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.