influencing the occurrence of hæmoptysis. The general statement by
Peacock, that the weight of the heart in phthisis, though less than in
acute diseases, is greater than that in other chronic diseases, needs
to be modified somewhat, as he did not make a distinction between
different forms of phthisis. The more the case approaches the fibroid
variety the more likelihood of some increase of size, particularly in
the right ventricle. Spatz,[66] a later authority, gives as the result
of his examination that phthisis diminishes the size of the left
ventricle--that an absolutely compensatory hypertrophy of the right
ventricle, which is apparent in special cases, does not as a rule
exist, although {289} the resultant decrease does not throughout stand
in relation to the decreased weight and volume of the whole body in
phthisis. The ratio between the depth of the left ventricle and
circumference of the aorta is diminished; and, as this is not
compensated for by hypertrophy of the walls of the ventricle, arterial
tension diminishes and the pulse becomes soft and small. The chance of
rupture of weak vessels by relatively excessive tension is thus much
weakened in the later stages of phthisis.

[Footnote 66: _Deutsches Archiv für klinisch Med._, vol. xxx. p. 154.]

Another element capable of modifying the hæmoptysical features of
phthisis is claimed by Jaccoud[67] as existing in the insufficiency of
the tricuspid valve, which compensates the increased tension in the
field of the pulmonary artery arising from obstruction of a
considerable part of it. The amount of blood passing from the right
ventricle is thus, by a reflux, proportioned to the area of obstruction
in the artery, and the tension is reduced so as to prevent rupture of
the weak vessels. His conclusions are based on 18 cases of measurements
of the tricuspid orifice. They varied from 111 to 130 millimeters. The
evidence obtainable during life was a systolic murmur heard at the
ensiform cartilage and cervical venous reflux.

[Footnote 67: _Clinique médicale_, vol. ii. p. 346, etc.]

DIAGNOSIS is mostly called for with regard to the chances of
hæmatemesis. Inspection of the blood is naturally an early point for
attention. Its bright-red color, frothy look, freedom from extraneous
matter, and its coming up by coughing are strong evidences easily
acquired of its pulmonary origin. Corroborative circumstances are the
family history of phthisis or hæmoptysis, the presence of pulmonary, or
in fewer instances of cardiac, physical signs, the immediately
premonitory symptoms spoken of before. Fever, the age of the patient,
and the continuance of the discharge of blood in its later gradations
of color and mixture of catarrhal elements, inspection of the mouth,
fauces, and larynx, would exclude those possible sources. Each has its
limitations, but together they are conclusive as against hæmatemesis.
Recent and accumulating experience attributes some diagnostic value to
the presence of bacilli tuberculosis in the expectorated blood.
Hiller[68] reports 6 cases of hæmoptysis in which the blood showed in
bacilli: 3 were completely initial. The bacilli were easily
demonstrated by preparations and also by inoculation on guinea-pigs.
They have also been found in the blood of cases of acute tuberculosis
by Weichselbaum.[69] Resort may be had to the well-known tests for the
presence of the elastic tissue of the lung in sputum.

[Footnote 68: _Centralblatt für die med. Wissenschaft_, March 24,
1883.]

[Footnote 69: _Wiener med. Wochenschrift_, No. 13, 1884.]

As positive data for hæmatemesis we have the dark color of the blood,
its firmer clotting, greater density and want of aëration, acid
reaction, the presence of extraneous matters of food and drink, their
ejection by vomiting, and pain or uneasiness at the epigastrium. As
corroborative we have the less frequent occurrence of hæmatemesis, the
individual history of gastric disease, such as ulcer of the stomach or
presence of hepatic cirrhosis from intemperate habits, and the history
of a blow on the abdominal surface: discharges of blood from the bowels
are more likely to occur in hæmatemesis.

Hæmoptysis may be simulated, as by scratches or cuts on some part of
the internal surface of the throat or mouth. The blood is then likely
to be thinned by secretion from the mouth. Inspection would detect the
imposture. The chance of blood from an epistaxis being swallowed and
afterward ejected by vomiting is to be remembered. Cardiac hæmoptysis
is distinguished in most cases by the presence of symptoms and physical
signs of valvular, usually mitral, disease in a considerable degree of
advancement. These are so pronounced as to exclude phthisical disease.
Other and fewer cases occur where the hæmoptysis is the first evidence
of the cardiac disease, and they require a careful exclusion of all the
features of tubercular disease, so as to be able to {290} arrive at a
correct conclusion. There are no conclusive considerations pertaining
to the amount and character of the blood. In the severe and copious
hemorrhages there is likely to be present a marked shock.

PROGNOSIS.--Hæmoptysis usually implies phthisis existing or imminent,
and yet it has in general a favorable effect on its course. This
applies more to its first stage than subsequently, and more to the
small than to the large hemorrhages. The gravity of the small ones
increases in proportion to their frequency. The family and personal
equation is of more importance than the mere quantity. We may have a
slight hæmoptysis and a large increase of the morbid condition
following it, and the reverse, the result depending on the individual
tolerance of and susceptibility to reaction. As in the second stage the
reactive elements are more potent, the small hemorrhages then are less
beneficial. They are the index of activity in the destructive lesions,
and yet may relieve the accompanying congestion. The easiest
appreciable symptom of the progress of the disease is the fever. We may
fail to properly interpret physical signs because of want of
familiarity with the individual case before us. If besides more fever
there be more cough, dyspnoea, and debility, the prognosis increases in
gravity. These remarks will apply with more force to the large
hemorrhages than the smaller ones, and are guides for prognosis in all
the clinical forms of hæmoptysis. In the special clinical form, the
hemorrhagic variety of phthisis, bleedings recur often and in large
quantities during years, and some of the cases end with final recovery.
The fever and constitutional irritation give way under seemingly very
unfavorable conditions. The fact that a great part of them have no
history of heredity, and that they come on at a late period of life,
may account for this, because they thus escape the influences which
heredity and age are known to impose upon the other classes of
phthisical subjects. Some interesting conclusions have been drawn from
the history of cases of profuse hemorrhages. Pollock[70] thinks that
they shorten the duration of the first stage and lengthen the duration
of the second and third. Out of his 351 cases, 204 occurred in the
first three months of illness: 45 had remained in the first stage when
examined, 142 having undergone softening, while 164 had cavities. Of
286 cases of profuse hæmoptysis classified by Williams,[71] the number
of cases in the first stage was 187, and the percentage of deaths was
13.95; 65 cases were in the second stage, and the percentage of deaths
was 24.61; 31 were in the third stage, and the percentage of deaths was
67.74, showing increased effect of hemorrhages upon pulmonary
structures advancing in destructive processes and upon constitutions
being progressively undermined by them. In other clinical varieties the
symptom is so clearly subordinated to the general process that it loses
its prognostic importance in the established disease. There is an
imminence of fatal hemorrhage in many of them, as in fibroid phthisis,
cancer, abscess, gangrene, and hemorrhagic infarction of the lungs. In
extra-pulmonary hæmoptysis or in that from rupture of pulmonary
aneurism there is seldom opportunity for prognosis.

[Footnote 70: _Elements of Prognosis in Consumption_, p. 139.]

[Footnote 71: _Pulmonary Consumption_, p. 150.]

If the condition be recognized, we can but say that the fatal attack is
liable to come at any moment. In cardiac hæmoptysis the hemorrhage is
an event coming toward the close of organic and obstructive changes
which are not much within our control. There are minor degrees, as
shown by expectoration of single small masses of dark coagulated blood
and by the absence of marked aggravation of the symptoms, which do not
prognosticate unfavorably for the immediate, but do show impending
dangers of a future, attack. Morbid anatomy shows traces of a recovery
from a number of premonitory threatenings. The elements of a serious
prognosis are the appearance of a shock, increased dyspnoea, a large
amount of hæmoptysis, increased perturbations in the heart-action, and
increased areas of dulness or râles at certain parts of {291} the lung
other than the usual sites of consumptive disease. These and other
evidences of constitutional initiation are not as available as in the
other varieties mentioned.

TREATMENT.--In the cases of the mildest form very little more need be
done than to keep the patient quiet. His apprehensions may require
attention. They may be allayed by assuring him that the hemorrhage will
be more of a security than a danger, because it is the expression of a
local congestion that will be relieved by the discharge. We have found
that a large dose of quinine (ten or fifteen grains) will answer the
double purpose of a nervous sedative and of controlling the congestion
and hemorrhage if the latter object be necessary. This suggestion
becomes still more applicable in the severe forms of hæmoptysis. The
dose may be repeated within twenty-four hours if needed. If congestion
be manifested by its symptoms of substernal heat, soreness, oppression,
dyspnoea, and cough to a greater degree, and if the hemorrhage is
becoming copious and the hemorrhagic pulse developed, and the
temperature elevated, the necessity of a more active interference is
evident. Absolute quiet in bed, fresh air, a calm and equable behavior
on the part of the family or friends in attendance so that no
excitement may be reflected to the patient, are essential. The
medicines selected should be such as may control the vascular
excitement, and hæmostatics. Ergot will fulfil such indications. It has
its limitations in its unpleasant taste, but it should be pushed to the
points of tolerance. Of the fluid extract one teaspoonful should be
given every hour or two until some effect is observed in slowing the
pulse or checking the hemorrhage. If the stomach rebel, ergotin pills
may be substituted in doses of three to five grains at the same
interval. Should all the resources of ergot medication be required or
the above mode of use fail or disagree, hypodermic injections may be
added. Two to three grains of the extract of ergotin would form a
proper dose, to be repeated every one or two hours. It has been quite
the exception in our experience to have serious irritation follow the
use of it in this way. Failure in this and other uses of ergot will
follow because we do not administer it with sufficient freedom.[72]
Another most valuable hæmostatic is turpentine. It should also be given
freely. From ten to thirty drops in an emulsion or in sugar may be
given every two to four hours, according to tolerance and to the
threatening character of the case. The ergot and turpentine are best
alternated at intervals of one to three hours, according to the
requirements of the attack. Some preparation of opium is often required
to quiet cough--morphine or codeine, one-fourth grain of the former and
one-half grain of the latter, repeated at intervals until their effects
are obvious. By adding the use of broken ice and the external
application of cold compresses frequently repeated, and, if time and
strength permit, the inhalation of persulphate of iron spray twenty or
thirty minims in half an ounce of water, we get a plan of treatment
adapted to the urgent cases. Some recent reports have confirmed the
confidence of the ancients in the use of ligatures. They may be applied
to both lower limbs. A dozen dry cups may be applied to the chest.
There is no occasion or time for the use of many medicines, but if a
general plan, such as the above, must be changed, acetate of lead in
doses of two grains every two hours would be an excellent substitute,
due regard being had to the possible toxic effects from too long
continuance of it in such doses; it is usual to add a little opium to
it. Gallic acid is an effectual remedy for the control of different
kinds of hemorrhages. Like ergot, it is usually given in too small
quantities. Twenty to thirty grains must be given every two to four
hours. {292} It is better borne by the stomach, and can often be
continued longer, than the medicines above mentioned.

[Footnote 72: A medical friend, T. C. Minor of Cincinnati, has in his
own case used three or four drachms of the fluid at a dose, with the
effect of reducing his pulse twenty beats in a few hours.]

We have already noted ipecacuanha as one of the survivals of ancient
practice. It has had warm advocates among modern physicians. Graves
places vivisection first and ipecacuanha next in his plan of treatment.
Trousseau strongly recommended it. Peter and the French practitioners
also strongly endorse its use in the severe forms. We have no doubt of
its efficacy. It is important to exclude if possible the existence of a
pulmonary aneurism or any such source of blooding, as there are no
special means by which this can be done. It is a good rule to use the
ipecacuanha in the cases of early or first-stage hæmoptyses. We would
give it as it is given in dysentery. Precede its administration half an
hour with thirty drops of laudanum, then give ten grains in water. If
vomiting comes on, repeat it in an hour, and again, if hemorrhage
continue, in two hours. The usual experience is that tolerance is
established after two or three doses. It has also an application in
small doses of one-quarter to one-half a grain in the milder forms,
with irritative cough and slight fever.

Graves calls attention especially to the excellent effect of opium in
all kinds of passive hemorrhage, hæmoptysis as well, but insists that
it should be given only after vivisection has been performed or when
the hæmoptysis has become rather passive, or in scorbutic and similar
cases. His direction on one occasion to a physician, in a case of
protracted bleeding of the gums, was, "Go home and give two grains of
opium immediately, and then half a grain every hour until the bleeding
stops." A combination applicable to the persistent bleeding recurring
day by day is the sulphate of magnesia made soluble in rose-water by
the free use of dilute sulphuric acid--one teaspoonful of the former,
fifteen drops of the acid, one-half to one ounce of the rose or plain
water. Many other remedies might be mentioned, and among them atropia.
After the bleeding has ceased it is necessary to be assured as to the
condition in which the lung has been left, and to counteract, if
needed, any persistence of irritation. Fever is the most valuable
evidence as to this point. If it exist, the use of quinia and ergot had
better be continued freely. A three-grain ergotin pill about three
times daily, and five grains of quinia morning and evening, can be
tolerated two or three weeks. Local irritation should be applied if
physical signs or pain warrants it.

{293}

PULMONARY APOPLEXY.

BY WILLIAM CARSON, M.D.

DEFINITION.--Escape of blood into the pulmonary parenchyma, with
laceration of its substance.

SYNONYMS.--Hemorrhage (pulmonaire) foyer (Jaccoud); Diffuse pulmonary
apoplexy or Diffuse pneumorrhagia (Fleich); Diffuse pulmonary apoplexy
(Loomis); Pneumo-hemorrhagie (Gendrin), etc.

HISTORY.--Latour[1] is quoted as being the first to use the words,
"apoplexie du poumon."[2] Yet Duguet[3] also quotes from Frank that
Dolocus had a long time before employed it. It is known that cases had
been described long before this, as by Corvisart in 1808, Allan Burnes
in 1809, among those of this century, and by Prosper Martiano, Bonet,
Morgagni, Haller, etc., among the more ancient authors.[4] Again,
Laennec gives the weight of his authority, and establishes Latour's use
of the name, until, as the synonyms show, modern usage has almost
abandoned it. Among the multitude of those who have treated of
pulmonary apoplexy, we will have filled the requirements of this brief
historical statement by mentioning Virchow and his pathological
investigations into embolism, and also Cohnheim,[5] and later
Litten's[6] studies on infarction, which have some indirect connection
with pulmonary apoplexy.

[Footnote 1: _Histoire philosophique et médicale des Hémorrhagies_,
1815, passage misquoted in _L'apoplexie pulmonaire_ by Duguet.]

[Footnote 2: _Op. cit._, pp. 220, 222, and 224.]

[Footnote 3: _Op. cit._, p. 11.]

[Footnote 4: Duguet, p. 10, etc.]

[Footnote 5: _Untersuchungen über die Embolischen processe_, 1872.]

[Footnote 6: _Zeitschrift für klinisch Medicin_, Erster Band, 131.]

ETIOLOGY.--Predisposing Causes.--The male sex affords predominance of
cases, because of greater liability to accidents, to the various forms
of ulcerative destruction of lung-tissue, and to aneurisms of the aorta
and pulmonary artery.

The adult age is most exposed for similar reasons. Ogston's
statistics[7] support in a general way, but not with strictly technical
force, their quotation by Herz.[8] Omitting the last 4 of his 20 cases
(2 of which were from poisoning, 1 from fracture of skull by a fall
down stairs, and 1 from drowning), the average for males (12) was 56.4,
and 55.3 for females (4).

[Footnote 7: _Brit. and For. Med.-Chir. Rev._, vol. xxxvii., 1866, p.
459.]

[Footnote 8: _Ziemssen's Handbook_, vol. v. p. 298. Ogston says (p.
465) it did not appear, however, that any distinct rent of their
substance had taken place--to any extent, at least. "When we consider
that the area of the extravasation was sufficient to involve often one
or two entire lobes, and that death was in most of them very sudden,
the cases may be adopted as showing the action of causes similar in
kind, if not in degree, to those operative in undoubted pulmonary
apoplexy."]

As more efficient predisposing causes than either age or sex, may be
mentioned aneurisms of the aorta and pulmonary artery, amyloid
degeneration of bronchial and pulmonary vessels, the influence of
Bright's disease in producing disease of blood-vessels, and
atheromatous diseases of the pulmonary artery.

Exciting Causes.--Penetrating and contused wounds of the chest by their
{294} direct mechanical effect, and diseases and injuries of the brain
through the medium of the nervous system, may produce pulmonary
apoplexy, the result in the latter case being usually an infiltration
or small infarction.

SYMPTOMATOLOGY.--Pulmonary apoplexy is the least common of the two
forms of distinctive pulmonary hemorrhage, the other being pulmonary
infarction, already treated of under HÆMOPTYSIS. A proportion of cases
is associated with mitral disease in its most advanced stages. At that
time we may expect pneumorrhagia, but whether from infarction or
apoplectic laceration even the event can only occasionally determine.
In the latter, if hemorrhage makes its appearance it will be copious
and generally overwhelming; at other times the hemorrhage may not
appear, and the patient dies suddenly with possibly other indications
of the internal flow. The physical signs cannot be relied on, for often
the pulmonary tissue is already changed by the long-continued
obstruction of circulation. Rupture of aneurism, particularly of aorta,
in the great majority of cases takes place into a bronchus, and not
into the parenchyma. In case of wounds of the contused variety a
laceration of parenchyma occurs at times sufficient to produce marked
hæmoptysis. If the blood be not ejected, there are no certain
indications of what has happened. If the case be seen immediately after
the accident, such physical signs as moist bubbling râles on the margin
of an area of feeble or suppressed vesicular murmur, possibly attended
with a dull, high-pitched percussion note over that area, would afford
a strong presumption in favor of ruptured lung and consequent
hemorrhage.

The same signs later might be due to a limited traumatic pneumonia. If
the internal hemorrhage, whether traumatic or spontaneous, has made its
way through the pleura, then, if the patient live long enough for
examination, besides such symptoms as great oppression and exhaustion,
the physical signs peculiar to pleural effusion may appear to a limited
degree. This opportunity seldom occurs, as such a rupture produces
almost invariably a fulminant and rapidly fatal result.

COURSE, DURATION, AND TERMINATION.--The course of the lighter cases is
much like that of pulmonary infarction, and that of the severe forms
too brief for observation. As to termination, it is quite possible
there are cases of laceration so limited as to allow complete recovery,
but clinical experience shows that pulmonary apoplexy is usually fatal.

PATHOLOGY AND MORBID ANATOMY.--With branches of the pulmonary vessels
weakened by long-continued heart disease, or with such vessels as are
found with chronic nephritis, a sudden increase of tension in them from
unusual effort or excitement will precipitate a fatal rupture.
Sometimes the progress of the degeneration is so insidious and complete
that a rupture may occur without obvious exciting cause. This is also
the natural history of aortic aneurism. An examination soon after the
laceration will show a mass of blood, usually coagulated, sometimes
partly fluid, lying in an irregular cavity with walls of the lacerated
lung-tissue. After a longer time the lung-tissue beyond the walls of
the hemorrhagic focus becomes oedematous to a certain extent. A
contraction of the cavity, with change of contents, may proceed to the
extent that an encapsuled mass of very small size will remain as the
final result (Rokitansky).

DIAGNOSIS from bronchial hemorrhage by the probable existence of
phthisical conditions and history. The quantity of blood ejected may be
profuse in either case, and therefore be no criterion. From pulmonary
infarction, as the other form of pulmonary hemorrhage, by the larger
amount of hæmoptysis. If there be no hæmoptysis, a presumption would
exist in favor of apoplexy in case of extreme dyspnoea or a fatal
result. The associated diseases or causes being similar, no inference
from the medical history would be reliable except in case of injuries.

{295} PROGNOSIS.--As we meet with it in recognizable form, the result
is almost invariably fatal. A qualification is allowed because of the
experience of such a pathologist as Rokitansky, who describes a process
of cure in a few cases. The prognosis in such would be determined
partly by the severity of the antecedent or accompanying disease, as in
heart lesions, and partly by the increased respiratory distress, pain,
exhaustion, and hemorrhage.

TREATMENT.--As has been before intimated, a case of pulmonary apoplexy
distinctive enough to be diagnosed is usually one that is beyond the
reach of treatment. Remedies that may relieve dyspnoea, exhaustion, and
hemorrhage are those to be relied on. External irritants, as
turpentine-stupe stimulants, ergot, turpentine internally, and such
other remedies as are of known effect in the treatment of the
associated heart troubles and of the incidental pulmonary infarctions.

{296}

ABSCESS OF THE LUNG.

BY WILLIAM CARSON, M.D.

DEFINITION.--A circumscribed suppuration of the lung, resulting in a
cavity.

SYNONYMS.--Abcés du poumon; Lungenabscess.

HISTORY.--The ancients described abscess of the lung, and placed it
among the terminations of the inflammation of that organ. They believed
that if the inflammation did not resolve itself by the fourteenth or
twenty-first day its termination was to be by suppuration. Hippocrates,
Van Swieten, and others are mentioned among those who maintained these
views and consequent frequency of such cases which prevailed until
physical methods and pathological investigation proved their
incorrectness. J. P. Frank, Bayle, and Cayol[1] are given credit for a
partial reversal of this opinion. Avenbrugger,[2] a pupil of Van
Swieten, in describing vomicæ, divides them into two kinds--the
ichorous and the purulent. By the purulent vomica he means an encysted
abscess of the chest resulting from the conversion of an inflamed spot
into a white, thick, glutinous, fatty matter. When these communicate
with the bronchi and discharge any of their contents by expectoration,
they are called open; otherwise, close or shut. He gives symptoms and
signs belonging to the respective varieties. Corvisart, in his comments
on these propositions, says: "In fact, the purulent vomica is always
the result of an inflammation, more or less acute, of the lung." He
makes distinctions between the various kinds of purulent vomica and the
ichorous vomica. Laennec, as in many other subjects of which he
treated, has the credit of placing this one on its modern basis, at
least so far as the frequent termination of pneumonia in abscess is
concerned. Among English writers Stokes deserves especial mention.
Abscess was the fifth and the last of the stages of pneumonia,
according to his classification. He treated largely of the perforating
abscess. Traube, Trousseau, and Leyden are among those who have
contributed largely to the elucidation of the subject. The latter has
especially claimed for this subject a more prominent place in the
literature of practical medicine, and has strongly enforced his views.

[Footnote 1: _Nouv. Dict. de Méd. et de Chirurgie_, tome xxix. p. 394;
and Leyden, "Ueber Lungenabscess," _Sammlung klinische Vorträge_, von
Richard Volkmann, Nos. 114, 115.]

[Footnote 2: _On Percussion of the Chest_, a translation of
Avenbrugger's original treatise by John Forbes, with comment by
Corvisart, 1761-1808, pp. 38, 43, etc.]

ETIOLOGY.--Predisposing Causes.--Everything tending to debilitate the
constitution may become a factor in the production of abscess of the
lung. Senile constitutions, Bright's disease, chronic alcoholism,
diabetes mellitus, and insanity are some of the predisposing causes.

Exciting Causes.--These may be divided, as in the case of gangrene,
into the pulmonary, or those originating in the lung or pleura, and the
intra-pulmonary, or those originating outside of the lung or pleura.
Among the former are included pneumonia and empyema, perforating and
discharging into the {297} lung, or one variety of Stokes's perforating
abscess, pulmonary apoplexy, and suppurating bronchial glands, opening
up a passage through the lung and bronchial tube. Either croupous or
catarrhal pneumonia may be associated with or terminate in pneumonia.
Among the latter, or extra-pulmonary class are included cases of
embolism from the right heart, producing infarction, or from the
systemic veins. These emboli carry with them the productive capacity of
suppuration. Abscess external to thoracic walls, as in deep-seated
mastitis, will at times perforate the walls and enter the lung.
Abscesses of the liver not infrequently perforate the diaphragm, and
are discharged through the lung.

Foreign bodies in the bronchi may ulcerate through them and produce
suppuration of the lung, which may finally open a way externally
through the chest-walls.

SYMPTOMATOLOGY.--The symptoms of abscess of the lung, as may be
inferred from the enumeration of causes, are divisible into two
categories--one including those symptoms with which the abscess may be
associated, but which do not necessarily prognosticate it; and the
other including the symptoms which indicate the abscess as a fact
accomplished. In the simplest and most frequent clinical form, that
following pneumonia, the early symptoms would be those of a severe and
irregular form, as shown by very troublesome and uncontrollable cough
or unusual pain or respiratory embarrassment, high fever, but at that
time fairly typical pneumonic temperature, great prostration, etc.
These may all diminish in due time, and mostly do without suppuration
following. A return of pain, dyspnoea, fever, and general distress
should awaken suspicion, yet they may be the result of an extension of
pneumonia to other portions of the lungs. Rigors and sweats and
increased depression would point to a suppurative process and under
such circumstances to the lung as the locality. We cannot, then,
positively predict an abscess. It is suspected when a more or less
copious eruption of purulent discharge occurs suddenly, and sometimes
the discharge is so abundant and pus-like that any other alternative
than abscess is very remote; at other times the discharge is small in
quantity. The proof of physical cavernous signs is the final step. This
is often difficult. A slightly greater increase of lung-density,
probably at the middle or upper part, with imperfect bronchial
breathing, the appearance of a few moist râles or crepitus, the gradual
increase of these and merging into coarser crepitus, and revelation of
more or less of the cavity signs, is the physical history of many cases
of abscess of the lung. Others have a much more pronounced course, such
as the cases of so-called gangrenous abscess--a sort of connecting link
between gangrene and abscess of the lung. The breaking down of tissue
is ostensibly very sudden, and the cavernous signs are very soon
unmistakable. Other clinical forms are the pyæmia, to be distinguished
by the antecedent history, which will reveal a source for infectious
emboli. The abscesses are usually multiple and small, so that their
precise locality cannot be made out. The proof of infectious
transportation is sudden pneumonic symptoms, as pain, tinged and
finally purulent expectoration. Rupture into pleura may occur and
produce empyema. Rupture of hepatic abscess and discharge through the
lungs is also a clinical form shown by this antecedent event, pointing
to hepatic inflammation. The egress of the pus is sometimes through a
narrow track, and not by a reservoir within the pulmonary tissue; at
other times the lung is really excavated. The discharge of pus is
usually copious and paroxysmal. Leyden recognizes as his third class a
form of chronic abscess, or one coming on during a case of chronic
pneumonia and bearing great resemblance to a variety of phthisis. Its
general symptoms are much the same as in the acute variety,
differentiated by the element of time.

COURSE.--It may be said, in a general way, that the etiology has much
to {298} do with its course. If the cause be pneumonia, the course will
be such as the detail of symptoms already given shows. In some unknown
way the natural course of the disease is interrupted, and what promises
to be an average case is followed by the characteristic features of
abscess. If pyæmia be the precedent condition, a peculiar form of
pneumonia, embolic in origin, appears, and abscesses again follow.
Greater septicity and rapidity of destruction are probable sequences.
The perforating abscesses are subject to modifying influences of
mechanical effect, such as gravitation and the resistance of tissues,
and have their peculiar course, which is often marked by great
chronicity.

TERMINATION.--In the course of seventeen years the reports of the
Cincinnati Hospital show that there have been 6 cases of abscess of the
lung treated there. Of these 4 died and 2 were discharged as improved.
These figures show the infrequency of such cases, and also represent a
greater mortality than probably occurs in the non-hospital class. We
know of no large statistics which show what is the percentage of
recoveries. Our own experience in private practice gives a majority of
recoveries. They were cases following typhoid fever, croupous and
catarrhal pneumonia, and hepatic abscess. A termination in a chronic
cavity now and then happens: perforation of the pleural cavity, with
subsequent pyo-pneumothorax, discharge externally through an
intercostal space, or even extension into the abdominal cavity, are
among the actual events of such abscesses.

DURATION.--The duration of an ordinary case is subject to wide
variations between one and six months. A few cases are recorded of
several years' duration. Previous constitutional condition has much to
do with this element. The degree of infectiousness in the pyæmic class
is important as to time. The abscesses become a subordinate condition
in the fate of the case. In this connection we may also refer to
Leyden's third variety, a so-called chronic abscess.

PATHOLOGY.--A close parallelism, etiologically and otherwise, is
observable up to certain points between gangrene and abscess of the
lung. Both are products of, or associated with, pneumonia. That which
finally determines whether the result shall be gangrene or abscess is
unknown to us. In the article on GANGRENE OF THE LUNG some
investigations are referred to which point to a probable solution in
the existence of specific forms having special pathogenetic force. The
tendency of experimental and clinical investigations is to connect the
suppurative process closely with the product of specific germs. Ogston
in 65 cases of acute abscess found micrococci present in all of them.
Obstruction of blood-vessels in the centre of the pneumonic area or on
the margin of the abscess walls is an important anatomical element in
the production of abscess, and it is claimed that it is often due to
colonies of micrococci within their calibre; so that it is probable
that there are both mechanical and biological or chemical influences at
work. If the view of the zymotic and infectious character of pneumonia
be tenable, the contingency of an abscess developing in its course
would seem not very remote. Yet the proportion of cases of abscess from
pneumonia is not more than 2 per cent. Leyden's high authority supports
the idea of the essential and specific differences in the chemical and
morphological peculiarities of gangrene and abscess of the lung, but
the subject is as yet on a hypothetical basis.

MORBID ANATOMY.--The fresh cavity, generally in the upper lobe, has
rough, ragged, and irregular walls, and may have bridles of the more
resistant structures, as bronchi and vessels, crossing it. Such a
cavity is quite likely to contain portions of undissolved parenchyma or
more or less malodorous pus. The older cavity becomes smoother walled,
and of more regular limits and cleaner contents. A gradation from
granular hepatization through congested to crepitant tissue is almost
uniform in the varieties of abscess, {299} whether simple or pyæmic. In
addition, some peculiarities are observable in the latter. These are
usually several, varying in size from a pea or less to a walnut, some
round and others wedge-shaped; others lying superficially and forming
slight elevations on the pleural surface. In proportion to the curative
progress the cavity will contract and disappear, occasionally leaving
behind a cicatricial mark. A lining pus-secreting membrane will
sometimes form, resulting in such a limitation of morbid action and
such a disappearance of reactionary symptoms as to make the disease
entirely local, but quite chronic.

DIAGNOSIS.--The more or less sudden and copious expectoration of pus,
without a specially offensive odor, in the course of a case having up
to that time the history of a pneumonia, would be considered as due to
the development of an abscess in the lung. Some degree of fetor in
breath and expectoration is observed, but it is far different from that
of gangrene. The detection of the débris of lung-structure in coarse
particles, and the microscopic discovery of elastic lung-tissue, are
important diagnostic points in contradistinction from the solution of
tissue that gangrene usually effects upon the parenchyma of the lung.
According to Leyden's[3] very complete investigations, the microscope
reveals fatty crystals, mostly in roundish fragments, of the size of
the epithelium of the lung and of a brilliant structure; pigment-débris
of a yellowish-brown or brownish-red color; hæmatoidin and bilirubin,
which Traube thought were due to hemorrhagic infarction, but which
Leyden has observed in all of his cases; and, lastly, micrococci, in
the well-known form of the round, granular micrococci colonies, which
differ from those in gangrenous fragments in that they show very little
movement and do not give the iodine reaction.

[Footnote 3: "Ueber Lungenabscess," _Volkmann's klin. Vorträge_, p.
994.]

Difficulties of diagnosis arise in the case of an empyema discharging
through the bronchi, or of an encysted empyema discharging through the
third or fourth intercostal space in front; also, between abscess of
the superior portion of the liver and one in the base of the lung, or
between the latter and a pyo-pneumothorax. Very careful study of the
history in each case is of the first importance. Where this is not
attainable the difficulty is often much increased. In the case of the
empyema the discharge is more profuse at each time, the whole amount in
a given period is much greater, and the time of opening is much delayed
beyond that of the pneumonic abscess. Trousseau gives the case of a
child who brought up for more than six months 200 grammes of pus daily.
He makes children an exception to the rule as to the late opening of
the pleural abscesses. In the encysted empyema discharging either
internally or externally the difficulties are greater. A portion of the
lung-tissue may be so near behind the deposit of matter as to make the
physical signs confusing if the pus has opened externally. Some of
these and of the interlobular deposits it is almost impossible to
diagnose.

In hepatic abscess opening into the lung and bronchi the discharge is
copious, dirty brown, paroxysmal, and will generally, on careful
observation, show the bile color or its chemical reactions or some
microscopic débris of the liver. In Leyden's third class, or the
chronic abscess arising in the course of chronic pneumonia, the history
is so much like that of some forms of phthisis as scarcely to serve in
diagnosis. He thinks there are some macroscopic and microscopic
appearances which may serve for diagnosis. There are in the
expectoration dark and compact pieces of greenish-black color, not
unlike plugs of pus, and larger, black-pigmented fragments of
parenchyma, from a pin's head to a hempseed in size. Microscopically,
they consist of a close and strongly-pigmented parenchyma, which seldom
reveals alveolar structure. They show fatty degeneration and
cholesterin plates. This class of cases is mostly without fever. The
application of the bacilli-tuberculosis test would seem to offer some
assistance in diagnosis.

{300} PROGNOSIS.--A grave prognosis may be formulated if there be a
history of feeble constitution, and especially if it be further
impaired by habits of intemperance, if the patient belong to either
extreme of age, if there has been a recent debauch, or if there be wide
variation from the typical form of pneumonia. Variations will be shown
in such a complexus of symptoms as follows: fever of low grade, subject
to extremes in range; feeble and frequent pulse, but not so marked as
in gangrene of the lung; dyspnoea, objective and subjective; typhoid
depression; tongue dryish; delirium; copious and fetid or difficult
expectoration; physical signs of extensive lesion, such as a large
cavity with a large outlying pneumonic area. A favorable prognosis
would be conditioned on the appearance of a fewer number of these
symptoms or on their evolution in a milder form.

The capacity of the patient to endure a long-continued suppurative
discharge is principally determined by his natural vigor and his
ability to assimilate food, other elements, such as extent of injury to
the lung, being the same. A well-defined superficial cavity would be
more favorable, because within surgical relief.

In the pyæmic variety the force of the infectious element will
determine largely the result. Chills and sweats are important
prognostic elements in such a case.

In the secondary abscesses of either the empyematous or hepatic variety
prognosis is grave--more so in the latter than in the former, because
surgical procedure would be more promising in the former, and because
of the implication of an organ so liable to destructive inflammation as
the liver. A long and tedious course of suppuration is possible in
either. The dangers in an established abscess arise from liabilities to
septic infection and exhaustion consequent on want of reparative power
and persistent suppuration.

TREATMENT.--The treatment of abscess differs little if at all from that
of gangrene of the lung. The tendencies of the two diseases toward
exhaustion and infection are similar, but are less pronounced in the
former. The same remedies are necessary in both, such as stimulants,
tonics, antiseptics, anodynes, and expectorants internally, inhalations
and drainage externally; brandy and malt liquors as stimulants;
nourishing and concentrated food at frequent intervals; quinine as
tonic and antiseptic; carbolic acid and turpentine as most valuable
antiseptics (the latter being also an excellent stimulant); eucalyptus
in cases of profuse as well as fetid discharge; carbonate of ammonia,
senega, as expectorants; morphine and codeine or anodynes to control
cough; carbolic acid for inhalation; and in cases of definitely
localized cavities a free opening to be made with antiseptic
injections.

Successful cases of surgical interference are reported, and such
treatment is now recognized as proper when the system is giving way
under septic poison, evinced in chills, sweats, and great prostration,
where the purulent discharge is fitful and imperfect, and where the
physical signs are clear enough to show the locality of the abscess.

{301}

GANGRENE OF THE LUNG.

BY WILLIAM CARSON, M.D.

DEFINITION.--Putrid necrosis of the lung-tissue.

SYNONYMS.--Lungenbrand, Gangrene du poumon, Gangræna pulmonum.

HISTORY.--By common consent, Laennec has the credit of first
identifying, naming, and classifying gangrene of the lung as a distinct
disease; yet Lieutaud[1] in 1707 describes imperfectly a case of
gangrene of the lung in a child: "the right lung, within and without,
appeared entirely putrid." Bayle[2] is considered, in his section on
his fourth variety of phthisis (phthisis ulcereuse), to have described
a rather chronic form of gangrene of the lung. Morgagni, Boerhaave,
Stoll, J. Frank, and Cullen considered gangrene as one of the
terminations of peripneumonia.[3] Laennec's development of the subject
has only in a few directions been enlarged. His classification is
universally adopted. His description is adopted generally as the most
complete. There have been, however, controversies on different points,
such as the relation of pneumonia and of the obstruction of the vessels
to gangrene of the lung.

[Footnote 1: _Historia Anatomica Medica_, 1787, Obs. 329, cited by
Louisa Atkins, 1872.]

[Footnote 2: Bayle, G. L., _Recherches sur la Phthisis pulmonaire_,
1809-10, p. 30.]

[Footnote 3: I. Straus, _Nouv. Dict. de Méd. et de Chir._, p. 403,
etc.]

In the pathology and etiology of gangrene Virchow's investigations on
embolism and thrombosis opened up important relations; in diagnosis,
Traube and Leyden and Jaffee; in medical treatment, also Traube; and in
surgical treatment, Haley and Lawson (1879),[4] S. C. Smith (1880), E.
Bull (1881), Fengar and Hollister (1881), Mosler and Voght (1882). The
antecedent development of pulmonary surgery, through important work
done by Mosler, Pepper, and others, had prepared the way for special
applications of it to gangrene and abscess of the lung. Spencer Wells
claims to have suggested similar proceedings nearly forty years ago.

[Footnote 4: _Lungen Chirurgie_, Mosler, xx. p. 67.]

ETIOLOGY.--Predisposing Causes.--Constitutional weakness is a common
predisposing influence: it may be a primary condition, but is more
often secondary or dependent on some recently-acting debilitating
cause, as typhoid fever, chronic lung disease, diabetes, etc. Chronic
alcoholism is a cause which, besides its effect on the system at large,
may add a special one on the lungs in producing hyperæmia or drunkard's
pneumonia.

Of 46 cases we have collected mostly from the Vienna Hospital report,
the youngest was nineteen years old and the oldest was forty-seven
years. Lebert[5] has collected altogether 60 cases, 32 of his own and
28 of others: 19 occurred between twenty and thirty years, and 1
between thirty and forty. Huntington[6] gives 32 cases from the
Massachusetts General Hospital Record between 1857 and 1875: 9 were
between twenty and thirty years, and 12 between thirty and forty; the
youngest was ten years old and the oldest sixty-four. It is noticeable
that these figures coincide largely with those {302} showing the
incidence of phthisis. Louisa Atkins[7] gives, as the youngest ages
among all the varieties, one of three months and another of two months.

[Footnote 5: _Klinik der Brustkrankheiten_, vol. i. p. 827.]

[Footnote 6: _Boston Med. and Surg. Journal_, vol. xcv. p. 486.]

[Footnote 7: _Gangræna Pulmonum bei Kindern_, 1872.]

Of the 46 Vienna Hospital cases, 43 were male and 3 female.
Huntington's cases were males 24, females 8. Of Lebert's own 32 cases,
22 were males; of the 32 others summarized by him, in 4 sex was not
mentioned, and of the remainder 17 were males and 11 females. These
figures show the large predominance of males in the liability to
attack.

Exciting Causes.--They may be classified as pulmonary and
extra-pulmonary. The influence of the alcoholic habit has been referred
to above among predisposing causes: debauches are a frequent
antecedent, especially in hospital cases, by means of resulting
pulmonary hyperæmia and drunkard's pneumonia. Its association with
croupous pneumonia may be assumed as settled after some warm disputes.
The pneumonia of Bright's disease and putrid bronchitis are
occasionally causative; bronchiectasies result in it not unfrequently.
Extension of diphtheritic inflammation from the tracheal and bronchial
mucous membrane is another form. The catarrhal pneumonia secondary to
measles may produce it in children.

Embolism is the most frequent cause in the class of extra-pulmonary
causes. It may be mechanical or infecting. A bronchial artery may be
plugged so as to produce a gangrenous slough from mechanical cutting
off of nutrition. Embolism of the pulmonary artery branches is more
frequent, and by bringing about infarction and apoplexy may produce
gangrene. Of the infecting variety may be mentioned emboli from the
peripheral veins, as in surgical or uterine phlebitis, or from cerebral
sinuses secondarily involved from otitis. Other causes acting from
without on the lungs are foreign bodies, as particles of food passing
beyond the trachea into the lungs, as in case of the insane or
drunkards, and blows on the walls of the chest. These latter are
capable of producing not only the ordinary phenomena of
contusion-pneumonia[8] but gangrene, and without evidence of external
injury or fracture of the ribs.

[Footnote 8: M. Litten, p. 26, vol. v., _Zeitschrift für klinische
Medicin_.]

SYMPTOMATOLOGY.--Gangrene of the lung is the termination of a process
the beginning and progress of which are not declared or cannot be
followed through characteristic symptoms. Even its final occurrence may
remain unknown if a communication be not established with a bronchus,
which event is followed by the true symptoms, the expectoration and its
odor. Whatever symptoms occur previous to that event may occur
independent of it. Adopting Lebert's dictum,[9] gangrene of the lung is
not a pathological unit. As its pathogenesis varies, so does its
symptomatology. A feature common to its several varieties is marked
constitutional depression and variations from the typical form of the
disease in which it occurs. If pneumonia, croupous or catarrhal, be the
precedent or associated disease, it will be marked by soft and feeble
and frequent pulse, restlessness, dulness or distress of countenance,
more or less cyanosis, cool and relaxed skin, possibly delirium, dry
tongue, unusual dyspnoea and pleuritic pain, copious prune-juice
expectoration, irregular or non-typical temperatures. Along with these
functional variations occur some in physical signs, as a lesser amount
of dulness or of bronchial breathing, indicative of less structural
density and corresponding exudation. A case with such an evolution may
afford a presumption of an outcome in gangrene, but appearance of the
characteristic expectoration and fetor is necessary to exclude it from
irregular forms of pneumonia, which have no such termination. The same
general remark applies to the cases of gangrene in bronchiectasic
cavities. Perhaps some aggravation of the general condition may excite
apprehension, but the characteristic phenomena of expectoration, odor,
etc. must decide. If the cause be of embolic origin, we {303} may
expect some suddenness and perhaps shock in the beginning, and later
the evidences of a more limited inflammation of the lung-tissue, such
as circumscribed dulness and modified respiratory sound, which finally
end in those indicating destruction of lung-tissue.

[Footnote 9: _Op. cit._, p. 803.]

The macroscopic characters of the expectoration are those of a putrid
or fetid liquid of varying shades of color, ashy gray, dirty green, or
greenish-yellow, prune-juice, or more or less hemorrhagic. The odor,
which is at first so fetid and penetrating, often disappears after the
expectoration has been standing a while. It is separable, as first
described by Traube,[10] into three principal layers. The uppermost,
covered with a layer of foam, consists of, first, dirty green,
crumbling, confluent lumps; second, of larger, homogeneous, green
muco-purulent masses; and, third, of whitish-gray, transparent, mucous
masses. The second layer is formed of a colorless fluid. At the bottom
is a fine yellowish-white sediment. Microscopically are found fat-acid
crystals, many large fat-drops, and finely granular débris, masses of
free, black pigment. It is said elastic tissue is nowhere to be found,
but to this statement there are no doubt exceptions. Other bodies have
been found by Leyden and Jaffee,[11] which they named Leptothrix
pulmonalis. Kannenberg,[12] besides the above forms, found constantly
infusoria of the family of monads in the sputa of 11 out of 14 cases of
pulmonary gangrene. He considers them peculiar to the processes of
decomposition in the lungs.

[Footnote 10: _Gesammte Beiträge zur Pathologie und Physiologie_,
Zweiter Band, p. 452, etc.]

[Footnote 11: _Deutsches Archiv für klin. Med._, Band ii. pp. 488,
etc., "Ueber putride Sputa."]

[Footnote 12: _Virchow's Archiv_, Band lxxv.; _Zeitschrift für
klinische Med._, Band i. p. 228.]

PROGNOSIS in general is unfavorable. Individually, the gravity of the
case is determined by the evidence bearing on previous habits and
constitution; by the violence of the onset, as shown in prostration,
severe pain in the chest, dyspnoea, persistent and violent cough,
delirium, feebleness and softness of the pulse; by the variations from
the typical standards of croupous, or especially catarrhal, pneumonia,
such as greater amount of septic or infectious or typhoidal element,
non-typical and low temperatures in the early stages and also in the
stage of disintegration; by the amount of the latter as shown in the
physical signs of extensive lesion and in the amount of gangrenous
sputum; and by the irritant effect of this in producing bronchial
catarrh, and consequent catarrhal secretion, which may of itself become
an element of danger in a system already much prostrated. Favorable
prognosis is allowable when these conditions are being gradually
reversed.

PATHOLOGY.--The pathology of gangrene of the lung is scarcely more
settled than it was forty years ago, when Stokes[13] published his
eighteen propositions, embodying his experience. Obstruction of vessels
and inflammatory exudations are present as important pathological
conditions, but of themselves are not pathogenetic of gangrene. Other,
as yet unknown, elements of putrefactive agency are present. Leyden and
Jaffee's observations and those of Kannenberg have been mentioned[14]
as efforts to throw light upon the pathogenesis of gangrene of lung,
but how far the bodies described by them precede, coincide, or follow
the familiar clinical phenomena are undetermined questions.
Filehne,[15] in his experiments to determine the reason of the almost
universal absence of elastic fibres in the expectoration of patients
with gangrene of lung, comes to the conclusion that there is a ferment
which, acting under alkaline conditions, destroys the fibres. The
agents of this ferment he does not try to determine. Stokes anticipates
the tendency of modern experimental pathology by announcing as an
alternative proposition that "a process of putrefactive secretion
precedes in many cases the death of lung." The constitutional debility
which is so early a symptom prepares the way for such {304} an
invasion. In reference to the relation between the septic material and
thrombosis in gangrene, Kohler[16] affirms that the septic material
produces the fibrin-ferment, and thereby capillary thrombosis.
Recklinghausen thinks that a special material capable of exciting
coagulation has not yet been found in gangrenous substances, but that
there may be several factors, such as anæmia, changes in the
vessel-wall, imbibition with foreign substances, etc. Other
experiments[17] and views point toward the conclusion that there are
substances formed in various diseased conditions which have the power
of ferments and of producing coagulation of blood in the lesser
circulation.

[Footnote 13: _Dublin Quarterly Journal Med. Science_, Feb. 1, 1850.]

[Footnote 14: _Op. cit._]

[Footnote 15: "Sitzungsbericht der Phys. Med. Soc." in _Erlangen
Schmidt's Jahrbucher_, 1877, No. 7.]

[Footnote 16: _Recklinghausen's Handbuch der Pathologie_, p. 136.]

[Footnote 17: Wooldridge, Du Bois-Reymond, _Archiv Centralblatt für
med. Wissenschaften_, No. 41, vol. xi. 1874, p. 734.]

MORBID ANATOMY.--The circumscribed variety, as it usually appears, is a
cavity irregular in outline, with ragged walls, made so by the unequal
invasion of the lung-tissue by the gangrenous process. Sometimes the
cavity itself contains loose fragments of lung-tissue, or the contents
may be of a dirty, greenish, or brownish color, with some of the odor
of the expectorated matters. If the case has been a chronic one, the
walls are smoother, with a more or less formed lining membrane and the
contents of a less characteristic color or odor. The cavity is usually
in the right lung, and in the middle or lower portion. There is much
variety of statement on this point. The tissue immediately adjacent to
the gangrenous walls shows more or less of the products of catarrhal
pneumonia. The vessels terminating in the walls are obstructed by
coagula. If the gangrenous part come to the pleural surface, belonging
to what Fournet calls the superficial variety, it may produce adhesions
there, or it may result in perforation, with the result that we have
the products of pleuritic inflammation united with the contents of the
gangrenous cavity. In multiple foci, some will show the less advanced
stages of disease, such as incomplete softening and local inflammatory
lesions. In the diffused variety the lesions are sometimes described as
being the same except in extent. The demarcations, however, from
surrounding tissue are not as well marked; the tissue is soft, breaking
easily under pressure, sometimes oedematous, dark or dirty black on
surface or on section of lung; at other times the surface is mottled
with lighter-colored patches. A secondary result is the production of
bronchitis by the contact of the irritant expectoration from the
gangrenous cavity.

DIAGNOSIS.--Abscess of the lung is the disease most likely to be
confounded with gangrene of the lung. In the former you do not have the
same amount of profound constitutional depression; the symptoms have a
more frank expression, as it were, because of better precedent
conditions usually; the first eruption of matter from the abscess is
more copious and sudden than the usual manner of expectoration of
gangrenous sputum; the appearance of the contents of the abscess is
that more nearly of healthy pus, though the latter has at times a dark
dirty brown or hemorrhagic look; the separation into layers is not apt
to occur; the odor is usually not so fetid; microscopically, elastic
fibres are much more abundant in abscess than in gangrene of the lung.
The cavernous physical signs are not reliable in either disease. There
are cases in which it is impossible, and in which it is of no practical
importance, to make a diagnosis between gangrenous abscess and
pulmonary gangrene. Gangrene supervening in phthisical cavities is
distinguished by the history of a chronic pulmonary disease in which a
cavity has been previously marked. It is phthisis advanced to the
destruction of tissue plus the unknown gangrenous element which has
found a lodgment in a favorable place. Stagnation of cavity contents,
depression of system, etc. are favoring conditions. The same remarks
apply to bronchiectasic cavities and putrid bronchitis, physical signs
in the latter being additional points of difference.

{305} Our experience proves that the essential SYMPTOMATOLOGY of
gangrene of lung, except the débris of lung-structure in the sputum,
can occur where there was no gangrenous destruction, either
circumscribed or diffuse, no bronchiectasic cavities or bronchial
dilatations, and no phthisical cavity. In the case alluded to the
gangrenous odor and general characters of the sputum and the separation
into layers and the consolidation of tissue were present, but the
post-mortem afforded no explanation of the fetid expectoration. It was
a case of debauch and alcoholic excesses and exposure.

COURSE, DURATION, AND TERMINATION.--The course of this disease is
essentially an acute one. Whatever the early condition be, the
gangrenous element hastens its progress, as in cases beginning with the
phenomena of acute pleuro-pneumonia. A pre-existing phthisical cavity
will take on acute phases, also the septic element will be reinforced,
and, as indicated in the enumeration of symptoms, clinical
irregularities will be introduced. The early prostration is increased,
and the patient dies from exhaustion after a period varying from three
days to six weeks from the time the gangrene became manifest. Various
complications, such as pleuritis and perforation of pleura and
pneumothorax, hemorrhage, or extensive, diffused gangrene may cut short
the patient's life within the average period. Occasionally the
gangrenous cavity becomes chronic and the patient may live for months
in imperfect health. The termination of the circumscribed variety is
usually death. Diffuse gangrene is invariably fatal.

TREATMENT should be directed, first, to the known precedent states of
constitutional weakness, bad habits, etc., which lay a foundation for
unhealthy inflammatory processes, and for the pathogenetic elements
that bring about the gangrenous and septic and exhausting conditions;
second, to the special symptoms, such as severe pain in the side,
harassing cough, dyspnoea, etc. Remedies of the first class are quinia,
turpentine, early alcoholic stimulation, carbonate of ammonium,
antiseptics, as carbolic acid, etc. An anticipation from the beginning
of any irregular form of acute pulmonary disease of its termination in
gangrene is impossible, and hence early treatment is necessarily
general. It would be properly confined to the use of quinia, which
would be useful, either before or after the gangrenous element had
developed, in small doses frequently given, unless high temperature or
the septic process indicate the use of large ones. Turpentine
internally is desirable in proportion to the infectious or typhoidal
character of the attack. Its use by inhalation is beneficial when
gangrenous destruction has already taken place. Brandy or whiskey in
moderate and frequent quantities, one-half to one tablespoonful every
three hours, and carbonate of ammonium, meet the requirements which the
tendencies to debility indicate. Milk, milk-punch, beef and chicken
extracts should be given in the intervals between the administration of
medicines. This general plan is applicable throughout the pre- and
post-gangrenous stages. In the symptomatic treatment pain and a general
respiratory distress often demand attention. Opium is then useful, both
in relieving pain and moderating dyspnoea and cough. As these symptoms
are often urgent in the later stages of gangrene of the lung, the
treatment of the disease harmonizes both in its constitutional and
symptomatic aspects. Prescriptions can also be readily prepared which
contain remedies that have a decided effect in correcting the fetor of
the breath and expectoration, and thus evincing an influence on the
putrefactive process or ferment, which has become the prominent feature
of the disease. The author recommends that carbolic acid, in the dose
of one grain every four hours, be given for that purpose, and also its
use by inhalation. Assistance can sometimes be given by putting the
patient in such a position on the side as to promote the emptying of
the cavity.

Tapping a gangrenous cavity and the introduction of drainage-tubes may
be successfully resorted to. The cases suitable for such surgical
treatment have {306} been described by Fenger and Hollister[18] as
those where, "the presence of a gangrenous or ichorous cavity having
been ascertained, it is found that notwithstanding an outlet through
the bronchi for a portion of the contents of the cavity, it steadily
fills up again; the partial evacuation does not relieve the patient;
the infection of the healthy portions of the lung from the decomposed
contents of the cavity has commenced or is evidently about to take
place; the breath and expectoration continue fetid; absence of
appetite; increasing weakness, with or without fever, etc." For the
steps of the operative procedure reference may be made to the complete
directions given by the same authors or to works on surgery. The double
opening advised by the above authors would be the most efficient plan.

[Footnote 18: _Amer. Journ. Med. Sci._, Oct., 1881, p. 385.]

{307}

CROUPOUS PNEUMONIA.

BY ALFRED L. LOOMIS, M.D.

SYNONYMS.--English and American: Acute sthenic exudative pneumonia;
Primary lobar pneumonia; Vera peripneumonia; and Pneumonitis. _Fr._
Fluxion du poitine and Fièvre pneumonique; _Ger._ Pneumonia lobaris and
Lobäre Lungenentzündung.

DEFINITION.--Croupous pneumonia is an acute general disease with a
characteristic local pulmonary lesion. Anatomically considered, it is
an acute inflammation of the vesicular structure of the lungs,
resulting in infiltration of the alveoli, with inflammatory products,
which renders them impervious to air. This condition is known as
hepatization.

HISTORY.--Until the time of Laennec, pneumonia and pleurisy were
described as one disease. Hippocrates said that pleurisy was "a disease
quickly fatal, and characterized by sputa of various colors." Although
these two diseases were undifferentiated, accurate descriptions of the
lesions and objective signs of pneumonia have come to us from the
earliest medical writers.[1]

[Footnote 1: Thucydides, _The Plague at Athens_, B.C. 430.]

Much of the early history of this disease is interwoven with the
detailed accounts of a great variety of pulmonary symptoms which
occurred in the epidemics and plagues which prevailed in Eastern Europe
in the centuries just preceding the Christian era, and in Western and
Southern Europe during the sixteenth and seventeenth centuries. The
black death has been regarded by some as an epidemic of pneumonia.
While it is probable that in most of these epidemics the lung was early
involved, and that its implication hastened death, yet no proof exists
to sustain the belief that they were other than epidemics of typhus
fever, dysentery, and those (as yet unknown) fevers which collectively
were named plagues. That many of these plagues were complicated by
pneumonia there is scarcely room for doubt.

French investigators were the first to separate the pneumonic process
from all other morbid processes which occur in the thoracic organs.
Valsalva, Morgagni, and Boerhaave gave accurate descriptions of
pneumonia, but they did not sharply distinguish it from pleurisy.
Bichat and Pinel separated collapse of the lung attending pleuritic
effusion from inflammation of the lung-substance.[2] Laennec was the
first to draw the line sharply between pneumonia and pleurisy, and to
him, more than to any other observer, is due the credit of describing
pneumonia as a distinct disease. With his labors begins a new era in
the history of pulmonary inflammations.

[Footnote 2: _Nos. phil._, ii., Pinel.]

Grisolle's work[3] is especially valuable in statistics relating to the
climatic element in the development of pneumonia and its comparative
frequency among different races. The elaborate treatise on the
geographical distribution of pneumonia by Ziemssen has furnished data
for a more accurate knowledge of its geographical boundaries. Following
in the footsteps of Laennec, {308} Chomel, Stokes, Addison, and many
laborers of our own day have furnished the material from which the
clinical and pathological history of pneumonia is now being
constructed.

[Footnote 3: _Traité de la Pneumonie_.]

Recently, Jürgensen has strongly advocated the infection theory of
pneumonia, and has presented strong arguments in support of his
opinions. Sturges of London and Cohnheim[4] advocate the use of the
term pneumonic fever, and the former gives a most interesting general
comparison between it and the affections which he regards analogous to
it. Careful pathological experiments have recently been made by
Heidenhain, Sommerbrodt, Schuppel, and Klebs[5] with a view to
establish the germ-theory of pneumonia.

[Footnote 4: _Leçons de Chir. méd._, 1877, p. 17.]

[Footnote 5: _Arch. für experiment. Pathol._, p. 420.]

The literature of the past ten years is richer in the development of
facts and experimental investigations than all the centuries that have
preceded; and these recent experiments, combined with modern statistics
and the results of the microscope in pathological histology, have given
to croupous pneumonia a separate and distinct place in the list of
pulmonary diseases.

MORBID ANATOMY.--Anatomically as well as clinically, there are three
recognized stages in croupous pneumonia: 1, Stage of engorgement or
congestion; 2, Stage of red hepatization; 3, Stage of gray
hepatization, resolution, or purulent infiltration (suppuration).

It has been claimed that the stage of engorgement is preceded by a dry
stage, or "stage of arterial injection," in which the lung-tissue is
dry and of a bright-red color. It is evident that congestion of the
minute branches of the pulmonary artery would not give to the
lung-tissue a bright-red color, and if such a condition exists it must
be due to injection of the bronchial vessels. It is by no means proven
that such injection ever precedes pneumonic engorgement. In the stage
of engorgement that portion of the lung which is involved in the
pneumonic process does not collapse when the thoracic cavity is opened.
The affected portion of lung is distended and firmer than normal
lung-tissue, and when pressed upon crepitates less, often remaining
indented after the pressure is removed. The lung is not entirely
airless, for by pressure the air can be forced from one portion of it
to another. Its color is darker than normal, usually being of a
brownish-red or purple. There is an increase not only in its actual
weight, but in its specific gravity. On section a thin, frothy,
blood-stained serum exudes, and sometimes on pressure flows freely from
the cut surface; occasionally this exudation is tenacious. When alcohol
is added to this fluid, it coagulates into a granular, amorphous mass.

The capillaries around the air-cells are distended, and dark blood
oozes from their divided ends. Occasionally, upon close examination,
there may be seen beneath the pleura and between the air-sacs small
points of blood-extravasation. A portion of lung in this stage, when
placed in water, does not float as near the surface as healthy
lung-tissue.

When examined with the microscope, the lumen of the alveoli are seen to
be diminished by the encroachment of the varicosed and tortuous
capillary vessels. As a rule, the air-sacs are uniformly dilated; some,
however, may be collapsed--a condition probably due to pressure during
the early period of the pneumonic process. The epithelia of the alveoli
are swollen, and contain a granular protoplasm with free nuclei. The
air-vesicles also contain exfoliated epithelial cells and white and red
blood-corpuscles. The serum which escapes into the alveoli from the
distended capillary vessels is the fluid in which these cell-elements
float. Since the enlarged epithelia often suffer a division of their
protoplasm, embryonic mono-nucleated cells are intermingled with the
other elements. It is still a disputed question whether the bronchial
or the pulmonary capillaries are the chief source of the pneumonic
exudation.

Physiology teaches that lung-tissue is nourished by the blood in the
{309} ramifications of the bronchial arteries, and that the pulmonary
capillaries are the passive media for the interchange of gases. Hence
it is claimed that the bronchial capillaries only are implicated in the
inflammatory process. Virchow has shown that the pneumonic process can
be completely established in places where pulmonic capillaries cannot
be traced on account of the plugging of a large branch of the pulmonary
artery;[6] yet even he admits that secondarily the pulmonary vessels
have much to do in the inflammatory process.

[Footnote 6: _Ges. Abhang._, p. 369, Virchow.]

On the other hand, it is claimed that in the early stages of the
pneumonic process the parts that are supplied by the bronchial
capillaries are not reddened or injected, as they would be were these
vessels primarily concerned in the inflammatory process. Reasoning from
the above, it would seem that both sets of vessels are involved, but
that usually one set is implicated at the very commencement to a
greater extent than the other.

It is often difficult, and sometimes impossible, to differentiate
between the anatomical appearances produced by pulmonary congestion and
oedema and the first stage of pneumonia. In pulmonary congestion and
oedema the fluid in the alveoli is serum, and contains none of the
pathological cell-elements found in the first stage of pneumonia. The
alveolar capillaries are turgid, and in this respect resemble the
capillaries in pneumonic congestion, but when a stream of water flows
over a portion of lung in the first stage of pneumonia its dark color
remains, while in hyperæmia of a non-inflammatory character this is not
the case.

On account of its color and its resemblance to liver-tissue the name
red hepatization has been given to the second stage of croupous
pneumonia. The lung in this stage has a dark liver or mahogany color,
and is slightly mottled, the mottling becoming more marked the farther
advanced is the hepatization. The color is of a brighter red when the
lung is first removed from the body than after it has been exposed to
the air.

The volume of the lung is increased--at times so as to bear the impress
of the ribs. It is solid and firmer than normal; pressure does not
indent but tears it; it is very friable, and its torn surface presents
a granular appearance. Its specific gravity is increased. It is
airless, and there is an entire loss of crepitation.

Upon section it is seen that the granular appearance of the cut surface
is due to the pneumonic exudation which fills the alveoli. This
granular appearance is not so well shown on the cut as on the torn
surface. The granules can be readily removed from the air-cells by
means of a fine needle. A dirty, red, viscid fluid slowly oozes from
its cut surface, which is more apparent after the lung has been exposed
to the air for twelve or twenty-four hours and has undergone
post-mortem changes. At any time this viscid, rusty-looking material
may be scraped from the cut surface, or it exudes when a portion of the
lung is firmly compressed. A portion of the inflamed lung quickly sinks
in water, and small spots of blood-extravasations may be seen scattered
here and there throughout its substance. When a stream of water is
poured over the cut surface of the implicated lung the color changes
from a maroon to a gray or yellow-gray, the usual color of fibrillated
fibrin.

Not infrequently the material in the infundibula and air-cells extends
into the minute bronchi, but these tubes are rarely completely filled
with the pneumonic exudation. When examined under the microscope the
alveoli are found filled with a solid material composed of a network of
fibrillated fibrin, in whose meshes are leucocytes, red blood-globules,
and changed epithelia. These latter are in various forms, usually round
or oval. They may, however, become quadrangular, triangular, or
irregular. They are granular, and may contain a single nucleus, a
nucleolus, or multiple nuclei. These cells finally become granular, and
fat-globules accumulate in them. {310} They also become discolored from
imbibition of blood-coloring matter, so that in the latter part of the
process there is quite an accumulation of pigment-granules, not only in
the free cells, but in the fixed epithelia. The larger cells discharge
their nuclei into the accumulation of corpuscular elements, and the
whole contents of an alveolus present a more or less round shape. The
alveolar walls remain unchanged, or are slightly thickened by the
capillary turgescence. All of these different cell-elements have been
regarded by different observers as characteristic of pneumonia. The red
globules give the color to the consolidated lung. The pus-cells are
always numerous.

The transition from red to gray hepatization is never well defined. The
mottling gradually becomes more marked, so that the affected portion of
lung assumes a marbled or granite appearance. As the deep-red color of
the second stage fades the density of the pneumonic consolidation
becomes less and less, until it is a mere pulp, breaking down under
slight pressure. The decoloration is due to the pressure on the
blood-vessels, to decoloration of the blood-corpuscles that were
present in the second stage, and to fatty degeneration of the other
cell-elements which occupied the air-sacs.

The weight and density of the affected lung-tissue are diminished, and
toward the end of this stage the lung crepitates. On section a nearly
uniform dirty-gray, bloodless surface is exhibited, from which flows
spontaneously or upon slight pressure a dirty-white or reddish-gray
puruloid fluid. The granular red hepatized look has disappeared or is
very indistinct. The amount of oedema in the affected portion of the
lung varies in different cases. When it is excessive a large quantity
of serum exudes from the cut surface, which then exhibits a smooth,
non-granular, glistening appearance, and it does not so readily break
down when pressed upon as do other forms of gray hepatization. When
examined under the microscope, the alveoli are seen to be filled with
numerous round mono-nucleated cells, the intercellular fibrils that
bound the elements together having disappeared; in other words (the
fibrillated having become granular fibrin), the alveoli are filled with
a fluid or semi-fluid mass in which numbers of discrete oil-globules
and protein granules are freely mingled.

The granular and fatty elements are due to the rapid degenerative
changes that occur in the cell-elements. In this stage leucocytes still
emigrate from the blood-vessels. The masses that occupy the alveoli are
now shrunken, and between them and the alveolar wall is a layer of
fluid, so that in a thin section the contents of the air-sacs are
readily lifted out by a camel's-hair brush. All of the affected portion
of the lung is rarely in the same stage of the inflammatory process,
and to distinguish red from gray hepatization, or the latter from the
beginning of some of the conditions next to be mentioned, is often
impossible.

The changes which take place subsequent to the stage of gray
hepatization, and the modifications due to age, remain to be
considered.

Croupous pneumonia may terminate--1, in resolution [recovery]; 2, in
suppuration, purulent infiltration; 3, in abscess; 4, in gangrene; 5,
and very rarely, in chronic (fibroid) pneumonia.

1. During resolution the lung is moist, lighter than in the stage of
hepatization, has a yellow or yellowish-green color, and still shows a
marked loss in elasticity. On section, the lung appears to be
non-granular, and a tenacious, puruloid fluid escapes when the section
is pressed upon. Some oedema may still remain. When examined under the
microscope the alveolar capillary vessels are seen to have returned to
their normal calibre; the alveolar epithelium is restored; the cells in
the air-sacs are degenerated, broken down, and resolved into a
detritus. The degeneration of these cells is both fatty and mucoid, and
the coloring matter of the blood gives origin to the granular {311}
pigment which is scattered throughout the disintegrated and liquefied
mass. Some of the pigment is supposed to come from the connective
tissue between the alveoli. In this condition the alveolar contents are
either expelled by expectoration or undergo absorption, the lung being
finally restored to its normal condition.

2. When purulent infiltration or suppuration of the lung occurs, its
surface becomes yellow--more so than in any of the preceding
conditions; it is soft, moist, and friable, and gives somewhat the
sensation of an abscess. It is well described as miry.[7]

[Footnote 7: _Pneumonia_, Sturges, 1876, pp. 110, 113.]

On section, a diffluent, purulent fluid exudes from a surface whose
yellow color is due both to the large number of cells which are
undergoing fatty degeneration, and to the anæmia which results from
over-distension of the alveoli with these cell-elements.

When examined under the microscope, the cells are found not only
crowding the alveoli, but infiltrating the inter-alveolar tissue. This
corpuscular infiltration of the alveolar walls may so interfere with
their nutrition that they will undergo softening and degeneration.
Whether these cells (in all respects resembling pus-cells) have
emigrated from the blood-vessels or are the result of epithelial
changes is still unsettled. Reason and analogy seem to point to a dual
origin. Now and then these cells are pigmented. Occasionally the
alveolar walls become thinned, indistinct, and finally rupture.

There has been much discussion over the term suppuration of the lung,
but the appearances reported by those who uphold, as well as by those
who protest against, the term are identically the same, all agreeing
that the "lung is filled with pus."

3. Abscess of the lung, as a termination of croupous pneumonia, is
exceedingly rare, and is always preceded by extensive cellular or
interstitial oedema; small abscesses are formed by the rupture of
several of the alveolar septa. It may follow purulent infiltration.
These abscesses vary in size from that of a pea to one which may occupy
the greater part of a lobe. They may have a thick, well-defined,
irregular wall, their interior being crossed by shaggy shreds of
broken-down lung-tissue, or they may form irregular excavations in
softened lung-tissue. They may be single or multiple. Several abscesses
are often found in the same lobe. They increase in size by peripheral
growth or by fusion of several small abscesses.

Abscesses are more common in the upper than in the lower lobes; their
frequency is variously estimated as 1 in 30 or 60 cases. These
pus-cavities, if of small size, may ultimately close by cicatrization,
in which case they may open into a bronchus of sufficient size to allow
of the discharge of their contents. Under such circumstances the
contents of the abscess are expectorated; interstitial inflammation is
set up around their site, which after a time encloses them in a firm
connective-tissue wall; contraction ensues, and finally only a line of
cicatricial tissue marks their former situation. Or if no such
bronchial opening occurs, the abscess becomes encapsulated in firm
cicatricial tissue, and the contents undergo cheesy and calcareous
transformation. Sometimes these abscesses perforate the pleura and
discharge their contents into the pleural cavity, causing
pyo-pneumothorax. External fistulous openings have occurred, but they
are a rare termination of pulmonary abscess.

4. Gangrene is said to be a termination of croupous pneumonia in about
2 per cent. of cases, but this estimate is based on too few statistics
to be wholly reliable. It is met with in bad constitutions where there
is very great vital depression, in chronic alcoholismus, and in cases
of intense septic poisoning. Interference with the blood-supply,
causing the formation of pulmonary or bronchial thrombi, leads to its
development.[8] While usually limited to a {312} small area of
lung-tissue, it may invade large tracts, and be either circumscribed or
diffuse.

[Footnote 8: Huss, _Pneumonia_; Carswell, _Ill. El. Forms of Disease_.]

The gangrenous portion of the lung is changed to a dark, dirty, pulpy
mass, sometimes wanting the fetor of gangrene. When the mass has become
diffluent, a sort of cavity is formed, in which are found fetid fluid
and shreds of gangrenous lung-tissue. Around the gangrenous mass there
is a zone of gray hepatized, friable tissue, which in turn is bounded
by a zone of red hepatized tissue. When the above-named zones are not
present in diffused gangrene, the cavities are large, and shreds of
tissue and vascular bands traverse the cavity, which swarms with
bacteria. Such a gangrenous mass may lead to sloughing of the pleuræ.
It has been denied that a croupous pneumonia can terminate in gangrene,
but modern pathologists all support the opposite view. It may be
mentioned that gangrene in croupous pneumonia of the horse is of
frequent occurrence.

5. Chronic (interstitial fibroid) pneumonia may result when the process
of resolution in croupous pneumonia is delayed and the inflammatory
process does not advance beyond the stage of gray hepatization. In such
cases the walls of the alveoli, and finally the inter-alveolar tissue,
become the site of new connective-tissue developments.

The peculiarly hard and oedematous condition that sometimes marks gray
hepatization is, by some observers, regarded as an intermediate stage
between croupous and interstitial pneumonia. An abundant
cell-production in the second or third stage of croupous pneumonia may
be followed by shrivelling of the alveolar contents, and subsequent
cheesy changes may bring about one form of phthisis. Whether this can
ever occur independent of tubercle is still a mooted question. This is
called (by those who believe in such an origin of phthisis) cheesy
infiltration, and is to be differentiated from tubercular infiltration.

In childhood croupous pneumonia is not of so frequent occurrence as
catarrhal. In its anatomical changes it does not differ from croupous
pneumonia in adults. In old age the pneumonic changes usually begin in
the upper lobes of the lung, and extend downward--the reverse of what
occurs in adult life. In the stage of engorgement crepitation is
usually wholly absent, and when the stage of red hepatization is
reached the color is found much darker than in adults, sometimes being
blue or black; the lung is much more strikingly marbled, and on section
the granules, in those cases where they are present, are much larger
than in adult life. Frequently in senile pneumonia the granular look is
absent. Gangrene is a far more frequent termination of croupous
pneumonia in old age than at any other period. The highly-rarefied
condition of the lungs at this period seems to favor the development of
small abscesses.

Croupous pneumonia involves either the whole lobe or a whole lung. Its
most frequent seat is the lower lobe of the right lung. Its next most
frequent seat is the lower lobe of the left lung, then the upper lobe
of the right, the middle lobe of this lung being least frequently
involved. Double pneumonia has been variously estimated as occurring in
from 5 to 50 per cent. of cases, but in all probability the percentage
rarely, even in epidemics, exceeds 12 or 15 (Huss, Grisolle, Barth,
Ziemssen). In old age the difference in point of frequency of attack
between the two sides is very slight, and some affirm that sthenic is
more frequent on the right and typhoid pneumonia on the left side.
Double pneumonia is more frequent in the senile period than during
adult life.

The average duration of the different stages is as follows: The stage
of engorgement lasts from two to three days; the stage of red
hepatization, from three to five days; and the stage of gray
hepatization, from two to six days. In old age the stages rapidly merge
into each other, and suppuration of the {313} lung may occur within
thirty-six or forty-eight hours from the onset of the pneumonia, while
it is not at all infrequent for complete red hepatization to occur
within the first six or eight hours.

The changes in the pleura over a pneumonic lung are quite
characteristic. An uneven, thin, downy-looking layer of plastic lymph
is spread over the pleural surface, which presents a fine arborescent
vascularity. At times this plastic layer may partially conceal the
liver-brown color of the pneumonic lung. As the stage of gray
hepatization is reached, pleuritic adhesions are apt to be formed,
which subsequently undergo absorption, and thus the pleuritic changes
follow, to a certain extent, those which are taking place within the
lung. The cell-elements in this fibrinous meshwork are chiefly pus- and
large endothelial-cells. The pleura itself is opaque, congested, and
ecchymotic, and may be so thickened as to give rise to a dull note on
percussion after the pneumonia has undergone resolution. If there are
adhesions from previous pleurisies, or pleuritic changes that have
occurred prior to the lighting up of a pneumonia, they will modify its
course and termination.

The right heart is dilated, and on inspection immediately after death
it is not unusual to find both ventricles filled with pale, firm clots
that insinuate themselves between the columnæ carneæ and sometimes
extend into the vessels. The pulmonary vessels running to the affected
portion of the lung may be the seat of thrombosis. Pericarditis is so
frequently found at the post-mortem of those who die of pneumonia that
its occurrence must be regarded as something more than either accident
or complication.

The blood is hyperinotic in croupous pneumonia, and, while the amount
of fibrin is only slightly increased at the very onset, the amount
obtainable goes on increasing until the eighth or ninth day; _i.e._ as
the amount of fibrinous exudation within the alveoli augments, so does
the same factor appear in greater quantity in the blood--a circumstance
whose opposite condition we should expect to observe. In infectious
diseases--_e.g._ variola--as the temperature rises the hyperinosis
increases. In pneumonia, however, the pyrexia and fibrin increase in
the blood and bear no relationship to each other. The amount varies
greatly in every case; it has reached 10.5 in 1000.

Around the zone of pneumonic inflammation it is not infrequent to
discover pulmonary oedema; and in many fatal cases extensive oedema
seems to be the direct mode of death.

Temporary compensatory emphysema may occur in the neighborhood of the
inflamed lobe or lobes. It may be mentioned that when emphysema has
previously existed the pulmonic granules observable in the second stage
are of unusually large size.

The bronchial glands are enlarged and congested, and in rare instances
they may suppurate. The lymphatics of the lung are choked with fibrin
and with red and white blood-corpuscles, and the deeper lymphatics
contain products identical with those in the pulmonary alveoli. In both
lymphatic vessels and in the lymph-glands (bronchial) at the root of
the lung there are always well-marked evidences of inflammation.

The liver and spleen are congested, the latter organ especially
presenting the characteristics which are found in it in cases of death
from fevers.

Finally, gastro-intestinal catarrh is occasionally observed, and in
rare cases it is attended by ulceration and hemorrhage. But there seems
no good reason for believing that there is any connection between
pneumonia and these intestinal changes. Indeed, most of the
observations bearing on this point were made during cholera epidemics.
Still, analogous influences might induce both at the same time.

No change in the brain accompanies pneumonia, except congestion. Pus
and inflammatory products when found in the meshes of the pia-mater are
in {314} all probability due to coexisting meningitis or cerebro-spinal
meningitis of an epidemic character.

ETIOLOGY.--The specific cause of croupous pneumonia is as yet
undetermined, and the very existence of such a cause is still a matter
of conjecture.

Among the predisposing causes age ranks first. There are three distinct
periods of life in which the liability to pneumonia is greatest--viz.
in early childhood, between the ages of twenty and forty, and after
sixty.

Notwithstanding the fact that catarrhal pneumonia is a very common
disease in childhood,[9] the statement that croupous pneumonia is rare
at this period cannot be received.[10] From a number of statistical
tables it appears that it is five times more frequent during the first
two years of life than in the succeeding eighteen.[11] It is met with
most frequently between the ages of twenty and forty, and after a lapse
of twenty years the predisposition to it increases, pneumonia being the
most fatal of all acute diseases after the sixtieth year. Nine-tenths
of the deaths from acute diseases after the age of sixty-five are from
pneumonia. Each year after sixty the liability to it is greatly
increased.

[Footnote 9: "Die lobuläre pneumonie ist im Sänglingsalter eine
ausserordenich häufige Krankheit" (Vogel, _Kinderkrankheiten_, p.
222).]

[Footnote 10: "Lobäre pneumonie kommt viel seltener vor" (Vogel, _loc.
cit._).]

[Footnote 11: _Klinik der Kreislaufs u. Athms. org._, Breslau, 1856.]

In early life, in what may be denominated the first period, anterior to
the second year, males and females are very nearly equally affected.
Between twenty and forty, the time when the condition of males and
females is most diverse, the proportion is 3 males to 1 female, or at
least 2 to 1. After sixty, when the hygienic condition of both sexes
again differs very slightly, this proportion is less striking, and the
disease is pretty evenly divided between old men and old women; still,
the male sex always furnishes more cases than the female. When women
work as men do, or when both sexes are huddled together (as in
prisons), then the difference between them is lost.

The puerperal state does not seem to increase the predisposition, but
pneumonia is more apt to occur at the time of the catamenia.

The general condition of the individual at and before the pneumonic
seizure seems to have some predisposing influence, although opinion is
divided as to whether the strong and robust or the feeble and sickly
are the more predisposed to it. Those who are convalescing from acute
and severe illnesses, those who are habitual alcohol-drinkers, and
those who are under the influence of malarial poison are far more
liable to pneumonia than those who are free from such taints.
Enervating habits, poverty, antihygienic surroundings and dyscrasiæ
(especially cancerous), and chronic nervous diseases act as
predisposing causes. Difficult dentition in children seems to act in a
similar manner. Diphtheria, erysipelas, measles, small-pox, and other
acute infectious diseases must be ranked as causes predisposing to
pneumonia.

Chronic and acute uræmia, pyæmia, septicæmia, and all that class of
diseases which depend upon the retention of excrementitious substances
in the blood, are also powerful predisposing causes. It is also of
frequent occurrence in chronic blood diseases, such as chronic
alcoholismus. Suppuration in the abdominal cavity, which opens into the
thorax, may lead to a pneumonia. Long-continued, passive pulmonary
hyperæmia from any cause becomes a predisposing cause to pneumonia. The
pneumonia which frequently occurs during acute articular rheumatism has
been regarded by some as metastatic from the joints; but the more
reasonable explanation is that the blood-changes in rheumatism
predispose to pneumonia.

One attack predisposes to others; as many as twenty-eight attacks have
been noted in the same individual, the time between the attacks and the
{315} number of them being governed by no rule and subject to the
widest variations.

When pneumonia follows a severe blow or injury to the chest or shock
from any traumatic cause, the injury (or the shock) must be regarded as
a predisposing cause. It is noteworthy to observe how often in the aged
fracture of the hip-joint is followed by pneumonia. Within four hours
after this injury croupous pneumonia has been established.

The influence of prolonged exposure to intense cold and sudden chilling
of the surface of the body as a predisposing cause of pneumonia is
still undetermined. Cold does not markedly affect the pneumonia-rate,
except in the very old. Nearly nine-tenths of the cases of senile
pneumonia occur between November and May. The January and February
statistics seldom exhibit the highest pneumonia-rate, as they would
were there any direct relationship between pneumonia and cold. In
elevated regions north-east winds favor the development of pneumonia,
and it is most prevalent in any locality during those periods of the
year when there are the greatest extremes of temperature. A
continuously low or a continuously high temperature has much less
influence in its production than great vicissitudes of temperature. In
New York City early spring and winter seem to be the periods when it is
most prevalent.

A glance at its etiology shows that it is a disease to which all things
predispose that depress the general vitality: this is evidenced by the
fact that children and old people are greatly depressed by the intense
cold of winter and the chilling winds of March and April. Almost
unknown in the polar regions, pneumonia is not an infrequent disease
along the Mediterranean coast; and one peculiarity is to be noted here,
that in cold as well as in warm climates moderate elevation above the
sea-level predisposes to its occurrence.

Rainy seasons or moist districts do not influence the pneumonia-rate to
any appreciable degree. Both these conditions have a direct effect in
increasing the prevalence of bronchial catarrh, but they do not
increase the pneumonia-rate.

The well-established facts that pneumonia occurs oftener among the poor
than the wealthy; in the sailor when on shore oftener than when he is
on shipboard; in soldiers oftener than among civilians at the same
military post,--these are explained on the ground of better hygienic
surroundings, better mode of life, nourishment, etc., of the one class
as compared with the other. And in studying the predisposing causes of
pneumonia one is led more and more to observe that it is the more
liable to occur the less resistance individuals are able to offer to
some (as yet unknown) specific pneumonic influence, and that depressing
influences of whatever kind unquestionably predispose to croupous
pneumonia.

The more dense the population in a district, the greater the
pneumonia-rate. Hirsch says: "The amount of the mean fluctuation in the
mortality from pneumonia is in inverse ratio to the density of the
population." When a city has attained a certain size, wind, weather,
seasons, and races have but a slight influence in varying the
pneumonia-rate. Thus, in New York City from 1840 to 1858 (eighteen
years) the mortality from pneumonia was 5.85 per cent., while from 1859
to 1877, inclusive, it was 6.2 per cent.

Before considering the exciting causes of croupous pneumonia, or their
relation to its predisposing causes, the question meets us, Is croupous
pneumonia an acute specific constitutional (infectious) disease or a
local inflammation?[12]

[Footnote 12: _Virchow's Archiv_, Bd. lxx., Heidenhain.]

That it is not a simple local inflammation appears from the following
facts: the experiments with the inhalation of hot air, moist warm air,
icy-cold air, {316} vapors of various noxious acids and gases;[13] the
tracheal injection of caustic ammonia[14] and mercury; and
traumatism,--have all resulted negatively as exciting causes. And these
experiments have all the more weight since they have been conducted not
only at different times, and in countries distant from each other, but
also because they have been repeated by various pathologists, and
always with a similar result--viz. the development of lobular or
catarrhal, and not of croupous, pneumonia. Section of the vagi
certainly produces hepatization of the lungs, but it is not the
hepatization of croupous pneumonia. Its distinctive microscopical
characteristics are always wanting in the part of the lung consolidated
by such experiments. A strong argument of those who adhere to the local
theory of pneumonia is, that cold occupies a prominent place in its
production. As exposure to cold and to draughts is a common experience,
it is easy to ascribe the origin of any disease to cold.

[Footnote 13: Sityl, _K. K. Akad. zu Wien_, 867, Reitz.]

[Footnote 14: Gendrin, _Hist. Anat. des Inflam._]

"Close rooms and bad air," says Squire, "more predispose than does
outdoor exposure, unless that be prolonged or the individual resistance
weakened by fatigue or intemperance." Both wet and cold invariably
heighten the bronchitis-rate and exacerbate catarrhal processes, but
neither of these can be proven to influence the pneumonia-rate.
Statistics show that croupous pneumonia is more prevalent in our
Southern States than in our Northern States. The epidemics in the West
Indies are as well known as, and have been more devastating than, those
in Iceland and in the Norse countries. The prevalence of pneumonia in
this continent progressively increases from the pole to the equator.

Hirsch's statistics and statement, that "the amount of the mean
fluctuation in the mortality from pneumonia is in inverse ratio to the
density of the population," is a strong argument in favor of the view
that croupous pneumonia is due to some specific pneumonic infection,
for all acute general diseases increase where there is over-crowding.

It is often stated that pneumonia is a far more frequent disease now
than it was twenty years ago. That I might arrive at something definite
on this point, I have carefully examined the death-reports of England
from 1840, also those of New York City, dividing them into two periods
of eighteen years each; and I find that the average mortality from
pneumonia in England from 1840 to 1858 was 5.57 per cent.; from 1859 to
1877, 4.77 per cent., an actual decrease of 14.3 per cent. In New York
City from 1840 to 1858 the average ratio of mortality from pneumonia to
all other diseases was 5.85 per cent., and from 1859 to 1877 it was
6.20 per cent., showing an increase in New York of 15.2 per cent. Thus
it is shown that while in England pneumonia is on the decrease, in New
York City it is on the increase.

Those who advocate cold as a cause of pneumonia base their argument on
the seasons of the year when it is most prevalent. The winter and
spring are pre-eminently the seasons of pneumonia, but cerebro-spinal
meningitis, diphtheria, influenza, measles, and other diseases of
similar general character occur with greatest frequency in the winter
months, yet it is not now claimed that cold causes them. While it is
not to be denied that cold is to a limited extent an exciting cause of
pneumonia, the belief that it is the primary or principal cause must be
held in abeyance if not altogether rejected. Again, the symptomatology
of pneumonia seems to militate against its being a local disorder.

There is no relationship between the amount of lung-tissue involved and
the intensity of the symptoms; high fever, delirium or convulsions, and
rapid heart-failure are often as well marked when a post-mortem reveals
only one lobe to be involved as when a double pneumonia exists. "The
local inflammation in its gradual extension and composite character
offers no sort of {317} parallelism to the fever which for a while
accompanies it." In local phlegmasiæ there is a direct ratio between
the amount of surface involved and the attendant constitutional
disturbances.

Rarely does a second chill occur when there is an extension of the
pneumonic process. "Small consolidations with high fever and severe
constitutional symptoms, and extensive infiltrations with a
comparatively slight fever and general disturbance, are the rule and
not the exception."[15]

[Footnote 15: _Ziemssen's Cyclop. Prac. Med._, vol. v. p. 146.]

The absence of regular and constant prodromata, the absence of a known
period of incubation, of a typical temperature-range, and of
characteristic surface phenomena, and the fact that it is not
contagious,--these must not be overlooked when we are tempted to regard
croupous pneumonia as an acute infectious disease.

The points of resemblance between croupous pneumonia and the acute
general diseases are the following: It has an initiatory chill, an
orderly pyrexia, and a somewhat typical course, inasmuch as there are
in many cases a day of abrupt crisis and a definite duration. The
symptoms follow in regular sequence.

There is a peculiar countenance, and here we note a resemblance to
typhus and typhoid; there are usually herpetic eruptions; the kidneys
are not infrequently the seat of a nephritis; and catarrhal pyelitis is
a common condition. The cerebral symptoms greatly resemble the
condition that accompanies the exanthems. The peculiarity of its
commencement in the very young and old--convulsions in the former and
coma and collapse in the latter--serves to point to an alliance with
those diseases where a specific morbific agent acts primarily and
principally on the nervous system. Etiologically, it often arises under
precisely similar circumstances as those which give origin to
cerebro-spinal meningitis and diphtheria, to both of which diseases it
is also allied, since the pathological changes are distinct from those
of any other inflammation.

Again, the influence of septic, miasmatic, and atmospheric conditions
is certainly almost universally acknowledged. A good example of this is
the sewer-gas pneumonia so often occurring in New York City, and of
which frequent mention is made by English writers. Again, there have
been frequent epidemics of pneumonia in certain districts in garrisons
and on board ship, where over-crowding, bad ventilation, and general
antihygienic surroundings prevailed.[16]

[Footnote 16: In the _U. S. Sanitary Commission Memoirs_, Russel
reports: "The surgeons on duty with the regiments in the barracks
(Benton, Mo., 1864) report that men occupying the same bunks with those
affected were very much more liable to be attacked than those more
remote. Some of the most intelligent surgeons were led to believe that
the disease was actually contagious."]

During the winter of 1881-82 I remember three instances where two
individuals in the same house were simultaneously attacked with
croupous pneumonia.

Pythogenic pneumonia is a form which arises under miasmatic influences,
and is contagious.[17]

[Footnote 17: _Dub. Med. Journal_, 1874, vol. i., Grimshaw and Moore.]

"The epidemic form of croupous pneumonia at certain times bears the
distinct characteristics of a specific infectious disease."[18]
Miasmatic and zymotic pneumonia are names which have also been given to
this form; and indeed it is now generally acknowledged that croupous
pneumonia does occur as an epidemic disease when it is, seemingly,
dependent upon a specific contagion. Huss thinks that during a typhus
epidemic pneumonia is apt to assume the low typhoid form.

[Footnote 18: _Berliner klinische Wochensch._, 1879, No. 37, A. Kühn.]

Moreover, as in typhoid and cerebro-spinal meningitis, so in pneumonia,
we {318} have abortive cases, and forms which are distinguished by the
names sthenic, asthenic, malignant typhoid, icteric, etc. Still, a
pneumonia epidemic is different from a typhoid or cholera epidemic: it
does not sweep over large districts and affect all ages and classes
indiscriminately.

Every acute general disease has its complications, and the occurrence
in pneumonia of peri- and endocarditis, as well as its cerebral and
renal complications, allies it to other acute general diseases.

Cerebro-spinal fever has its characteristic lesion in the membranes at
the base of the brain and about the cord; typhoid fever, in the
lymph-structures of the intestinal tract; diphtheria commences in and
chiefly involves the epithelia; and pneumonia has its characteristic
local lesions in the vesicular structure of the lungs. Croupous
pneumonia is occasionally met with in intrauterine life, and it is to
be remembered that acute general diseases occur far oftener in the
foetus than local inflammations. Again, the accepted treatment of
pneumonia at the present day is an indication of its specific
character. Thus the weight of evidence leads to the opinion that
pneumonia is an acute specific general disease caused by a specific
poison. The nature and action of the pneumonia-poison may be indicated
by the following facts and experiments: Hyperinosis does not seem
capable of causing croupous pneumonia; the fibrin increases as the
consolidation is completed, and does not antedate either the pyrexia or
the hepatization. Excessive bleeding increases the amount of fibrin
obtainable from the blood; and when, in pneumonia, we find one lung
weighing three pounds more than the other, may not the blood-elements
effused into the alveoli have much to do with the hyperinosis?

Pneumonia resembles quinsy[19] in its pyrexia, temperature-curves,
duration, its constitutional as compared with its local symptoms, and
its rapid and abrupt decline. Both have a similar herpetic eruption,
and in both the amount of chlorides in the urine is subnormal, the urea
(in both) being increased.

[Footnote 19: Sturges, _Pneumonia_, _loc. cit._]

An analogy has been noted by some observers between pneumonia and acute
rheumatism. Trousseau sees an analogy between erysipelas and
pneumonia.[20] But apart from their etiology it is difficult to
recognize any constant resemblances between them. Sturges places
"pneumonia in a middle place between the specific fevers, so called,
and the local inflammations," and adds that it has something in common
with both. Cohnheim classes croupous pneumonia among the miasmatic
contagious diseases.

[Footnote 20: _Clinical Lectures_, vol. iii. p. 353.]

The idea of its being a specific disease dates from the latter part of
the eighteenth century:[21] it is not by any means a modern thought,
although it has within the last ten years received a new impulse and
given rise to extended discussions.

[Footnote 21: C. Strackius in _Nov. Theo. Morg._, 1786.]

It seems to me that the resemblance of pneumonia to the acute general
diseases is to be found for the most part in its nervous phenomena, and
that the complications which render pneumonia dangerous are those which
interfere directly with the muscular power of the heart or diminish its
nerve-supply.

In order that the influence exerted by an abnormal nerve-supply upon
the contractility of the cardiac muscles may be more apparent, let us
glance at a few modern physiological facts. When the inhibitory nerve
of the heart, the pneumogastric, is cut, the heart beats wildly. When
the peripheral cut end is stimulated, the heart stops in diastole. But
neither of these phenomena instantly follows the operations, on account
of the intervening cardiac ganglia, the part of the vaso-motor system
which has its centre in the medulla oblongata. Afferent inhibitory
filaments (the depressor branch) of the vaso-motor centre are also in
the vagus. Now, by injecting atropine into the blood we so influence
these cardiac ganglia (which intervene between the conditions of the
vagus and the resulting action upon the heart-beat) that the inhibitory
{319} action is entirely checked. Thus an intimate connection is
apparent between the local heart-mechanisms, the general vaso-motor
system, and some filaments of the vagus. Again, we know that the
natural explosive decompositions of the nerve-cells of the respiratory
centre may be either augmented or enfeebled according to the condition
of the blood supplying this ganglion. Now divide the cervical portion
of the pneumogastric, and there results, after a more or less prolonged
period, an extensive pulmonary consolidation (hepatization), which is
not accompanied by the least sign of heart-failure. It is to be
remembered that such pulmonary consolidation has none of the essential
pathological characteristics of croupous pneumonia.[22]

[Footnote 22: Michael Foster, Wagner, Goetz, Heidenhain, Du
Bois-Reymond, Ludwig, and Pflüger.]

From these experiments the following deductions seem at least
reasonable: The tonic influence normally held by the vaso-motor system
of nerves over the vascular system is either lessened or destroyed by
an altered blood-state or by some morbific agent in the blood
introduced from without. The large quantity of blood which would then
be retained in the arterioles throughout the body, and which could not
be returned to the heart, may cause so great a diminution in the
blood-pressure as in itself to cause heart-failure. But in addition,
and in connection with this, may not the action of a morbific material
in the blood upon the intrinsic cardiac ganglia so interfere with their
function, or so act upon the medullary vaso-motor centre itself, that
the movements of the heart are deranged and its power is more or less
diminished?

It would seem that this materies morbi in the blood may as well act
upon both the medullary centre of the vaso-motor system and the ganglia
in the wall of the heart as upon either alone. The phenomena of
asphyxia are brought about by influences acting solely on the medullary
centre. Again, the large amount of urea excreted, the result of
excessive tissue-change throughout the body, may also be due to
deranged nerve-function.

Klebs[23] even claims that he has found the infectious agent--a monas
pulmonale--which can be inoculated, with the result of developing
croupous pneumonia. This has been credited so far as to lead to the
subcutaneous injection of carbolic acid to destroy the pneumonic germ.
Incidentally, it may be remarked that it has been shown that the
contagion of the pleuro-pneumonia of cattle, according to Parkes, "has
been found in the pus- and epithelium-cells of the sputa." The true
nature of the pneumonia poison, if one exists, is as little determined
as that of the other acute contagious general diseases. But, whatever
its nature may be, its primary action seems to be on the nerve-centres.

[Footnote 23: _Arch. für exper. Path. u. Pharm._, vol. iv., 1875.]

SYMPTOMS.--The symptoms of croupous pneumonia may be considered under
two heads--Subjective, or rational symptoms; and Objective, or physical
signs.

Subjective Symptoms.--In only a small proportion of cases are there
prodromata. Grisolle found that prodromata occurred in 50 out of 205
adult cases, or in about 25 per cent.; and Fox says that he finds the
proportion to be about 28 per cent. In old age they seem to be more
frequent, the proportion being about 60 per cent.[24]

[Footnote 24: Durand-Fardel, _Mal. des Viellards_.]

There may be for a day or two, or even for a week, preceding a
pneumonic seizure a feeling of general malaise, accompanied by
anorexia, headache, dull pains in the limbs, back, and lumbar region,
vertigo, epistaxis, or slight diarrhoea. Sometimes the skin assumes a
slightly jaundiced hue, and there may be flashes of heat accompanied
by, or alternating with, slight rigors. Flying pains in the limbs and
chest and epistaxis are common in senile croupous pneumonia. When
prodromes have existed more than three or four days, they will be vague
and undefined.

{320} Rise in temperature as a prodrome is by some thought to be caused
by a deep-seated and undiscoverable hepatization. But let us take one
example from many in support of a contrary view--viz. the case of an
inmate of Bellevue Hospital during the winter of 1880-81. For three
days preceding the first appearance of consolidation the temperature
ranged at 102° and 103° F. During this time there were several slight
rigors followed by flashes of heat.

Wilson Fox[25] states that he knows of but one case--the one referred
to by Monthus in his _Essai sur la Pneumonie double_.

[Footnote 25: _Reynolds's System_, art. "Pneumonia."]

In epidemics febrile symptoms and diarrhoea often precede for some two
or three days the first sign of consolidation.[26]

[Footnote 26: _The Lancet_, vol. ii., 1878, p. 701, Couldrey.]

In the great majority of cases croupous pneumonia is ushered in by a
distinct chill. Huss and Grisolle found a chill in 80 per cent. of
their cases; Fismer and Louis in about 77 per cent. of theirs; and
Lebert in over 92 per cent. of his. In 84 out of 100 cases admitted to
my ward in Bellevue Hospital, a distinct chill marked the invasion of
the disease.

Generally, the patient retires in his usual health, to be seized with a
severe chill during the night. The chill lasts from half an hour to two
or three hours. Its abruptness and severity are almost characteristic
of the pneumonia.

In children, headache, nausea, vomiting, delirium, and convulsions may
take the place of the chill; its onset then closely resembles that of
the exanthemata, indicating the action of some irritating poison upon
the nerve-centres. When these symptoms are not present there will be
more or less anorexia, thirst, and a tendency to stupor. The child will
awake in the middle of the night with a burning skin, a bounding pulse,
flushed face, and hacking cough. When there are convulsions, followed
by a loss of consciousness, the pneumonia is usually at the apex of the
lung.[27]

[Footnote 27: Rilliet and Barthez.]

If an old person is seized with a severe chill during the night, it is
almost a certain indication that pneumonia is developing. Although the
chill of invasion is of less frequent occurrence, it is more
significant than in adult life. A protracted fit of shivering and pain
in the side are the two diagnostic symptoms of acute sthenic senile
pneumonia. They occur in about 50 per cent. of all cases, and from
statistics taken from the Salpêtrière it seems that in March and April
these two symptoms are almost always present.

In the other half of the cases of senile pneumonia the onset is marked
by a frequent, irregular respiration, slight rise in temperature, short
hacking cough, and signs of great exhaustion. Nausea, vomiting,
diarrhoea, and collapse or a semi-comatose condition may usher in a
senile croupous pneumonia.

Durand and Fardel give the following statistics of the mode of advent
in 35 cases of senile pneumonia: 7 began with distinct rigors; 8 with
rigors and pain in the side; 6 with rigors and vomiting; 8 with pain in
side alone; and 6 with vomiting only. When a chill is the initial
symptom, either in childhood, adult life, or at the senile period, it
is rarely repeated.

In adults, following the chill there is usually pain underneath the
nipple of the affected side; sometimes the earliest symptoms following
the chill are headache, vomiting, and diarrhoea, dyspnoea, a hacking
cough, and pain that simulates that of lumbago. Within twenty-four
hours after the invasion the aspect of the patient becomes
characteristic: there is a rapid rise in temperature, attended with
great prostration; the pain in the side is aggravated by coughing and
deep inspirations; and the respiratory movements are accelerated. The
countenance assumes a dull or anxious expression, with a tendency to
lividity; the pulse is accelerated, full, and soft; there is complete
anorexia and great thirst; speech is difficult, and often there is
great restlessness. The urine becomes scanty and high-colored, the
bowels are constipated, and the tongue is dry and covered with a white
coating.

{321} These symptoms either increase in severity or are attended by
exacerbations and remissions until the day of crisis, which usually
occurs between the third and the ninth day; when, if recovery is to
take place, there is a sudden remission of all the pneumonic symptoms;
the temperature falls abruptly; the surface becomes moist; the flush of
the countenance disappears; the pulse and respiration become normal;
and the patient rapidly passes on to complete convalescence.

In some cases the decline in the symptoms is gradual and the disease
terminates by lysis and not by crisis. In unfavorable cases signs of
heart-failure appear within the first few days, and the patient sinks
rapidly into collapse and dies.

With this brief outline of the disease I will pass to an analysis of
its prominent symptoms.

Respiration.--The respirations are more constantly increased in
frequency in croupous pneumonia than in any other acute disease. In
most febrile diseases the respirations increase in frequency with the
pulse-rate. In pneumonia there is no uniform ratio between pulse and
respiration; this is regarded by some as an important diagnostic
sign.[28] In some cases the respirations will be 80, and the pulse only
90, per minute. The acceleration in the respiration is not in
proportion to the amount of lung-tissue involved, but seems to be due
to a peculiar condition of the nervous system which existed prior to
the pneumonic seizure or is caused by a poison acting upon the
nerve-centres. Traube[29] thinks that it is due to the pain and to the
high temperature. This theory would not explain its occurrence in those
cases where the pleura is not involved--_i.e._ when no pain is
present--and yet the shallow, panting, rapid breathing is well marked.

[Footnote 28: _Dis. of Lungs_, Walshe, 1860, p. 366.]

[Footnote 29: _Annal. de Charité_]

In other pulmonary diseases, when there is high temperature, as in
acute phthisis, the respirations are not so much accelerated as in
pneumonia. The character of the respiratory acts is also peculiar: they
resemble the panting of a dog. Accelerated breathing may or may not be
accompanied by dyspnoea; in many cases the dyspnoea seems to be
independent of it, for extreme dyspnoea is often present where the
respirations are but slightly increased in frequency.

In children the acceleration of respiration is more marked than in
adults, and the ascent of the chest occurs during expiration, and not,
as normally, with the inspiration. The diaphragm is markedly contracted
with each expiratory act, and the diagnosis will as often be made by
the character of the respiration as by the physical exploration of the
chest, for in children the early physical signs of pneumonia are often
unsatisfactory.

The hurried breathing prevents a young child from nursing; it takes the
mother's nipple for an instant, nurses greedily, and then drops back,
gasping for breath.

It is to be remembered that in pneumonia in children the pulse and
respiration discrepancy will not be so well marked as in adults: the
pulse may be 150 to 160 per minute, while the respirations are 80 or
90. In children there will early be noticed the peculiar expansion of
the nostrils which comes on late in adults. In senile pneumonia the
chest enlarges vertically during inspiration. The whole act has a
panting character, and the expiration is prolonged.

In perfectly healthy old people the inspiratory movements are jerky in
character. The lungs become fully expanded only after a succession of
interrupted efforts. An exaggeration of what is physiological in old
age--_i.e._ catchy breathing--is the most frequent form of abnormal
respiration in senile pneumonia.

Dyspnoea, although frequently accompanying accelerated respiration, is
by {322} no means a constant attendant of it. When urgent it is not in
proportion to the amount of lung involved, since double pneumonia may
be accompanied by less dyspnoea than when but one lobe is involved. It
can be due only in small degree either to the diminution in the total
breathing capacity, to the pain, or to the rapid and destructive
tissue-metamorphosis; for on the day of crisis it ceases, although the
lung at this time is not relieved of its obstructive exudation. The
most intense dyspnoea usually occurs in those cases where there is
extensive nervous prostration, and must always be regarded as a symptom
of great gravity.

In secondary pneumonias, especially where there is coexistent disease
in any part of the respiratory tract, the dyspnoea is usually more
marked than in primary and uncomplicated pneumonia. It differs from the
labored dyspnoea of general capillary bronchitis. A diagnosis between
these two diseases can often be made by the character of the dyspnoea.

When the summit of the lung is involved, the dyspnoea is always greater
than when the pneumonia is at the base. In pneumonia of the apex in
children the dyspnoea is so great that the nostrils are widely dilated,
the mouth is open, and its corners are drawn downward and outward. In
senile pneumonia, even when the respirations are 70 per minute,
patients do not complain of difficulty in breathing.

When persons over seventy who have been asthmatic or are the subjects
of chronic bronchitis develop a pneumonia, they often suffer less from
dyspnoea than before the pneumonic attack. They feel exhausted, are
unable to move about, and on lying down to rest often suddenly expire.

Immediately after the initial chill pain is present in over 85 per
cent. of the cases. It is of a sharp stabbing character, and is usually
located over the seat of the pneumonia; it is intensified by coughing,
sneezing, and deep inspirations. In some cases there is tenderness on
pressure over the seat of the pain. The pain usually disappears after
the third or fourth day of the disease; if it continues until the
eighth day, it may be regarded as evidence of pleuro-pneumonia. If the
pneumonia is central there will be no pain. In old age, even in a
pleuro-pneumonia, pain is never severe. It is rather a dull, uneasy
sensation referred to the whole chest, or if localized by the aged
patient is referred to the pit of the stomach, the nipple, the loins,
the hypochondrium, or even to the side opposite to the one involved.

Cough is generally present within twenty-four hours after the accession
of croupous pneumonia. At first it is short, ringing, or hacking in
character, and increases the pain in the side. It sometimes entirely
ceases just before a fatal termination. In children a hacking cough is
more constant than in adults. Within a few hours it becomes painful and
urgent, and occasionally assumes a paroxysmal character, resembling
whooping cough.

Old people with pneumonia often have no cough. When present it is
slight, and may escape the notice of the patient as well as of the
physician. When an aged person suffering from chronic bronchitis or
asthma, who has had a chronic cough, develops a pneumonia, the cough
generally becomes less severe, and may entirely cease.

Expectoration.--The sputum in pneumonia is characteristic. During the
first forty-eight hours it is simply frothy mucus; then it becomes
semi-transparent, viscid, gelatinous, and tenacious, but never opaque.
Streaks of blood often appear early, mixed with the sputa. So tenacious
is it that the cup which contains it may be inverted without spilling
the mass. It can be drawn out between the thumb and finger into thin
strings, and its tenacity undoubtedly is one cause of the difficulty in
its expectoration. Its color varies: generally on the second day the
brick-dust or rusty sputa are observed; still, there are numerous
exceptions. The color is due to admixture of blood which extravasates
from the capillaries of the alveoli. The rusty sputa are preceded {323}
in some cases by a transient brighter red expectoration. In other cases
it is of a creamy-yellow color, resembling in this respect ordinary
catarrhal sputa; or, again, it becomes dark and of a prune-juice color.
A severe pneumonia may have none other than a purulent sputum.

Prune-juice sputa of an offensive odor are indicative of a depraved
state, and occur only in grave forms of pneumonia. In alcoholismus and
in those markedly septic forms of pneumonia which are to end fatally,
the prune-juice or burnt-sienna sputum is usually present. In some
instances prune-juice sputa appear before the physical evidences of
hepatization.

A watery and blood-stained expectoration indicates pulmonary oedema and
congestion, and is an unfavorable symptom. When a case is tending to a
fatal termination, the sputa become scanty, less tenacious, more
diffluent, and often of a greenish color. But a greenish color may be
present during the stage of resolution, and may temporarily occur in
the middle period of a pneumonia, without being indicative of serious
changes. It is usually present in the so-called bilious pneumonia when
there is jaundice.

Pre-existing or complicating lung diseases may mask or alter the
ordinary rusty pneumonic sputa. On the day of crisis, when resolution
occurs, the sputa usually become abundant and of a creamy-yellow color.
But purulent creamy sputa may occur with a complicating abscess and in
some cases of purulent infiltration. During the whole course of the
disease there may not be a single characteristic sputum, or it may not
be present until the fifth, sixth, or even the twelfth day of the
pneumonia. Again, the sputa may continue of a brick-dust hue until the
ninth or tenth day. There is frequently an entire absence of
expectoration in the pneumonia of acute articular rheumatism and in
pneumonia of the apex.

Lastly, the sputa may be more or less pigmented, or when venesection or
purgation has been extensively practised expectoration may suddenly
cease.

In children expectoration is rarely present, but the brick-dust masses
may often be detected in the ejected matter after an attack of
vomiting. In senile pneumonia expectoration is never an early symptom,
and it is liable during any period of the disease to suddenly cease.
Rusty sputa occur in only about 33 per cent. of senile pneumonias. They
are at first scanty, gray, and frothy, then yellow or catarrhal (sputa
cocta). In severe and fatal cases profuse bloody expectoration may be
present at the onset. The reason why the viscid (pathognomonic) sputum