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
of pneumonia is so often absent in senile pneumonia is that the stages
pass rapidly into each other, and purulent infiltration takes place
very early. The day of crisis is not marked by the same changes in the
expectoration that mark the crisis in pneumonia of adult life.
A chocolate-looking serous expectoration usually accompanies the
so-called typhoid pneumonia.
When examined under the microscope, the sputum is found to contain
swollen epithelia, both spheroidal and columnar, red and white
blood-globules, minute spherules of fat, and the other elements which
were described as filling the alveoli during the stage of red
hepatization. (See Morbid Anatomy.)
Walshe affirms that pus-cells are not found in the brick-dust
expectoration of pneumonia. The mucoid cells will often be stained by
the liberated coloring matter of the blood, and pigment-granules may be
found mingled with the granular débris of its resolving stage. In about
75 per cent. of the cases there will be found in the sputa, when
floated in water, casts of the alveoli and bronchioles.[30]
[Footnote 30: _Diagnost. u. Pathognos. Untersuch._, 1845, Remak.]
The chemical constituents of the sputa are albumen, mucus, and mucin.
Different observers have found the sputa to contain tyrosin and sugar.
There are two explanations of the acid reaction of pneumonic sputa.[31]
{324} Verdeil thought it due to the excess of pneumic acid in the
inflamed lung. Bamberger claims that it is due to the deficiency in
alkaline phosphates.[32]
[Footnote 31: _Gaz. méd._, 1851, p. 777, Robin et Verdeil; _Chem. Anat.
Phys._, vol. ii. p. 460 _et seq._]
[Footnote 32: _Wurtzburg Med. Zeitschr._, ii., No. 506.]
It may be noticed that the following differences exist between
pneumonic and catarrhal sputa: catarrhal sputa contain 10 to 14 per
cent. of alkaline earths; pneumonic sputa contain no alkaline
phosphates. In catarrh the ratio of the soda to the potash is 31 to 20;
in pneumonia the ratio is 15 to 41. There is 3 per cent. of sulphuric
acid in catarrhal and 8 per cent. in pneumonic sputa.
Early in pneumonia there is an increase of the fixed salts, notably
chloride of sodium, in the serum of the blood. It has been thought that
from the rapid and excessive cell-transformation in the lung the
chloride of sodium is attracted to that organ. In one case where no
sodium chloride was found in the urine 10 per cent. of the solid
material of the sputa consisted of that salt. Still, the presence of it
in the sputa and blood, and its absence from the urine, are facts that
still need elucidation.[33]
[Footnote 33: Beale gives the following analytical table of a case of
acute pneumonia:
Chloride of Sodium. Per cent. of Solids.
Urine 0.
Blood from heart 0.68
Hepatized lung 2.59
Healthy lung 1.43]
The expired air in croupous pneumonia is colder than normal, and, as in
many acute general diseases, there is a diminution in the amount of
carbonic acid excreted.
Temperature.--The temperature-range of a typical case of croupous
pneumonia shows it to belong to the remittent or subremittent type of
diseases rather than to the class of febrile disorders marked by a
continuous pyrexia. In rare instances it is intermittent.
As in most acute general diseases which are ushered in by a distinct
chill, the temperature rises rapidly during the chill. In two or three
hours after the chill it may range from 102° to 105° F. After
twenty-four hours it is subject to evening exacerbations and morning
remissions, but the morning temperature is rarely more than 2° F. lower
than the evening. Indeed, the difference in the subremittent type may
amount to only ½° F., and in the remittent type to only 1° F. At
midnight a second exacerbation may occur, but not so marked as that
occurring early in the evening. Occasionally the remissions occur in
the evening and the exacerbations in the morning.
[Illustration: FIG. 33. A Typical Case of Lobar Pneumonia in the Adult:
Recovery by Crisis.]
The temperature is usually highest on the evening of the third day. In
some cases the maximum range may not be reached until a few hours
before the crisis, on the fifth or sixth day. {325} In fatal cases,
just preceding death, the temperature may reach 107° or even 109° F.
An (average) typical temperature-curve is shown on the preceding page
(Fig. 33).
If after the fourth day of a pneumonia an unusual remission is followed
by a high temperature-range, either an extension of the pneumonia or
the occurrence of some active complication is indicated. If in an
otherwise mild pneumonia the temperature suddenly rises to a high
point, a grave complication is indicated. The sudden fall of
temperature on the fifth or sixth day indicates a crisis and the
beginning of convalescence; it may occur in the morning or after the
evening exacerbation.
In a typical case it is usual to find the temperature on the morning of
the fifth, sixth, or seventh day two or more degrees lower than on the
preceding night, and subsequently it falls until a normal, or not
infrequently a subnormal, temperature is reached. The crisis may occur
by successive and increasing remissions, while the exacerbating
temperature remains constant (Fig. 34); and indeed it is common for the
remissions to be excessive immediately preceding the crisis.