the greatest surgeons, and but seldom resorted to except in extreme cases. Notwithstanding the servile obedience to tradition in those days, some important points were advocated in regard to the propriety of allowing the openings for empyema to remain unclosed for an indefinite period. From the seventeenth to the eighteenth century the operation of paracentesis was the topic of many surgical treatises.

Early in the seventeenth century practitioners became less distrustful of {588} puncturing the chest, and were led to believe in the harmlessness of the operation (Trousseau). As a consequence of this tendency, physicians began to study the question of puncturing the chest in hydrothorax. In 1624, Gérome Goulée alleged that he succeeded more frequently in hydrothorax than in abdominal paracentesis. Twenty years later, Zacutus Lucitanus asserted that paracentesis was as necessary in cases of serous effusion into the chest as incision in empyema. In 1663, Robin and Duval recommended thoracentesis as the best treatment for hydrothorax. Some time afterward this practice was put in force by Willis. Lower also mentions a case, and subsequent authors quoted these cases as an encouragement to the performance of paracentesis of the chest for the removal of serous effusions. Jean de Vigo brought out again the pyulcon. Druin about the year 1665 proposed the use of the trocar as a substitute for the actual cautery in opening the chest.