Chapter XXI: Part 21

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 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.

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.

Just before the final fall the fever may be greater than at any time preceding.[34] When the decline in temperature is gradual (lysis), the normal temperature is usually reached by the ninth day, but it may be delayed until the twelfth or fourteenth day. A very slow or protracted lowering of the temperature is attended by a coincident slow disappearance of the physical signs of consolidation. There is no explanation for this, except that it is met with oftenest in the weak, debilitated, and dissipated where venesection has been practised or a depressing plan of treatment has been resorted to.

[Footnote 34: See Fig. 33, where a temperature of nearly 105° F. is followed on the evening of the fifth day by the final fall.]

A high temperature persisting after the tenth day indicates purulent infiltration (see Fig. 38).

Pneumonia involving the apex of the lung is usually marked by a higher average range of temperature than when it is confined to the lower lobes. Statistics show that the fifth and seventh days are the days of crisis in the majority of uncomplicated pneumonias. Of 867 cases terminating by crisis, in 677 the crisis occurred before the eighth day. Neither the height of the temperature-range nor the amount of lung involved affects the critical day.

In the form of pneumonia sometimes called bilious--a form that prevails in miasmatic regions--the temperature is markedly paroxysmal.