MORBID ANATOMY.--The constant lesion in fatal cases of caisson disease

is congestion of the brain or spinal cord. This congestion may be

pretty evenly distributed or it may vary in intensity in different

localities. This is especially true as regards the cord. It affects

both the meninges and the substance of the brain or cord. In most cases

there is more or less of serous effusion into the arachnoid. The

tissues of the scalp and those surrounding the spinal column are

sometimes engorged.

When sufficient time elapses before death the brain may be softened in

spots. This is probably due to the occlusion of vessels by coagula

formed during the primary congestion.

Congestions also occur in other localities, and especially in the solid

abdominal viscera. The liver and spleen have been found engorged in

nearly every case. Jaminet has found clots of blood in the kidneys.[2]

The mucous membrane of the stomach, intestines, and bladder is often

injected and marked with patches of ecchymosis. The lungs in cases of

true caisson disease, though occasionally found in a state resembling

red hepatization, seldom present any other change than simple

hypostatic congestion.

[Footnote 2: _Physical Effects of Compressed Air_, p. 20.]

PATHOLOGY.--It is probable that the pathology of this disease is not

entirely uniform in all cases. Doubtless the chief element in it is the

congestions already described, and especially of the brain and spinal

cord. The mechanism, therefore, of these congestions becomes a subject

of paramount importance.

It was suggested by François[3] that the morbid phenomena might be due

to the liberation in the vessels of air which had been absorbed by the

blood while under pressure, but which was set free again when the

pressure was removed. This theory has been reasserted by Paul Bert,[4]

with this difference: that he claims that bubbles of nitrogen instead

of air are the cause of the interruption of the circulation. These

bubbles he has discovered after death in the vessels of the brain and

cord. But he states that when the pressure does not exceed five

atmospheres three minutes allowed for the restoration of the normal

pressure will be found to prevent the formation of these globules of

nitrogen. Now, we find the caisson disease occurring when the pressure

does not exceed two atmospheres and when six to eight minutes are

allowed for locking out.[5] It would seem that under these conditions

the gas should escape through the lungs as rapidly as it is disengaged

from the blood. Moreover, we find that the attack often comes on

several minutes or even hours after leaving the caisson. During this

time any free nitrogen in the blood should be constantly becoming less

by diffusion through the {856} pulmonary membrane, and if enough were

not present at first to cause obstruction, such an effect could

scarcely take place at a later period.[6]

[Footnote 3: _Annales d'Hygien publique et de Méd. legale_, t. xiv.,

1860.]

[Footnote 4: _Comptes Rendus_, August, 1872, and February and March,

1873.]

[Footnote 5: _I.e._ passing from the caisson into the open air through

the lock, or antechamber, where the pressure is gradually reduced.]

[Footnote 6: In a private letter to the writer, T. Lauder Brunton

suggests that a bubble of air might pass from a larger vessel, which it

had only partially obstructed, into a smaller branch, which would be

entirely occluded by it, or that additional nitrogen might be

disengaged when the pressure was lessened by relaxation of vascular

tension.]

It is also very difficult to reconcile with Bert's theory the fact of

the comparative immunity from danger which results from repeated

exposures to the effects of compressed air. If the action were that of

purely physical causes, habit could make no difference. The obstruction

of the vessels, as described by Bert, is a condition of which the

system could never become tolerant by frequency of repetition.

In the writer's view, the explanation is to be found in the changed

conditions of the circulation, which result first from the increased

pressure upon the surface, and then from the sudden removal of the

pressure. While the subject is in the caisson the blood is driven from

the peripheral vessels toward the interior of the body, where the

pressure is less than at the surface.[7] It is also forced from the

more compressible tissues into the solid and resisting organs, such as

the liver and kidneys; and lastly, it flows toward bony cavities, for

the reason that their walls resist the effect of direct pressure, and

equilibrium of pressure can be restored within them only by an afflux

of blood. Thus the distribution of the blood is everywhere changed, and

the size of the vessels is no longer determined by the muscular action

of their walls, but by the amount of blood forced into them, the vital

action which should regulate the circulation being entirely overpowered

and set at naught by an overwhelming physical force operating from

without. The vessels become merely passive tubes, distended in some

places where they are protected from pressure, and compressed in others

where the tissues about them are compressible. By this transfer of

blood from one part to another the equilibrium of pressure is restored

and the circulation goes on, though without any regard to the

physiological demands of the different organs. There is no stasis

anywhere so long as pressure and counter-pressure are equal, thus

allowing fair play for the action of the heart.

[Footnote 7: This is shown by the marked pallor of the skin and the

shrunken and wrinkled appearance of the hands.]

If, now, the external pressure is suddenly removed, what will be the

result? Vessels which have been compressed and almost emptied of blood

will now offer new channels through which the blood can rush, and

vessels overcrowded with blood, with their walls paralyzed by

over-distension, will have the current within them slowed almost or

quite to the point of stopping. The vessels of the brain and spinal

cord, being within bony walls, where the direct pressure of the

condensed air could not affect them, will be found the most distended

and the most helpless to relieve themselves. They will get little aid

from the vis a tergo of the circulation, for the blood will find easier

courses by other ways, vascular tension being almost nil and the

vaso-motor system out of use.

The longer the sojourn in the caisson has been, the more entirely

passive the vessels will have become, and the longer will be the time

they will require to resume their normal condition. At some points the

circulation will be greatly slowed or entirely interrupted, and

nerve-elements lying beyond and deprived of their blood-supply will

express their want by pain or paralysis. Areas of stasis once formed

will be likely to extend, and may thus affect nerve-elements which at

first escaped. This would explain those cases in which the attack is

deferred until some time after leaving the caisson.

It is readily conceivable that in persons beginning work when the

pressure is slight and continuing day by day, as the pressure slowly

increases the {857} vessels should acquire the power of adaptation to

the variations in the amount of their contents, since this is only an

extension of the physiological principle which we see exemplified in

all organs having an intermittent function.

The influence of the trophic system of nerves also, as the connecting

link between central nerve-lesions and peripheral vascular

disturbances, must not be forgotten in this connection. Suspension of

function in trophic cells, either in the cerebral cortex or in the

anterior horns of the cord, could easily be brought about by the action

of the mechanical causes already described, and would result in areas

of vaso-motor paralysis and consequent congestion at the termination of

the corresponding nerve-fibres. The proneness of the large joints, and

especially the knees, to be attacked is suggestive, in view of the like

circumstance in chronic degeneration of the cord.

CAUSES.--The one essential cause without which the disease can never be

developed is transition to the normal atmospheric pressure after a

prolonged sojourn in a highly-condensed atmosphere. Hence we have to

consider two elements, pressure and time, the danger in these cases

being as the degree of pressure to which the person has been exposed

multiplied by the duration of the exposure.

But inasmuch as a prolonged sojourn in the caisson does not in every

case produce the disease (many of the men employed escaping it

entirely), it follows that there must be concurrent causes which

determine its development.

The first of these is a special predisposition. This is occasionally

strongly marked, some persons being affected by a short exposure to a

low pressure from which there would generally be experienced no

inconvenience whatever.

Perhaps the most frequent exciting cause of the caisson disease is too

rapid locking out. Indeed, it is altogether probable that if sufficient

time were allowed for passing through the lock the disease would never

occur. But what is sufficient time for one is too short for another;

and all that can be done is to fix upon a duration for the process

which shall be proportioned to the pressure, and as great as is

consistent with the circumstances, and then to see that the rule is

rigidly observed. At least five minutes should always be allowed for

each additional atmosphere of pressure.

Newness to the Work.--Unquestionably, the liability to the caisson

disease is greatest in those exposed for the first time to the

influence of the compressed air. New hands are very apt indeed to

suffer more or less during the first week. Those least affected are

such as begin work when the pressure is comparatively slight, and

continue without intermission as the pressure increases. It seems that

the system after a time becomes adapted to the changed conditions, and

is protected in a measure from their effects. Nevertheless, some

serious cases occur among old hands, especially when for any reason

their stay in the caisson is prolonged beyond the usual time, thus

showing that their immunity is merely relative. A sudden increase of

pressure also, even though very slight, is certain to develop new

cases, men thoroughly inured to the work often being affected under

such circumstances.

Fulness of Habit.--During the progress of the work on the East River

Bridge in 1872 the writer, who had medical charge of the men, observed

that among those taken sick there was a very marked preponderance of

men of heavy build and with a tendency to corpulency. Of 39 men of this

build, only 3 escaped illness, while of 53 lank and spare men 25

escaped. Of the 39 stout men, 8 were more or less paralyzed; of the 53

slender men, only 2 were paralyzed. The deaths, 3 in number, were all

of heavy men.

These figures show unmistakably that a tendency to fulness of habit

renders work in a compressed atmosphere much more hazardous. Persons of

this build have more fluids in the body, the distribution of which is

changed by the pressure in the manner before stated, and it is

therefore not surprising {858} that the effect upon them should be

greater than upon lean and sinewy persons, whose bodies contain a

minimum of fluid.

Severe Exertion immediately after Leaving the Caisson.--As at the

moment of going out of the compressed air the system undergoes a

violent reaction, it is manifestly unfitted to bear in addition a

severe tax upon the muscular strength. Hence the ascent of a long

flight of stairs immediately after leaving the air-lock is as wrong in

theory as it has proved bad in practice. Triger, whose apparatus at

Chalonnes was so arranged that the ascent of the ladder took place in

the compressed air, the lock being placed at the top instead of the

bottom of the shaft, found that the men ascended a distance of seventy

feet without becoming in the least out of breath--making the ascent, in

fact, more easily than if it had been in the open air.[8]

[Footnote 8: _Comptes Rendus_, t. xiii., 1841.]

The Abuse of Alcohol.--Several writers have remarked that habitual

drinkers are more likely to be affected than those who used spirits

moderately or not at all. It is stated by the director of the work at

Douchy[9] that the attacks from which the men suffered were "almost

always coincident with some excess committed in the interval of the

shifts." It is easy to perceive that, as the disease is characterized

by cerebral congestion, the abuse of alcohol, which has a tendency to

produce the same result, would act as a predisposing cause.

[Footnote 9: _Annales d'Hyg. pub. et de Méd. legale_, 1854.]

Entering the Caisson Fasting.--Jaminet insists very strongly upon the

influence of this cause, and cites instances to prove his position.

Several cases corroborative of his views occurred under the observation

of the writer. One of the rules for the men working in the New York

caisson prohibited entering the compressed air without having taken

food, and in addition to this each new hand was especially cautioned as

to the danger of disregarding this precaution, and the foremen were

directed to use every effort to secure its observance. Yet,

notwithstanding all this, a number of very severe attacks were found to

be coincident with, if not dependent upon, violations of this rule. In

these cases epigastric pain and retching were prominent symptoms.

TREATMENT.--The treatment of this disease will depend upon the severity

of the case and the presence or absence of gastric symptoms or of

paralysis. If we have to deal with the neuralgic pains only, the chief

reliance must be upon anodynes administered with a liberal hand.

Fortunately, the pain, though very severe while it lasts, is in most

cases of short duration, the attack passing off usually in a few hours.

It is therefore quite practicable to keep the patient under the

influence of morphine during the whole time, and thus enable him to

escape entirely all extreme suffering. But large doses will be

required, the intense pain inducing a remarkable tolerance of the drug.

Half a grain may be given at the outset, and a quarter of a grain every

half hour afterward until relief is obtained. When employed

hypodermically somewhat smaller doses may be used.

In some instances the very best results are obtained from hypodermic

injections of atropine at the seat of pain, but in other cases they

fail to procure relief, and, upon the whole, atropine is inferior to

morphine.

Jaminet, regarding the affection as wholly the result of exhaustion,

relies entirely upon stimulants and concentrated nourishment, ignoring

the aid of anodynes altogether. It is difficult to see the reason for

this, even admitting to the fullest extent his theory of the disease,

for nothing can be more exhausting than the intolerable pain which

characterizes this affection, and nothing could act more promptly as a

restorative than an efficient anodyne.

Starting from the theory already given as to the mode in which the

disease is produced, the writer was led to the idea that benefit would

be derived from {859} the use of an agent that would induce contraction

of the capillaries, and thus correct the want of tone which was

considered to lie at the foundation of the difficulty. For this purpose

ergot was employed, with the belief that it would be useful, first, by

contracting the vessels of the brain and spinal cord and relieving

their congested state; and, secondly, by restoring tone to the

superficial vessels, and thus imparting vigor to the circulation.

An extended trial warrants him in saying that the results justified the

theory. In his hands, though not always successful, ergot was certainly

very useful in a considerable number of cases. He has seen very severe

pain completely relieved within half an hour after the administration

of a drachm of the fluid extract. In other instances unsteadiness of

the limbs, which seemed about to usher in paralysis, yielded promptly

to one or two doses. A teaspoonful of the fluid extract may be given,

and the dose repeated in half or three-quarters of an hour, unless the

pain is relieved.

Frictions, with or without stimulating liniments, are very generally

resorted to, and seem sometimes to give momentary relief, but it

appears to be rather by occupying the attention of the patient than by

any action occasioned in the part. In some instances, when the pain is

confined to a particular locality, having the part immersed in hot

water will afford temporary relief. But the use of the general hot bath

is not advised, as it is unsafe to increase the already existing

relaxation of the vessels. In several of Jaminet's cases paralysis came

on while in the hot bath. In two of the writer's cases cold was applied

to the spine, with apparent benefit in each.

Epigastric pain is almost always relieved at once by the use of an

alcoholic stimulant with ginger, as employed by Jaminet.

Vomiting is best treated with sinapisms to the epigastrium and

swallowing small bits of ice.

When paralysis occurs it is to be treated on general principles. Cups

or leeches, with douches and frictions to the spine, may be useful;

and, if the case be protracted, the use of strychnine may be called

for. Electricity may be of service in preserving the nutrition of the

muscles. The bladder will almost certainly be involved, requiring the

constant use of the catheter.

The cerebral symptoms which occasionally occur are, with the exception

of coma, so transient in their nature as to call for no special

treatment. Coma, when it takes place, is to be managed according to the

circumstances of the case, as when proceeding from other causes. If

accompanied by a full, strong pulse, venesection may be expedient.

There remains to be considered a plan of treatment originally suggested

by Pol, and carried out to some extent by Foley--viz. returning the

patient at once into the compressed air. Foley says, as the result of

his experience, "A true specific is returning to the caisson, through

which means all such accidents (pains, vertigo, etc.) speedily

disappear. It is to be resorted to unhesitatingly in all threatening

cases, and the pressure should be admitted rapidly." But the means of

access to the caisson are usually such that it would be difficult to

remove a patient into it, even if he could be comfortably cared for

while there or if his presence would not interfere with the work. It

would therefore be desirable to have facilities for employing

compressed air at some point above ground which would be easily

accessible.

Of course the secondary effects which arise in protracted cases would

not be capable of direct relief by simply reproducing the physical

conditions existing in the caisson. The most that might be hoped for in

such cases would be that the pressure might result in giving a new

impulse to the circulation in the congested part, and thus favor

resolution.

Reasoning from his view of the pathology of the disease, Bert has

proposed the inhalation of oxygen in order to displace the free

nitrogen from the blood by diffusion. Experiments upon animals

demonstrated that the sounds {860} produced in the heart by the

presence of free nitrogen speedily disappeared when the animal was made

to inhale oxygen, the nitrogen diffusing into this gas much more

readily than into common air. But, though immediate death was averted

by this expedient, paralysis nevertheless occurred, and the post-mortem

examination showed the presence of bubbles of nitrogen in the vessels

of the cord.

{861}

DISEASES OF THE MEDIASTINUM.

BY EDWARD T. BRUEN, M.D.

Inflammation of the Mediastinum.

SYNONYMS.--Mediastinitis. _Fr._ Médiastinite; _Ger._ Mediastinitis.

Lesions caused by inflammatory processes in the mediastinum may,

theoretically, occur in the duplicatures of the pleura, separating the

pleural from the mediastinal cavity. This condition may terminate in

resolution or in effusion of plastic lymph, as in a case reported by

Wildemann, in which the anterior mediastinum was filled with layers of

solid exudation, the pericardium inflamed, and its cavity distended by

six ounces of pus. The effusion appeared to have been occasioned by

long-continued pressure on the sternal region. The process is

practically unrecognizable during life, or at least possesses no

described clinical features.

Abscess of the Mediastinal Space.

Galen has alluded to trephining of the sternum for caries or necrosis

inducing the formation of pus; and Petit[1] has furnished many

instances of mediastinal abscess from the warfare of preceding

centuries.

[Footnote 1: _Traité des Maladies chirurgicales_, tome i. p. 143.]

ETIOLOGY.--I. Predisposing Influences.--Mediastinal abscess is very

rare, at least of such dimensions as to simulate tumor. The condition

is sometimes idiopathic, possibly due to sudden exposure to cold,[2] or

is associated with the rheumatic diathesis, but in these cases some

forgotten injury may have been received.

[Footnote 2: Gunther, _Oesterreich Zeitschrift f. Prak. Heilk._, 1859;

Gross, _System Surgery_.]

Symptomatic or secondary purulent collections may occur in connection

with operations upon the neck, as tracheotomy, also from softening

gummata or glanders, or they may be due to a constitutional cause, the

so-called metastatic inflammation of the mediastinal connective tissue

in the course of pyæmia.

Scrofulous suppuration of the lymphatic glands may result in secondary

abscess.[3]

[Footnote 3: Bristowe, _Path. Soc. Trans._, London, vol. ix. p. 46.]

II. Exciting Causes.--The mediastinum has been penetrated by balls and

sabres, and in one case the shaft of a carriage passed through the

anterior space, yet without damage to the contained viscera. Gunshot

fracture of the sternum, recorded in the history of the Civil War in

America, seems to have been very rarely followed by suppuration, even

though the tissues have been exposed to such a degree as to render the

arch of the aorta distinctly visible.

The anterior mediastinum may be threatened with inflammation, which may

sometimes terminate in abscess, as in cases of caries, necrosis, or

fracture of the sternum.

{862} Warner[4] reports a case in a boy aged thirteen in which two

weeks after fracture of the sternal bone a separation of the edges of

the fracture was observed, the interval being occupied by a tumor of

considerable size, which contracted and dilated with as much regularity

as the heart. It receded on palpation, and on removal of the pressure

the tumor immediately resumed its former size. It subsequently

ruptured, discharged the contents of an abscess, and the patient

recovered.

[Footnote 4: _Amer. Journ. Med. Sci._, Apr., 1873.]

Goodhart[5] records a case of acute mediastinal abscess resulting

apparently from injury produced by the sticking of a piece of meat in

the oesophagus. A case illustrating the possibilities of direct injury

to this region by a blow or fall has been recorded by Bennett. In a

middle-aged lady, previously in good health, an abscess slowly formed

and presented a prominence over the upper part of the sternum. Two

months before the lady had fallen in going up stairs, and struck the

sternum against the stone edge of the stairs. These examples have been

selected because they seem to cover the possibilities of directly

determining causes.

[Footnote 5: _Path. Trans._, London, vol. xxvii.]

SYMPTOMS.--There are three separate groupings under which the symptoms

may be classified: _(a)_ The latent symptoms, which include chiefly

manifestations of intra-thoracic irritation or pressure; _(b)_ the

fulminating phenomena; _(c)_ the physical signs.

A system of practical medicine. By American authors. Vol. 3 · 第 134 / 161 段