[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.

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