and may be carried out upon the principles usually applied in the
treatment of hydrothorax. Bird recommends that the trocar should be not
less than six inches long and of the smallest diameter that is made,
always providing that it is strong enough to bear the strain of a firm
pressure. Cysts can be tapped in this manner even when they are
separated from the chest-wall by quite a deep layer of lung-substance.
This treatment should be practised at the earliest possible period in
the life of the cyst. Speaking of the aspirator, he says that cases
always do so well if tapped early enough with the simple trocar and
canula that aspiration is not required. The gradual expansion of the
lung as the cyst is emptied is sufficient to expel all the fluid,
especially if aided by the effects of coughing. In exceptional cases of
old standing, where there is a thick adventitious external wall to the
cyst, which is generally closely adherent to the ribs, or again in
cysts of the pleura, a free antecedent incision of the external tissues
is sometimes required. It has been suggested by different authors that
tincture of iodine should be injected after {471} aspiration to secure
the obliteration of the cyst by inflammation. The injection of carbolic
or salicylic acid under the same conditions has been practised with
success by Mosler and others.
The treatment of old suppurating cysts is rather different. The centre
of the sac, as nearly as can be judged, is fixed upon, and an incision
is then made through the skin and muscles, and the largest-sized trocar
and canula that will pass between the ribs is introduced into the sac.
This gives exit to a quantity of pus, even chalky substances and
fragments of cysts of different sizes. The opening must be free and
kept patulous for some weeks, and the sac should be daily washed out
with some disinfecting solution through the drainage-tube. Some delay
is always necessary to allow of the separation of the parent cyst from
its nidus and the gradual expansion of the lung. Immediate attempts at
its removal by forceps are generally unsuccessful, and portions are
very apt to be left behind. Several complications may interfere with
the success of the operation. One is the unavoidable piercing of a
small bronchus by the trocar. After the operation the wound of the
bronchus may remain patulous and a violent paroxysmal cough comes on,
with subsequent possible evacuation of the cyst through this channel.
The bronchial tubes, however, have been opened in operative treatment
of pulmonary cavities without serious result. When the parent cyst has
progressed to maturity quite unhindered, and is stuffed full of
daughter cysts, it has been recommended in such cases to introduce the
stylet and endeavor with its sharp point to stir up and break down the
smaller cysts as much as possible. The thermo-cautery has recently been
used successfully by Mosler to afford a means of penetrating the cyst
in the treatment of pulmonary hydatids. The tissues of the thoracic
wall must be first divided down to the pleura, as recommended in the
opening of pulmonary vomica by the thermo-cautery. Resection of the
ribs should be practised in case sufficient drainage cannot be
accomplished through an interspace.
Before applying to these operative measures it is desirable that
adhesions should have occurred between the visceral and the parietal
pleura. Fenger and Hollister recommend the introduction of a needle as
a means of diagnosis: if there be adhesions, it is unaffected by
respiration; if no adhesions exist, it is moved synchronously with the
breathing. There are, however, no absolutely reliable signs by which
this adhesion can be determined. Paracentesis of suppurating sacs has
been performed in cases in which the pleural surfaces have not been
adherent. In some instances the lung has been stitched to the opening
in the pleura, and after partial adhesion has occurred the purulent
collection has been punctured. In certain other cases, when pleural
adhesions have been absent, paracentesis has not been followed by
serious pneumothorax, possibly because the apposition of the pleural
surfaces is maintained by the tendency to cohesion which exists, and
after operative interference these surfaces are united by adhesive
inflammation.
{472}
ACUTE MILIARY TUBERCULOSIS.
BY JOHN S. LYNCH, M.D.
Acute miliary tuberculosis may be defined to be an acute disease
characterized by an eruption in one or all of the organs of the body of
small nodular or granular masses called tubercles, attended with fever
and various other functional disturbances.
The fact which Villemin and Klebs were the first to show,[1] and which
hundreds of others have since verified, that tuberculosis can be
conveyed by inoculation to certain animals, and the additional fact
that Koch and his followers seem to have identified the infective
material in the micro-organism which he has named bacillus
tuberculosis, would seem to justify our placing tuberculosis, along
with variola, measles, etc., among the acute contagious infectious
diseases. But since some able pathologists still deny the correctness
of Koch's conclusions; since in certain animals indifferent irritants
have excited a disease which could not be distinguished from
tuberculosis by the ablest pathologists of Europe and America; since to
some species of animals even more nearly allied to man by their
organism than rabbits and guinea-pigs the disease cannot be conveyed at
all, and that even to some of the latter inoculation fails to transmit
it; and, above all, since there is, as far as we know, not one single
case on record in which the disease has been clearly and unmistakably
traced from man to man in the order of infection,--we do not think that
as yet we are justified in defining it as a contagious infectious
disease purely and only. Everybody will take small-pox if not protected
by vaccination or inoculation, and this disease may be transmitted in a
modified form to many of the lower animals. The same may be said of
measles, scarlatina, and nearly all other diseases known to be
contagious and infectious. Since, then, so few persons take
tuberculosis that the evidence of its contagiousness rests upon a vague
popular belief, and since even some animals of a species known to be
peculiarly susceptible to the disease fail to take it even by
inoculation, we think that we are justified in assuming that there must
be something else besides a contagium required to produce the disease.
This is evidently a predisposition which depends upon some peculiar
diathesis, cachexia, or dyscrasia, congenital or acquired. It has been
assumed that scrofula constitutes the particular diathetic condition
which predisposes to tuberculosis, and it is common for scrofulosis and
tuberculosis to be spoken of as convertible terms. In the article on
SCROFULA in this work we have already given our reasons for dissent
from this view, and to that article the reader is referred. Farther on
we shall give our views as to what constitutes the tubercular diathesis
when we shall speak of the mode of formation of tubercle.
[Footnote 1: But Buhl had long before advanced the doctrine that
tuberculosis was a resorption disease.]
While, then, we cannot as yet admit that acute miliary tuberculosis is
always and only set up by a contagium, it is unquestionably true that
it is in a large majority of instances caused by an infective material,
which, however, {473} does not come from without, but is produced
within the system. This material is the purulent detritus resulting
from the softening and breaking down of the inflammatory and other
cellular hyperplasias which have undergone the caseous degeneration. It
seems to make little difference whether the caseous product was derived
from scrofulous glandular hyperplasia, catarrho-pneumonia, inflammation
of serous membranes with a cellular exudation, or ordinary cellular
inflammation; the only essential prerequisites being that there shall
exist a cellular exudation or proliferation, and that these cells shall
undergo the caseous degeneration.
The inoculation of this material into certain species of the lower
animals or its absorption into the blood of a human being predisposed
to tuberculosis will, as a rule, produce tuberculosis. Koch and his
disciples add to the foregoing another prerequisite--viz. that the
caseous matter must contain the bacillus tuberculosis. But as the
bacillus is generally found in all the cheesy inflammatory products we
have mentioned, they have (ignoring Virchow's definition of tubercle)
declared that all these are tubercle, thus very much enlarging the
hitherto accepted doctrine upon this subject. But if any of the cheesy
products are found not to contain the bacillus, then such product is
not tubercle, whatever may be the apparent identity or dissimilarity in
their etiology, microscopical appearances, or clinical history. This
seems to us to be a begging of the whole question of the relation of
the bacillus to tubercle, and in the absence of fuller experimentation
and investigation involves an assumption which cannot yet be admitted.
While the absorption of caseous pus is undoubtedly by far the most
frequent cause of miliary tuberculosis, it cannot be inferred that all
who may happen to have foci of caseous degenerations will necessarily
be attacked by tuberculosis. On the contrary, a vast majority escape,
and it is almost surprising how few of those who suffer from scrofulous
inflammation of glands, joints, etc. become the subjects of miliary
tuberculosis. Many cases of pulmonary phthisis also, originating as a
cheesy pneumonia, run their course without any distinct tubercular
complication. We can only explain these exemptions from the tubercular
process by supposing that in such cases the predisposition to
tuberculosis does not exist--they do not have the tubercular
diathesis--or that such persons possess a peculiar means of resistance
to the entrance of the infecting material into their blood.
Other diseases are supposed to favor the tubercular process, either by
directly exciting or increasing the predisposition to it. Among others,
measles, whooping cough, and typhoid fever have been regarded as
specially liable to be followed by tuberculosis. Bad air, poor or
insufficient food, onanism or other forms of sexual excess, severe
study with insufficient exercise, and, in short, anything which impairs
the strength or lowers the vitality, have been heretofore considered as
excitants or predisposers of the disease. Admitting all these causes as
effective in either exciting it or increasing the predisposition to it,
there still remains quite a large residuum of cases in which the
disease can be traced to none of these causes, and which, for the want
of more accurate knowledge, we are compelled to call idiopathic or
spontaneous. Such are those cases of tubercular meningitis occurring in
young children heretofore in apparent good health, and in whom no
traces of caseous degeneration can anywhere be found. It is true that
it may be asserted that these children may have been infected through
kissing by persons suffering from pulmonary consumption; but if this
were so the disease ought to be far more frequent than it is, since the
habit of kissing babies is universal and consumption the most
prevailing of all diseases. In the absence of any proof to the
contrary, we think that we are justified in believing that these are
cases of spontaneous tuberculosis, occurring in consequence of
intensity of the diathesis, either inherited or acquired.
{474} Miliary tubercles are found in the form of small roundish nodules
ranging in size from 1/500 to 1/250 inch (submiliary tubercles), up to
the size of a millet-seed or even of a pea. When of the latter size
they are always made up of a number of submiliary tubercles. Much
larger masses are found usually in the lungs and in the mesentery, but
these will generally be found to consist not of miliary or submiliary
tubercles alone, but of cellular new formations derived from
endothelial or lymphatic proliferations excited by the presence of
tubercles, and therefore mixed with them. When first formed they are
grayish in color, somewhat translucent, and tolerably firm to the touch
(gray granulations). They soon, however, undergo partial fatty
degeneration (this degeneration usually commencing in the centre of the
mass), and subsequently are converted into a dry, yellowish-white, and
somewhat crumbly mass which from its resemblance to cheese is called
caseous. This sooner or later softens (the softening process beginning
also in the centre), and the mass breaks down into a fluid
detritus--tubercular pus. In some situations they never reach the
caseous and purulent stage (notably in the cerebral meninges), because
the interference with the organs or nerve-centres of animal life
excited by their presence destroys the patient before there is time for
the accomplishment of these changes. The subsequent history of tubercle
depends upon the condition of the patient, his powers of resistance,
the intensity of the tubercular diathesis, the injury inflicted by the
first eruption, and the appearance of secondary eruptions. If all
conditions are favorable, the patient placed under proper hygienic
conditions and properly treated, the first eruption will also be the
last, and the tubercle dries up into an earthy mass (calcareous
degeneration), or it may remain for months, and even years, in its
caseous stage without undergoing the softening process.
If we examine a fresh tubercle under the microscope, we find, according
to Woodward[2] and Zeigler,[3] that it is usually made up of three
different kinds of cells: first and most abundantly, lymphoid cells
(Woodward) or white blood-cells (Zeigler); second, endothelioid cells;
and third, embryonic cells. In addition to these there is often found
(but not always) a few so-called giant-cells, generally occupying the
centre or circumference of the tubercle, and sometimes both. These
cells, which usually contain two or more nuclei and are much larger
than the ordinary lymphoid cell, were thought at one time to constitute
an essential histological feature of tubercle, and have been named
tubercular cells. But the frequent absence of these cells in genuine
tubercle has led to the conclusion that they do not possess any special
significance and are purely accidental. Each submiliary tubercle is
usually surrounded by a proliferating zone in which multinuclear
(giant) cells and fibro-plastic or spindle-form elements can be
distinguished (Cornil and Ranvier[4]). According to Rindfleisch,[5]
Woodward,[6] and Zeigler,[7] the cellular elements of tubercle are
always found included in a trabeculum of fine fibrillar (connective)
tissue, while Cornil and Ranvier deny the existence of any such
trabeculum, maintaining that its appearance is due to the action of
hardening agents used for preparing it for microscopic examination.
Virchow and Woodward believed that tubercle always takes its origin in
a lymphatic vessel, while Rindfleisch, partially agreeing with this
view, maintains that they most generally occur in the lymphatic sheaths
of the blood-vessels and follow the course of the latter, and that the
cells which compose the tubercle are formed by proliferation of the
endothelia of the lymphatics.
[Footnote 2: _Medical and Surgical History of the War of the
Rebellion_, Part 2, Medical Volume, p. 593.]
[Footnote 3: _General Pathological Anatomy_, London, 1883, p. 171.]
[Footnote 4: _Pathological Histology_, Philadelphia, p. 116.]
[Footnote 5: _Textbook of Pathological Histology_, Philadelphia, 1872,
p. 125.]
[Footnote 6: _Op. cit._]
[Footnote 7: _Op. cit._, p. 168.]
{475} Zeigler has not been able to demonstrate this relation of the
tubercle to a blood-vessel--that is, to an artery--but leaves us to
infer that they always arise from a capillary vessel, since he
maintains that the tubercle is primarily and principally made up of
emigrated leucocytes.
Such is a brief résumé of our knowledge as to the histology and mode of
formation of tubercle, and such are the opinions--in some particulars
agreeing, in others discordant--of those whose investigations and
observations the world regards as most complete and accurate. This
résumé is doubtless unnecessary and out of place in this article, since
this question (the histology and mode of formation of tubercle) has
been already discussed in the first volume of this work; but, as in the
explanation which is to follow of our views as to what constitutes the
tubercular diathesis and what is the mode of formation of tubercle we
shall have to frequently refer to the facts above stated, we have
thought it best, in order to save repetition and too frequent reference
to authorities, to give the above résumé of the present state of the
views of pathologists upon the histology of tubercle.
A careful consideration of the foregoing facts ought, it seems to us,
to enable us to arrive at a rational and probably correct conclusion as
to the mode of formation, as well as the principal etiological factors
concerned in the causation, of the miliary tubercle; and we venture to
offer the following explanation of the subject as more in consonance
with the facts above related than any view which we have seen upon this
question:
1. Miliary tubercles always occupy a lymph-space surrounding a
capillary blood-vessel. When found, as they quite often are, occupying
the wall of a larger vessel, artery or vein, it is still in the
lymph-sheath of a capillary of the vasa vasorum that they primarily
originated. And it may be said that this is the most dangerous site a
tubercle can occupy, because when softening takes place it is so apt to
burst into the lumen of the vessel and so produce a general infection.
2. The tubercular process consists at first of an undue or excessive
emigration of leucocytes through the walls of a capillary which runs
through a lymph-space, and where, of course, the walls of the vessel
are less firmly supported. Those cells whose vitality is lowered by the
causes which have preceded and excited the process can neither undergo
any process of differentiation nor wander on through the lymphatics;
they remain in the lymph-space, which they crowd and block up, and
finally by their pressure occlude, the capillary vessel from which they
emigrated. Until this event occurs they still retain a feeble vitality,
and even abortive attempts at proliferation are seen, which, however,
only reach the stage of division of the nucleus, the body of the cell
meanwhile swelling up by imbibition and thus forming the so-called
giant-cell. As soon as the capillary vessel becomes occluded further
addition to the incipient tubercle from this source ceases; nutrition
is now entirely cut off, and the cells, dying, become a foreign
substance, and soon undergo the caseous degeneration. But by their
presence they now excite a quasi-inflammatory process in the endothelia
lining the lymph-space, and hence we have a secondary addition to the
tubercle derived from the proliferating endothelia. Lastly, the
inflammatory process extends to the connective-tissue cells around the
lymph-space, and embryonic cells (the only cells capable of resulting
from connective-tissue inflammation) are added to the mass. This
constitutes the proliferating zone, consisting of many nucleated cells
and fibro-plastic and spindle-form elements, described by Cornil and
Ranvier.[8]
[Footnote 8: _Loc. cit._]
As soon as one capillary vessel becomes entirely occluded, the
neighboring ones become distended by a collateral hyperæmia, and the
same process of cell-exudation or emigration begins; and thus the
process goes on until all the capillaries supplied by a single arterial
twig take part in the process, and {476} one of the larger tubercles is
thus formed by an almost innumerable number of smaller (submiliary)
ones. It would seem to be quite probable that the trabeculum which
Rindfleisch, Woodward, and Zeigler described, and which Cornil and
Ranvier denied, consists of the remains of the connective-tissue fibres
which originally existed between the capillaries successively attacked
by the tubercular process.
In the lungs this process is usually complicated by a true
catarrho-pneumonic inflammation. The tubercle deposited beneath the
lining membrane of the air-sacs sets up inflammation in that membrane,
giving rise to abundant proliferation of the endothelia as well as
emigration of leucocytes, so that the air-sac becomes packed with cells
which may finally undergo caseation, and then cannot be distinguished
from the original tubercle which started the process. If the eruption
of tubercles should be very abundant, life may be destroyed by the
pneumonic process before caseation has even begun in the inflammatory
products. We have quite recently observed a case of this kind. A man
came to the city hospital (Baltimore, Md.) who presented all the
rational and physical signs of tuberculosis of the lungs. After about
three weeks, during which there was only moderate fever, no notable
dulness, and only a few scattered crepitant râles, the temperature
suddenly rose to 104° F.; dulness appeared first over the lower third
of the right lung, which rapidly extended over that side, and
subsequently to the left side, and the man speedily died, comatose and
cyanotic. The autopsy showed the most extensive miliary tuberculosis we
had ever seen in the human lung; but in addition to the tubercles,
which were found in almost every lobule of the right lung, the air-sacs
were almost universally filled with a soft, purulent-like matter which
oozed from the cut surface, and which could be squeezed out in enormous
quantities; myriads of Koch's bacilli were found. It was interesting to
note that the apparent starting-point of this tuberculosis was two
small cavities in the apex of the left lung surrounded by
firmly-indurated walls. Neither of these cavities was larger than the
kernel of an ordinary-sized almond, and, as the induration surrounding
them did not extend to the surface of the lung, their existence was not
recognized before death. The man gave a history of cough and fever,
which had lasted several weeks, about three years before his admission
to the hospital.
More frequently, however, the reverse of the process above described
takes place. That is, a catarrho-pneumonia terminating in caseation and
softening sets up tuberculosis through absorption of the caseous pus.
Indeed, in the case above related the order of pathological processes
was, first, a catarrho-pneumonia of limited extent, a cavity or rather
cavities; second, general tuberculosis; and lastly, a secondary
catarrho-pneumonia caused by the tubercles. We believe, therefore, that
Niemeyer's remark, that "the greatest danger for the majority of
consumptives is that they are apt to become tuberculous," is not so
absurd as a distinguished American author would have us believe.
The formation, then, of tubercle we believe to be an inflammatory
process, in which we have--1st, an exudation of lymphoid cells
(leucocytes) into the lymph-spaces, and occlusion by pressure of the
capillary vessel from which the cells have escaped; 2d, inflammation
and proliferation of the endothelium lining the lymph-space; and 3d,
inflammation of the tissues nearest adjacent to the space. If this is
simple areolar connective tissue, we have a "proliferating zone
consisting of many-nucleated cells and fibro-plastic and spindle-form
elements;" if a mucous or serous membrane, the usual products of
inflammation of such membrane in other and ordinary cases.