CROUPOUS PNEUMONIA.
BY ALFRED L. LOOMIS, M.D.
SYNONYMS.—English and American: Acute sthenic exudative pneumonia; Primary lobar pneumonia; Vera peripneumonia; and Pneumonitis. Fr. Fluxion du poitine and Fièvre pneumonique; Ger. Pneumonia lobaris and Lobäre Lungenentzündung.
DEFINITION.—Croupous pneumonia is an acute general disease with a characteristic local pulmonary lesion. Anatomically considered, it is an acute inflammation of the vesicular structure of the lungs, resulting in infiltration of the alveoli, with inflammatory products, which renders them impervious to air. This condition is known as hepatization.
HISTORY.—Until the time of Laennec, pneumonia and pleurisy were described as one disease. Hippocrates said that pleurisy was "a disease quickly fatal, and characterized by sputa of various colors." Although these two diseases were undifferentiated, accurate descriptions of the lesions and objective signs of pneumonia have come to us from the earliest medical writers.1
1 Thucydides, The Plague at Athens, B.C. 430.
Much of the early history of this disease is interwoven with the detailed accounts of a great variety of pulmonary symptoms which occurred in the epidemics and plagues which prevailed in Eastern Europe in the centuries just preceding the Christian era, and in Western and Southern Europe during the sixteenth and seventeenth centuries. The black death has been regarded by some as an epidemic of pneumonia. While it is probable that in most of these epidemics the lung was early involved, and that its implication hastened death, yet no proof exists to sustain the belief that they were other than epidemics of typhus fever, dysentery, and those (as yet unknown) fevers which collectively were named plagues. That many of these plagues were complicated by pneumonia there is scarcely room for doubt.
French investigators were the first to separate the pneumonic process from all other morbid processes which occur in the thoracic organs. Valsalva, Morgagni, and Boerhaave gave accurate descriptions of pneumonia, but they did not sharply distinguish it from pleurisy. Bichat and Pinel separated collapse of the lung attending pleuritic effusion from inflammation of the lung-substance.2 Laennec was the first to draw the line sharply between pneumonia and pleurisy, and to him, more than to any other observer, is due the credit of describing pneumonia as a distinct disease. With his labors begins a new era in the history of pulmonary inflammations.
2 Nos. phil., ii., Pinel.
Grisolle's work3 is especially valuable in statistics relating to the climatic element in the development of pneumonia and its comparative frequency among different races. The elaborate treatise on the geographical distribution of pneumonia by Ziemssen has furnished data for a more accurate knowledge of its geographical boundaries. Following in the footsteps of Laennec, Chomel, Stokes, Addison, and many laborers of our own day have furnished the material from which the clinical and pathological history of pneumonia is now being constructed.
3 Traité de la Pneumonie.
Recently, Jürgensen has strongly advocated the infection theory of pneumonia, and has presented strong arguments in support of his opinions. Sturges of London and Cohnheim4 advocate the use of the term pneumonic fever, and the former gives a most interesting general comparison between it and the affections which he regards analogous to it. Careful pathological experiments have recently been made by Heidenhain, Sommerbrodt, Schuppel, and Klebs5 with a view to establish the germ-theory of pneumonia.
4 Leçons de Chir. méd., 1877, p. 17.
5 Arch. für experiment. Pathol., p. 420.
The literature of the past ten years is richer in the development of facts and experimental investigations than all the centuries that have preceded; and these recent experiments, combined with modern statistics and the results of the microscope in pathological histology, have given to croupous pneumonia a separate and distinct place in the list of pulmonary diseases.
MORBID ANATOMY.—Anatomically as well as clinically, there are three recognized stages in croupous pneumonia: 1, Stage of engorgement or congestion; 2, Stage of red hepatization; 3, Stage of gray hepatization, resolution, or purulent infiltration (suppuration).
It has been claimed that the stage of engorgement is preceded by a dry stage, or "stage of arterial injection," in which the lung-tissue is dry and of a bright-red color. It is evident that congestion of the minute branches of the pulmonary artery would not give to the lung-tissue a bright-red color, and if such a condition exists it must be due to injection of the bronchial vessels. It is by no means proven that such injection ever precedes pneumonic engorgement. In the stage of engorgement that portion of the lung which is involved in the pneumonic process does not collapse when the thoracic cavity is opened. The affected portion of lung is distended and firmer than normal lung-tissue, and when pressed upon crepitates less, often remaining indented after the pressure is removed. The lung is not entirely airless, for by pressure the air can be forced from one portion of it to another. Its color is darker than normal, usually being of a brownish-red or purple. There is an increase not only in its actual weight, but in its specific gravity. On section a thin, frothy, blood-stained serum exudes, and sometimes on pressure flows freely from the cut surface; occasionally this exudation is tenacious. When alcohol is added to this fluid, it coagulates into a granular, amorphous mass.
The capillaries around the air-cells are distended, and dark blood oozes from their divided ends. Occasionally, upon close examination, there may be seen beneath the pleura and between the air-sacs small points of blood-extravasation. A portion of lung in this stage, when placed in water, does not float as near the surface as healthy lung-tissue.
When examined with the microscope, the lumen of the alveoli are seen to be diminished by the encroachment of the varicosed and tortuous capillary vessels. As a rule, the air-sacs are uniformly dilated; some, however, may be collapsed—a condition probably due to pressure during the early period of the pneumonic process. The epithelia of the alveoli are swollen, and contain a granular protoplasm with free nuclei. The air-vesicles also contain exfoliated epithelial cells and white and red blood-corpuscles. The serum which escapes into the alveoli from the distended capillary vessels is the fluid in which these cell-elements float. Since the enlarged epithelia often suffer a division of their protoplasm, embryonic mono-nucleated cells are intermingled with the other elements. It is still a disputed question whether the bronchial or the pulmonary capillaries are the chief source of the pneumonic exudation.
Physiology teaches that lung-tissue is nourished by the blood in the ramifications of the bronchial arteries, and that the pulmonary capillaries are the passive media for the interchange of gases. Hence it is claimed that the bronchial capillaries only are implicated in the inflammatory process. Virchow has shown that the pneumonic process can be completely established in places where pulmonic capillaries cannot be traced on account of the plugging of a large branch of the pulmonary artery;6 yet even he admits that secondarily the pulmonary vessels have much to do in the inflammatory process.
6 Ges. Abhang., p. 369, Virchow.
On the other hand, it is claimed that in the early stages of the pneumonic process the parts that are supplied by the bronchial capillaries are not reddened or injected, as they would be were these vessels primarily concerned in the inflammatory process. Reasoning from the above, it would seem that both sets of vessels are involved, but that usually one set is implicated at the very commencement to a greater extent than the other.
It is often difficult, and sometimes impossible, to differentiate between the anatomical appearances produced by pulmonary congestion and oedema and the first stage of pneumonia. In pulmonary congestion and oedema the fluid in the alveoli is serum, and contains none of the pathological cell-elements found in the first stage of pneumonia. The alveolar capillaries are turgid, and in this respect resemble the capillaries in pneumonic congestion, but when a stream of water flows over a portion of lung in the first stage of pneumonia its dark color remains, while in hyperæmia of a non-inflammatory character this is not the case.
On account of its color and its resemblance to liver-tissue the name red hepatization has been given to the second stage of croupous pneumonia. The lung in this stage has a dark liver or mahogany color, and is slightly mottled, the mottling becoming more marked the farther advanced is the hepatization. The color is of a brighter red when the lung is first removed from the body than after it has been exposed to the air.
The volume of the lung is increased—at times so as to bear the impress of the ribs. It is solid and firmer than normal; pressure does not indent but tears it; it is very friable, and its torn surface presents a granular appearance. Its specific gravity is increased. It is airless, and there is an entire loss of crepitation.
Upon section it is seen that the granular appearance of the cut surface is due to the pneumonic exudation which fills the alveoli. This granular appearance is not so well shown on the cut as on the torn surface. The granules can be readily removed from the air-cells by means of a fine needle. A dirty, red, viscid fluid slowly oozes from its cut surface, which is more apparent after the lung has been exposed to the air for twelve or twenty-four hours and has undergone post-mortem changes. At any time this viscid, rusty-looking material may be scraped from the cut surface, or it exudes when a portion of the lung is firmly compressed. A portion of the inflamed lung quickly sinks in water, and small spots of blood-extravasations may be seen scattered here and there throughout its substance. When a stream of water is poured over the cut surface of the implicated lung the color changes from a maroon to a gray or yellow-gray, the usual color of fibrillated fibrin.
Not infrequently the material in the infundibula and air-cells extends into the minute bronchi, but these tubes are rarely completely filled with the pneumonic exudation. When examined under the microscope the alveoli are found filled with a solid material composed of a network of fibrillated fibrin, in whose meshes are leucocytes, red blood-globules, and changed epithelia. These latter are in various forms, usually round or oval. They may, however, become quadrangular, triangular, or irregular. They are granular, and may contain a single nucleus, a nucleolus, or multiple nuclei. These cells finally become granular, and fat-globules accumulate in them. They also become discolored from imbibition of blood-coloring matter, so that in the latter part of the process there is quite an accumulation of pigment-granules, not only in the free cells, but in the fixed epithelia. The larger cells discharge their nuclei into the accumulation of corpuscular elements, and the whole contents of an alveolus present a more or less round shape. The alveolar walls remain unchanged, or are slightly thickened by the capillary turgescence. All of these different cell-elements have been regarded by different observers as characteristic of pneumonia. The red globules give the color to the consolidated lung. The pus-cells are always numerous.
The transition from red to gray hepatization is never well defined. The mottling gradually becomes more marked, so that the affected portion of lung assumes a marbled or granite appearance. As the deep-red color of the second stage fades the density of the pneumonic consolidation becomes less and less, until it is a mere pulp, breaking down under slight pressure. The decoloration is due to the pressure on the blood-vessels, to decoloration of the blood-corpuscles that were present in the second stage, and to fatty degeneration of the other cell-elements which occupied the air-sacs.
The weight and density of the affected lung-tissue are diminished, and toward the end of this stage the lung crepitates. On section a nearly uniform dirty-gray, bloodless surface is exhibited, from which flows spontaneously or upon slight pressure a dirty-white or reddish-gray puruloid fluid. The granular red hepatized look has disappeared or is very indistinct. The amount of oedema in the affected portion of the lung varies in different cases. When it is excessive a large quantity of serum exudes from the cut surface, which then exhibits a smooth, non-granular, glistening appearance, and it does not so readily break down when pressed upon as do other forms of gray hepatization. When examined under the microscope, the alveoli are seen to be filled with numerous round mono-nucleated cells, the intercellular fibrils that bound the elements together having disappeared; in other words (the fibrillated having become granular fibrin), the alveoli are filled with a fluid or semi-fluid mass in which numbers of discrete oil-globules and protein granules are freely mingled.
The granular and fatty elements are due to the rapid degenerative changes that occur in the cell-elements. In this stage leucocytes still emigrate from the blood-vessels. The masses that occupy the alveoli are now shrunken, and between them and the alveolar wall is a layer of fluid, so that in a thin section the contents of the air-sacs are readily lifted out by a camel's-hair brush. All of the affected portion of the lung is rarely in the same stage of the inflammatory process, and to distinguish red from gray hepatization, or the latter from the beginning of some of the conditions next to be mentioned, is often impossible.
The changes which take place subsequent to the stage of gray hepatization, and the modifications due to age, remain to be considered.
Croupous pneumonia may terminate—1, in resolution [recovery]; 2, in suppuration, purulent infiltration; 3, in abscess; 4, in gangrene; 5, and very rarely, in chronic (fibroid) pneumonia.
1. During resolution the lung is moist, lighter than in the stage of hepatization, has a yellow or yellowish-green color, and still shows a marked loss in elasticity. On section, the lung appears to be non-granular, and a tenacious, puruloid fluid escapes when the section is pressed upon. Some oedema may still remain. When examined under the microscope the alveolar capillary vessels are seen to have returned to their normal calibre; the alveolar epithelium is restored; the cells in the air-sacs are degenerated, broken down, and resolved into a detritus. The degeneration of these cells is both fatty and mucoid, and the coloring matter of the blood gives origin to the granular pigment which is scattered throughout the disintegrated and liquefied mass. Some of the pigment is supposed to come from the connective tissue between the alveoli. In this condition the alveolar contents are either expelled by expectoration or undergo absorption, the lung being finally restored to its normal condition.
2. When purulent infiltration or suppuration of the lung occurs, its surface becomes yellow—more so than in any of the preceding conditions; it is soft, moist, and friable, and gives somewhat the sensation of an abscess. It is well described as miry.7
7 Pneumonia, Sturges, 1876, pp. 110, 113.
On section, a diffluent, purulent fluid exudes from a surface whose yellow color is due both to the large number of cells which are undergoing fatty degeneration, and to the anæmia which results from over-distension of the alveoli with these cell-elements.
When examined under the microscope, the cells are found not only crowding the alveoli, but infiltrating the inter-alveolar tissue. This corpuscular infiltration of the alveolar walls may so interfere with their nutrition that they will undergo softening and degeneration. Whether these cells (in all respects resembling pus-cells) have emigrated from the blood-vessels or are the result of epithelial changes is still unsettled. Reason and analogy seem to point to a dual origin. Now and then these cells are pigmented. Occasionally the alveolar walls become thinned, indistinct, and finally rupture.
There has been much discussion over the term suppuration of the lung, but the appearances reported by those who uphold, as well as by those who protest against, the term are identically the same, all agreeing that the "lung is filled with pus."
3. Abscess of the lung, as a termination of croupous pneumonia, is exceedingly rare, and is always preceded by extensive cellular or interstitial oedema; small abscesses are formed by the rupture of several of the alveolar septa. It may follow purulent infiltration. These abscesses vary in size from that of a pea to one which may occupy the greater part of a lobe. They may have a thick, well-defined, irregular wall, their interior being crossed by shaggy shreds of broken-down lung-tissue, or they may form irregular excavations in softened lung-tissue. They may be single or multiple. Several abscesses are often found in the same lobe. They increase in size by peripheral growth or by fusion of several small abscesses.
Abscesses are more common in the upper than in the lower lobes; their frequency is variously estimated as 1 in 30 or 60 cases. These pus-cavities, if of small size, may ultimately close by cicatrization, in which case they may open into a bronchus of sufficient size to allow of the discharge of their contents. Under such circumstances the contents of the abscess are expectorated; interstitial inflammation is set up around their site, which after a time encloses them in a firm connective-tissue wall; contraction ensues, and finally only a line of cicatricial tissue marks their former situation. Or if no such bronchial opening occurs, the abscess becomes encapsulated in firm cicatricial tissue, and the contents undergo cheesy and calcareous transformation. Sometimes these abscesses perforate the pleura and discharge their contents into the pleural cavity, causing pyo-pneumothorax. External fistulous openings have occurred, but they are a rare termination of pulmonary abscess.
4. Gangrene is said to be a termination of croupous pneumonia in about 2 per cent. of cases, but this estimate is based on too few statistics to be wholly reliable. It is met with in bad constitutions where there is very great vital depression, in chronic alcoholismus, and in cases of intense septic poisoning. Interference with the blood-supply, causing the formation of pulmonary or bronchial thrombi, leads to its development.8 While usually limited to a small area of lung-tissue, it may invade large tracts, and be either circumscribed or diffuse.
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 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 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.
9 "Die lobuläre pneumonie ist im Sänglingsalter eine ausserordenich häufige Krankheit" (Vogel, Kinderkrankheiten, p. 222).
10 "Lobäre pneumonie kommt viel seltener vor" (Vogel, loc. cit.).
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 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
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, vapors of various noxious acids and gases;13 the tracheal injection of caustic ammonia14 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.
13 Sityl, K. K. Akad. zu Wien, 867, Reitz.
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 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
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
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
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.
18 Berliner klinische Wochensch., 1879, No. 37, A. Kühn.
Moreover, as in typhoid and cerebro-spinal meningitis, so in pneumonia, we 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 quinsy19 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.
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.
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.
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 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
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.
Klebs23 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.
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
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.
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 Fox25 states that he knows of but one case—the one referred to by Monthus in his Essai sur la Pneumonie double.
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
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
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.
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. Traube29 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.
28 Dis. of Lungs, Walshe, 1860, p. 366.
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 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 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
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 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
31 Gaz. méd., 1851, p. 777, Robin et Verdeil; Chem. Anat. Phys., vol. ii. p. 460 et seq.
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
33 Beale gives the following analytical table of a case of acute pneumonia:
| Chloride of Sodium. | Per cent. of Solids. |
| Urine | 0.00 |
| 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.
| 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. 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.
| FIG. 34. |
| Lobar Pneumonia, where the Crisis was marked with Evening Exacerbations, reaching nearly the highest pyrexia of the second stage: Recovery. |
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.
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.
In children the temperature rises very rapidly, sometimes reaching 106° F. within the first twelve hours. The highest recorded temperature in the pneumonia of children, with recovery, is 106°–107° F. The average temperature of pneumonia at this period of life is 104° F., the range being higher than in adult pneumonia.
In children the day of crisis is oftener the seventh than the fifth day. The fall of temperature during the crisis is somewhat remarkable; it often falls two and a half degrees below the normal, and this exceedingly low temperature may be maintained for two or three days, and yet the child recover.
The accompanying charts show ordinary temperature-curves from children with pneumonia (see Figs. 35, 36).
| FIG. 35. |
| A Typical Case of Lobar Pneumonia in a Child: Recovery. |
| FIG. 36. |
| A Case of Lobar Pneumonia in a Boy ten years old, in which thermometrical observations were made every four hours: Crisis on the sixth day. |
In old age it is often difficult to determine the exact day of the invasion of pneumonia except by the temperature. The rectal temperature rises to 103° or 104° F., or even higher, on the first days, and continues at about the initial point for three or four days, with daily morning and evening oscillations of a degree or a degree and a half. The temperature-rise does not begin for several hours after the initial chill, if a chill occur (see Fig. 37).
| FIG. 37. |
| A Typical Case of Senile Lobar Pneumonia: Recovery. |
Relapse in pneumonia is a rare event; it is quite phenomenal for it to occur four days after the crisis. The temperature suddenly rises, but usually returns to normal in three or four days.
Pulse.—The pulse in pneumonia varies with the type and extent, as well as with the stage, of the disease. In an ordinary mild case the pulse-rate is usually between 90 and 120 per minute. When the pulse-rate for any length of time is above 120, the case must be regarded as an exceedingly grave one.
The pulse at the onset of croupous pneumonia is usually full and soft. As the disease progresses it becomes small and feeble. In severe cases, and when the nervous system is markedly implicated, it is rapid, and may be 130 to 140, or even 160, at the onset of the disease. In such cases it will also be small and feeble.
A high temperature is usually accompanied by a rapid pulse, and a low temperature by a moderately frequent, full pulse. At the day of crisis, when the temperature falls, the pulse will fall; and this occurs in the severe as well as in the mild cases.
Subsequent to the third or fourth day in severe cases the pulse, in addition to its frequency and feebleness, may exhibit dicrotism, or it may be jerky, very compressible, and intermittent. Sometimes just before death the pulse becomes markedly slow. The feebleness of the pulse is ascribed by some to cardiac depression, the result of the high temperature; by others it is claimed that the afflux of blood to the left ventricle obstructs, and causes a deficiency in, the aortic circulation. In other words, hepatization is adduced as a cause of the feeble pulse. In chronic wasting diseases, in feeble, weak individuals, or in those already suffering from cardiac disease, weakness of the pulse is a very marked symptom.
I cannot regard a feeble pulse in pneumonia as due to the pulmonary hepatization, for it is not that pneumonia which is most extensive that is accompanied by the greatest heart-flagging. Heart-failure may exist before, or just as, consolidation is beginning. In many pulmonary affections the obstruction to the pulmonary circulation is greater than in pneumonia, and yet there is no heart-failure. The pneumonia with the highest temperature-range is not necessarily the pneumonia in which heart-failure is most marked or earliest to develop. There are many diseases in which there is a much higher range of temperature and yet no evidence of heart-failure occurs.
If a prolonged high temperature is the cause of feeble heart-power by the parenchymatous changes which it induces in its muscular fibres, such a high fever is not met with in pneumonia, and the heart is rarely found at post-mortem to exhibit such changes. May not the heart-failure, as indicated by a rapid, feeble, and intermittent pulse in pneumonia, be due to the presence in the blood of a morbific agent (as in certain infectious diseases) which so affects the nerve-centres which supply the heart that its contractile power is diminished and its rhythm disturbed? The pulse early shows commencing heart-failure by each cardiac pulsation producing a variable filling of the arteries with blood; hence the beats first vary in force, then waves occur, then true intermissions. I have been able to detect this heart-insufficiency by these variations of the pulse within twenty-four hours after the onset of a pneumonia, and occasionally during the initiatory chill.
In children the pulse-rate is greatly increased; it may reach 200 in a minute. It is very small, unequal and irregular, but never intermittent.
In senile pneumonia the pulse is not a reliable indication. The pulse may be only 50, and yet this would be a rapid pulse for the particular case in which it occurs.
In old age, both in health and in disease, the pulse has a fictitious hardness on account of arterial changes. The pulse may not be intermittent or irregular, yet the heart may be very irregular and intermittent in its action. Again, the pulse may be feeble and intermittent and the heart be acting regularly.
Remittence of the pulse is quite common in senile pneumonia independent of cardiac changes. The action of cold upon the surface in the aged is very quickly indicated by the radial pulse lessening its volume and strength, so that if the pulse at the wrist is taken it should be from the arm which has been covered. To avoid error, the pulse in senile pneumonia must be counted at the heart.
The surface of the body may be pungently hot and dry until the crisis is reached, or it may be bathed in perspiration from the onset of the disease. A moist surface has been regarded as a very favorable sign, but when in the height of the disease the parched skin becomes moist and the patient is not relieved, it is an unfavorable rather than a favorable symptom, and is met with more often in fatal cases than in those that recover.
In most cases of croupous pneumonia the expression of the countenance is characteristic. It is one of anxiety, and over the malar bones is a mahogany flush—not, as in typhus fever, diffused, but well defined and circumscribed, so that it is sometimes called the pneumonic spot. While the cheeks exhibit a spot of this dusky hue, the rest of the face may have an earthy pallor. Bouillard states that the pneumonic flush on the cheek is most marked when the pneumonia has its seat at the apex of the lung. Some authorities state that the cheek flushes most or solely on the affected side, while others35 have shown that the cheek on the side opposite to that affected is the one that is usually flushed. In this connection it is interesting to mention the case of Jaccoud, who, suffering from an attack of pneumonia himself, noticed for twenty-four hours preceding the pneumonia signs a flush and a burning sensation in the cheek opposite to the side affected. Usually one cheek is more flushed than the other, and this is undoubtedly due to disturbance of the vaso-motor system.
35 Barthez and Rilliet.
When the impediment to the circulation is excessive, or when vaso-motor disturbance is marked, the lips become cyanosed. At the time of crisis the face becomes paler.
In about one-half the cases pneumonia is attended by an herpetic eruption upon the lips, nose, cheeks, or eyelids. It rarely appears before the second or third day. It may not appear until the crisis is reached. Herpes occurs with varying frequency in different years, but is more commonly met in pneumonia than in any other febrile state. One winter nearly every case of pneumonia in Bellevue Hospital was accompanied by herpes labialis. When sweating exists and involves the entire body, it is very frequently accompanied by sudamina, which are either abundant or sparse, and seem to have a critical significance.
In children, while the surface of the body is hot and dry the extremities are cool. The pneumonic flush instead of having a mahogany tint assumes a bluish-white tint. Cyanosis of the extremities is more frequent than in adults, and herpes labialis more common. All the cutaneous symptoms are exaggerated in children.
In old age the pneumonic flush is often the first objective sign of pneumonia. The eyelids alone are cyanotic. If the face is dusky at first, it subsequently assumes a sallow hue, and the surface-heat, which is greatest in the morning, is succeeded by a cold, clammy perspiration.
Cerebral Symptoms.—The cerebral symptoms in the early stage of pneumonia are not very significant. Headache is usually present at the onset, and may continue throughout the disease. It usually steadily diminishes after the third day. If it is severe in the evening, there will be slight delirium at night—so slight as often to escape notice. Delirium and convulsions rarely occur except in debilitated subjects and in persons of enervating habits. It is most frequently met with in alcoholic subjects, and then it assumes the character of delirium tremens. It is an active, busy, restless delirium: the patient is constantly talking, but seldom in a coherent manner. Sometimes, in those who are not alcoholic subjects, the delirium may assume an active and violent character. Whenever active delirium is present, it is important to make careful and diligent search into the previous habits of the patient.
Pneumonia of the apex is more apt to be accompanied by severe cerebral symptoms than when it has its seat at the base.
Delirium may pass into coma. When delirium and headache are marked symptoms, muscular tremors (subsultus tendinum) are very apt to occur, with insomnia and frightful hallucinations. Indeed, these cerebral symptoms are often so prominent in alcoholic pneumonia, and occur so early, that the pneumonia may be wholly masked, and will only be discovered by the temperature-range and by a careful physical exploration of the chest.
When delirium is present in feeble patients, it assumes a low muttering typhoid type, and a state of stupor is soon reached.
Among the rare nervous symptoms met with in pneumonia may be mentioned photophobia, disturbances of vision, and deafness.
In children the cerebral symptoms are more prominent than in adults, and they do not seem to be influenced by the extent of lung involved. Stupor and restlessness on the one hand, or headache, delirium, and convulsions on the other, may usher in pneumonia in children without any prodromata.
Sometimes children pass rapidly into a semi-comatose condition which has not been preceded by delirium or convulsions. Convulsions are as common in children as they are rare in adults, and occur with greatest frequency and severity during dentition. The convulsions may be general and resemble those of epilepsy (pneumonie éclamptique of Barthez and Rilliet), or they may attack single muscles or groups of muscles, the child occasionally passing into a tetanic or opisthotonic condition.
If convulsions do not occur until late they are quickly followed by a deep and fatal coma. A very rare occurrence is partial paralysis of the muscles which were involved during the convulsive period. Such paralysis is often permanent. Again, the cerebral symptoms may closely resemble those which attend cerebro-spinal meningitis—viz. headache, constipation, great prostration, delirium, convulsions, opisthotonos, and strabismus. As in meningitis, there is a peculiar cry, and all the symptoms may point directly to the brain. These symptoms are most likely to be present in the pneumonia of the apex in children from five to seven years of age.36
36 This form is the pneumonie méninges of Barthez and Rilliet.
In senile pneumonia headache may persist throughout the entire attack; it is usually accompanied by delirium of a mild type, especially when the apex of the lung is involved. These patients are very loquacious and have a constant desire to get out of bed.
Alimentary Tract.—The symptoms referable to the digestive apparatus are neither diagnostic nor important. Nausea and vomiting are not infrequent, and in about 15 per cent. of all cases are among the initial symptoms. Gastric symptoms, when severe and persistent, greatly endanger life. There is no characteristic appearance of the tongue: it may be normal throughout, or covered with a creamy-white fur, which becomes dry and brown as the disease advances. In severe cases and toward the end of the disease the lips and tongue become brown, dry, and cracked, and sordes collect on the teeth. Anorexia is marked at the onset, and the thirst is intense. When convalescence commences the tongue becomes clean and the appetite returns. Occasionally there is a catarrh of the oral mucous membrane. Diarrhoea may occur as one of the initial symptoms. It is most apt to be present when there are nausea and vomiting. As a rule, the bowels are constipated and the stools dry. In young children nausea and vomiting are more common, and in 50 per cent. of the cases usher in the disease. They usually cease on the second day, although they may persist until the crisis occurs. Excessive and violent diarrhoea may precede a fatal termination.
In senile croupous pneumonia the tongue early becomes dry, shrivelled, and covered with a thick brown coating, and is protruded with difficulty. Although these patients do not complain of thirst, they take with avidity fluids that are placed to their lips. As the period of crisis is reached critical diarrhoea is of frequent occurrence.
Loss of strength occurs earlier and is more marked in pneumonia than in any other acute disease except typhus fever. Pneumonia patients become very weak within the first five days. The recovery of strength during convalescence is rapid.
Urine.—The urine at the onset of pneumonia is scanty, high-colored, and of high specific gravity. The amount of urea excreted is twice or three times more than the normal. The excess of urea increases until the crisis, and then suddenly diminishes with the fall in temperature, often below the normal standard.37
37 The daily amount of urea normally excreted is subject to great variations: it ranges between 355 and 460 grains. Parkes gives the result of 25 different observations: the lowest estimate was 286.1 gr. and the highest 688.4 gr.
Uric acid is also increased, and follows the same course as that of the urea. The inorganic salts of the urine, especially the sodium chloride, are diminished, and during the height of the pneumonia may be wholly absent. Much has been written concerning this diminution, which is by no means peculiar to pneumonia, but in no other acute disease is its diminution so constant and marked a symptom. Sodium chloride is probably retained in the system, for when the salt has been administered in large quantities none has appeared in the urine. The reappearance of the chlorides in the urine marks the approach of convalescence, and when the crisis occurs they appear in excess, following an opposite course to the urea and uric acid.
Although these last two ingredients are in very rare cases retained, the same as the chlorides, to appear when the crisis occurs, their retention is usually accompanied by a critical diarrhoea, which is followed by a prolonged convalescence. The diarrhoea is undoubtedly due to the irritation caused by the urea.
Parkes38 states that sulphuric acid is increased and phosphoric acid is diminished, but Huss affirms that both acids are diminished. With the increase of the urea and uric acid, and diminution of chlorides, biliary pigment will appear in the urine, and occasionally the biliary acids.
38 On the Urine.
Slight albuminuria is an ordinary phenomenon of pneumonia, and, though usually met with in the second stage, it may appear at any time. This symptom is present in 35 per cent. of all cases. Its presence is a point of resemblance between pneumonia and other acute blood diseases. The more severe the pneumonia, the more marked is the albuminuria. Some have ascribed its presence to passive hyperæmia the result of the pulmonary obstruction. This is questionable, except in those rare cases where venous engorgement is indicated by cyanosis, enlargement of the liver, jugular pulsation, etc.
In children the amount of urine corresponds to the quantity of fluid taken.
Critical Phenomena.—At the end of the first week, during which all the symptoms have increased in severity, the continued fall of temperature tells us that convalescence is established. As the temperature falls, profuse (critical) sweating occurs. Both of these phenomena may occur to such an extent that for hours the condition of the patient is one of collapse.
In rare cases death has occurred in the midst of these symptoms. The respirations and pulse-rate are diminished in frequency, the pulse being small and frequently exhibiting dicrotism. The cough becomes loose, the dyspnoea abates, the flush disappears from the cheek, the sputum is more copious, and is expectorated with less difficulty; it loses the rusty color from metamorphosis of its hæmoglobin, diminishes in viscosity, and no longer adheres to the side of the vessel, but becomes more opaque, of a creamy consistency, and resembles that of simple bronchial catarrh. When resolution is retarded, the creamy-yellow tint may give place to an almost black hue, on account of the excessive amount of pigment present. As convalescence advances, the sputa become scantier, more mucous, watery, transparent and colorless. At the time of crisis the intense thirst diminishes, the appetite returns, pain in the side subsides, and the patient passes into a quiet, natural sleep, to waken fully convalescent, suffering only from extreme exhaustion.
Epistaxis, hæmaturia, and hemorrhage from the bowels sometimes occur at the critical period, and may be regarded either as accidents or as the result of the defervescence. After the crisis the amount of urea in the urine (which during the height of the disease was augmented) falls to normal or nearly to normal. Sodium chloride appears in the urine as soon as the crisis occurs.
The critical phenomena in children are the same as in adults, and frequently the fall in temperature is so great that for hours after the crisis they lie half unconscious, with a cold surface covered with a colliquative sweat. With the critical sweat there is often a catarrhal flow from the nose. When children have been extremely restless or delirious the crisis is marked by the patient passing into quiet sleep.
In old age, when recovery occurs, it is generally by crisis, and a critical diarrhoea is much more frequent than a critical sweat.
In adults and in children the recovery of strength and flesh is rapid; in the aged the period of convalescence is very prolonged, and often does not begin (when the pneumonia is of the asthenic—typhoid—type) until the fourteenth or fifteenth day; still, complete recovery may be reached.
Symptoms indicating Danger.—When croupous pneumonia is to terminate fatally, dyspnoea is greatly increased; the patient suddenly sinks; the pulse becomes extremely small, rapid, irregular, intermittent, and dicrotic. Large moist râles are heard over the larger bronchi and trachea, while the auscultatory signs of pulmonary oedema become more and more apparent. The sputa become frothy, liquid, and blood-stained, or are entirely suppressed. The respirations become more and more hurried, the face is sunken and livid, the extremities are cold, and the superficial capillary circulation is more and more interfered with, as is indicated by the cyanosis. The body is bathed in a profuse cold perspiration. The fatal issue is usually preceded by coma.
The temperature may steadily rise up to the time of death, or death may occur in the defervescence. In alcoholic pneumonia death is preceded by cerebral symptoms, such as somnolence, numbness of the limbs, a sense of formication, and slight convulsive attacks.
In children death is often preceded by convulsions or coma. If the disease is protracted, death may be preceded by extreme exhaustion and collapse. Cyanosis and extreme rapidity of the pulse are usually present in children just before the fatal issue.
Senile pneumonia may end fatally within a few hours after its onset in a most unexpected manner. The aged patient walks apathetically about, totters to the bed, lies down, and dies. If the pneumonia has existed for a number of days, the signs of a fatal termination are sallowness of the face, a cold clammy skin, expansion of the alæ nasi, and a sudden rise or fall of the temperature. The inspirations become mere gasps, and, following the apathy, the patient gradually lapses into complete coma.
Symptoms which attend the Termination of Pneumonia in Abscess.—Acute pneumonia terminates in abscess in from 1 to 2 per cent. of all the cases. It is therefore a rare termination. It is most frequent in debilitated, weak subjects and in those who have received a depressing plan of treatment. The expectoration is exceedingly copious and fetid, and the sputa are yellowish or yellowish-gray in color, consisting almost wholly of purulent matter. Pigment is usually found in the expectorated masses, and when shreds of pulmonary tissue are present the diagnosis is established. The fever assumes a hectic type and is accompanied by rigors and sweats.
After these symptoms have continued for a time, the patient grows weaker and emaciated, and death results from exhaustion, from asphyxia (when a large bronchus is plugged with pus), or from the discharge of the abscess into a neighboring cavity.
DaCosta states that "pulmonary pneumonic abscesses are at the base of the lung;" Fox locates them "at the apex;" Green, "on the upper lobe;" I have found them in both situations.
The physical evidences of a lung-cavity are the most reliable signs of pneumonic abscess. Abscess is a very rare termination of croupous pneumonia in children. In old age the formation of abscesses is never evinced by any well-marked symptoms. The finding of elastic fibres in the sputa with the physical signs of a cavity are the only diagnostic signs.
Symptoms which attend the Termination of Pneumonia in Gangrene.—Gangrene as a termination of pneumonia has been found in about 14 per cent. of cases.39 This must be regarded as an exceptionally high percentage. Its occurrence is usually accompanied by symptoms of sudden collapse. The pulse becomes rapid, feeble, and intermittent, the face is pale and of a deathly hue, and there is a profuse expectoration of blackish-green masses containing shreds of decomposed and decomposing lung-substance of an exceedingly fetid odor. The breath is fetid and the whole body emits a cadaverous smell. The rapidly-increasing prostration is sometimes accompanied by hemorrhage.
39 In 28 out of 200 cases (Guy's Hospital Reports, Sec. vii., 1848).
The sickening and indescribable odor of pulmonary gangrene is most perceptible after an attack of coughing. Gangrene has its most frequent site in the lower lobes of the lung, and it is here that a careful search must be made for the rather ill-defined physical signs which attend its development. In old age, when a pneumonia is to terminate in a gangrene, typhoid symptoms appear very early, and death occurs with symptoms of the profoundest collapse within five days from the initial chill.
Symptoms which attend the Termination of Pneumonia in Purulent Infiltration.—The symptoms of purulent infiltration differ but slightly from those of the third stage of pneumonia. When resolution does not take place at the period of crisis, and the temperature remains high, accompanied by symptoms of prostration and profuse putrid expectoration, with none of the physical signs of resolution, purulent infiltration is to be suspected. Death may result from exhaustion, or recovery take place after a prolonged convalescence (see Fig. 38).
| FIG. 38. |
| Croupous Pneumonia in the Adult, terminating in Purulent Infiltration: Death on fourteenth day. |
Mild delirium is a frequent symptom during the stage of purulent infiltration. The sputa contain a large number of cells in various stages of fatty degeneration. The temperature has regular evening exacerbations, and often ranges higher than during any preceding period of the disease. The tongue becomes brown and dry, sordes collect upon the teeth, and the patient passes into a typhoid state.
Typhoid pneumonia is a term which has been applied to a variety of croupous pneumonia which is attended by typhoid symptoms. It has also been called asthenic, low, or nervous pneumonia. There are symptoms of extreme prostration from its onset. After well-marked pneumonic symptoms have been present for a few days, the patient passes into a condition of extreme prostration.
There is little or no expectoration, no dyspnoea, no pain, no cough. Sordes collect on the teeth and gums; the tongue becomes thickly coated with black crusts; the pulse becomes small, feeble, and rapid, and there is a tendency to the formation of bed-sores; and then occur stupor, somnolence, and a continuous low muttering delirium. This form of pneumonia is met with most frequently in the aged. In some cases there is marked disturbance of the special senses.
Tremors and subsultus tendinum frequently coexist. It may be accompanied by glandular swellings, by sharp and darting muscular pains, by arthritic symptoms, or by great gastric disturbance. It is not infrequent in epidemics, and it may follow or accompany erysipelas, Bright's disease, alcoholismus, or phlebitis. It is always a grave condition, but recovery is possible. Convalescence, which is very tedious, may commence as early as the twelfth or fourteenth day. Sometimes a modification of typhoid pneumonia accompanies dysentery, intestinal catarrh, or a phlegmonous gastritis. There are great sweating, profuse diarrhoea (colliquative), and high fever. The odor of the sputa resembles that of gangrene of the lungs. Such cases commonly end fatally.40
40 Cyclo. Pract. Med., iii., art. "Gastritis."
Bilious or Gastric Pneumonia.—Croupous pneumonia occurring in malarial districts, accompanied by gastro-enteric or hepatic symptoms, is known as malarial or bilious pneumonia. It has all the characteristic symptoms of pneumonia of a very severe type, but the fever is paroxysmal. The tongue is heavily coated; nausea and vomiting are common, and may persist throughout its entire course; the epigastrium is distended and tender; the skin is jaundiced; the liver is enlarged, and there is usually an exhausting diarrhoea, attended by greenish, black, viscid, and inodorous stools. The hepatic congestion and jaundice are due to a coincident gastro-duodenal catarrh.
Bilious pneumonia may be of a sthenic or asthenic type. The theory that the liver becomes inflamed by extension from the lung is untenable.
The symptoms of bilious pneumonia have frequently led to a diagnosis of typhoid gastric fever or some severe acute affection of the intestinal tract. But a reference to the physical signs will remove all doubts.
Bilious pneumonia runs a more protracted course and has a much longer period of convalescence than ordinary croupous pneumonia. In old age this form is not infrequent. The vomiting is distinctly bilious in character, and at this period of life somnolence and stupor are quite common, and are exceedingly unfavorable symptoms.
Latent Pneumonia.—Pneumonia in adults is seldom latent unless it complicates some disease whose symptoms are so severe, and the attending prostration is so great, as to obscure the characteristic signs of the pneumonia. Intercurrent senile pneumonia is always latent, and Grisolle says that an exploration of the thoracic organs in the majority of such cases gives negative results. If, then, an intercurrent senile pneumonia runs its course without expectoration, without dyspnoea, without the pneumonic flush, and without any of the physical signs of pneumonia, its diagnosis must rest—first, on the extreme frequency of pneumonia in old age; secondly, on the fact that of all the phlegmasiæ of advanced life pneumonia is the one which is oftenest latent; thirdly, that of all the acute diseases in old age pneumonia is attended by the highest range of temperature and the greatest prostration. When an old person has a slight rigor followed by febrile movement, with great prostration, for which no explanation can be found, pneumonia may be suspected, even though all its diagnostic signs are absent.
Intermittent or remittent pneumonia, which is described by some authors as a distinct type, is a form of acute pneumonia in which a malarial element is so pronounced that all the pneumonic symptoms, even the physical signs, undergo distinct intermission, returning each day with increasing severity. Occasionally, instead of the quotidian it assumes the tertian type. During the intermission the temperature may fall to normal. Severe chills and sweating are often present, and the pneumonia is not infrequently double.
The malarial conditions which give rise to this type of pneumonia occur more frequently in our Southern and Western States than in any other part of the world.
PHYSICAL SIGNS.—By studying the physical signs of croupous pneumonia in connection with the different stages of its morbid anatomy, their importance as elements in diagnosis and prognosis can best be appreciated.
Stage of Engorgement.—The physical signs indicative of the first stage of croupous pneumonia are usually present within twenty-four hours after its invasion. If the pneumonia is central, their appearance may be delayed until the third day.
Inspection.—On inspection the movements of the affected side are noticed to be more or less restricted, while the unaffected side moves as in health. In double pneumonia the respiratory movements will assume a costal type, attended by an increase in the abdominal breathing.
Palpation.—On palpation there is more or less increase in the vocal fremitus on the affected side. The degree of increase corresponds to the extent of the engorgement. It must always be remembered that normally the vocal fremitus is more marked on the right side than on the left.
Percussion.—There is slight dulness over that portion of the chest-wall which corresponds to the affected portion of lung: its extent varies with the amount of lung involved. It is never well marked until the end of the first stage, although the pulmonary capillaries are engorged with blood from the commencement. Even at the end of this stage the intensity of the percussion sound, although diminished and muffled, has a slightly tympanitic quality, due to the fact that the exudation has not completely displaced the air in the distended alveoli. Very extensive central pneumonia may fail to give either increase in vocal fremitus or dulness on percussion until the second stage is well advanced. Absolute dulness during this stage is of rare occurrence.
Auscultation.—During the dry stage, which according to some41 is said to precede the exudation stage, there will be noticed a feebleness and unnatural dryness of the respiratory murmur. Sometimes it is harsh, at others feeble and loses the peculiar breezy, rustling quality of the normal respiratory sound. If it is less intense over the affected portion of the lung, it is exaggerated over the unaffected portion. These changes are apt to pass unrecognized unless auscultation is practised frequently and early in the disease. As soon as the engorgement is well marked and exudation takes place into the air-cells, fine crackling sounds are heard at the end of inspiration. These sounds are called crepitant râles, and are regarded as the characteristic sign of the first stage of pneumonia. They resemble those produced by throwing salt on live coals or rubbing the hair in the neighborhood of the ear between the fingers. These râles do not necessarily depend upon the presence of fluid in the alveoli, but may arise from the sudden separation of the alveolar walls at the end of inspiration when they have been agglutinated by a tenacious exudation. They are as numerous as they are minute, are unaffected by coughing, and remain audible over a circumscribed space from twelve to twenty-four hours. Whenever the pneumonic stages follow each other in rapid succession, the crepitant râle may not be heard. It is rarely present in a pneumonia which is developed during an attack of acute articular rheumatism. With the crepitant râle the respiratory murmur is feeble or assumes a broncho-vesicular character.
41 Stokes.
When, as often happens, pneumonia has been preceded by or complicates any other thoracic affection, the crepitant râle will be mingled with the sounds arising from that particular condition. It is said42 that bronchial breathing is sometimes heard in this stage of pneumonia. The voice-sounds undergo slight increase in their intensity over the seat of the pneumonic engorgement.
42 Traube, Annal. der Charité, i. 286.
In children the crepitant râle is frequently absent, and, though it may be heard at the end of a full inspiration after coughing, it is never so fine or distinct as in adults. In children there will be no increase in vocal fremitus if, as often happens, a large bronchus leading to the inflamed spot is plugged with mucus.
In old age the physical signs of adult pneumonia are modified by certain physiological changes which occur in the lungs and chest-cavity of the aged. The more complete bony union of the chest-walls, the curvature of the spine, the rigidity of the bronchial tubes, the rounded form of the chest, and the senile rarefaction of the lungs, give rise to extra resonance on percussion as compared with an adult chest. On account of the great arching of the sternum and the deposition of carbonaceous material at the apex of the lung, the clavicular region near the median line gives a dull percussion sound. The scapular and supra-scapular regions are less resonant than in the adult, on account of the tilting of the scapulæ due to curvature of the spine. There is a loss in the vesicular element of the respiratory murmur, and it resembles the sound produced by a forceful expulsion of air from the compressed lips. When the septa or the alveoli are torn and greatly distended, it has a bronchial character. Its intensity varies: at one moment it is loud, at another hardly perceptible; the variation occurs not only in the same individual, but in different individuals of the same age. The vocal sounds are loud and bronchophonic in character, and have a vibration closely resembling oegophony. It is also to be mentioned that it is almost a physiological condition for old people to have bronchorrhoea; hence mucous râles may be present during the whole period of advanced life, and if one relies on the usual crepitating râles of adult pneumonia for a diagnosis he will be misled.
Inspection and palpation in the first stage of senile pneumonia furnish little positive information. Percussion will give little dulness until the lung has reached the stage of red hepatization, and even then it may be so slight as to pass unnoticed. Very early in the disease the respiratory murmur is feeble and indistinct over the affected portion, while the portion of lung that is not involved assumes, for the time, all the characters of a normal adult respiratory murmur. Again, the breathing over the pneumonia may be intensely puerile and interrupted.
The crepitant râle is rarely present in the first stage of senile pneumonia, but subcrepitant râles and large moist râles resembling those of bronchitis are heard during the whole of this stage. The explanation of the absence of the crepitant râle is to be found in the physiological condition of the air-cells just referred to. Sometimes, on a deep inspiration after violent coughing, fine crepitation is heard, but upon careful examination it will not be found to differ from the râles of capillary bronchitis. It may be stated as a general rule that the feebler and more superficial the respirations the less distinct will be the adventitious sounds.
The physiological rigidity of the bronchi in old age favors the early development of bronchial breathing, which is often the first physical sign of senile pneumonia. One of its peculiarities, when occurring in the stage of engorgement, is that it is most distinct at the root of the inflamed lung.
Stage of Red Hepatization.—The physical signs of the second stage of croupous pneumonia are more diagnostic than those of either of the other stages.
Inspection shows the expansive movements of the affected side to be more markedly diminished than in the first stage, while those of the healthy side are increased. Frequently there is absolute loss of motion over the inflamed lung.
Palpation.—By palpation the vocal fremitus is usually increased on the affected side over the consolidated lung-tissue. In some instances it may be only slightly increased, and in rare instances it will be found less marked upon the affected side than upon the healthy. Palpation may also reveal slight displacement of the heart from the pressure of the distended lung; and in rare cases well-marked pulsation is felt over the affected lung.43
43 Skoda, Stokes, and Graves regard this as the result of increased pulsation of the arteries in the inflamed spot; and Walshe and Fox rather admit it, but Grisolle denies it.
It is evident that the vibrations of the vocal cords can be transmitted from the trachea through the bronchi and lung to the chest-wall, and there is no reason why the cardiac impulse may not likewise be transmitted through a solidified lung to the chest-wall.
If the pneumonia is central, the vocal fremitus may not be increased. It is diminished when there is an abundant pleuritic exudation over the pneumonic lung.
Percussion.—On percussion there will be marked dulness over that portion of the lung which is the seat of the pneumonia, while over the healthy portion, as well as over the opposite lung, there will be exaggerated resonance. The nearer the hepatization approaches the surface of the lung, the more marked will be the dulness. There is a peculiar sense of resistance on percussion over a completely airless hepatized lung which is not present in solidification from other causes. The exact outline of an hepatized lobe can often be traced on the chest-wall.
The tympanitic quality which is sometimes present during the stage of engorgement may continue anteriorly during the second stage, and yet posteriorly the dulness will be complete. A tympanitic percussion sound is sometimes elicited over that portion of lung which is adjacent to the consolidated lobe. When an upper lobe is consolidated, forcible percussion may elicit a tympanitic sound, for the column of air in a large bronchus will vibrate under forcible percussion. The cracked-pot sound (bruit de pot fêlé) is occasionally met with over those relaxed and permeable parts of the lung in the immediate vicinity of the consolidation. When this sound is present over the consolidated portion, it is due to the sudden expulsion of air from one of the larger bronchi. It is most frequent in young persons with thin, elastic chest-walls. The cracked-pot sound in pneumonia is not increased in intensity when the patient's mouth is open.
In basic pneumonia the subclavicular percussion note may be distinctly amphoric in character. Dulness may appear within twelve or twenty-four hours after the onset of a pneumonia, or it may be delayed until the fourth day.
Auscultation.—As soon as the air-cells are completely filled by the pneumonic exudation, the crepitant râle ceases and bronchial respiration is heard over the affected lung. The bronchial breathing is due to the fact that the vesicular element of the respiratory sound disappears on account of the complete consolidation of the vesicular structure, and the tracheal element of the respiration is conveyed to the chest-walls through the consolidated lung. It often has a metallic element, or may sound like the tearing of a piece of linen. Bronchial respiration is more intense in pneumonia than in any other disease.
Laennec taught that bronchial respiration was due to the superior conducting power of condensed lung. Skoda combats this view, and says that bronchial respiration is generated or magnified in caverns and in the bronchi of condensed lung-substance by the air in these cavities and in the bronchi vibrating in consonance with that within the trachea. The condition necessary for this consonance is provided in the circumstance that the air is pent up in confined spaces whose walls reflect the sonorous undulations.
The more complete the consolidation, the more intense is the bronchial respiration. At the commencement of this stage the tubular breathing only attends expiration, while later it accompanies both acts. Pleuritic exudation may mask or render this sound very indistinct. It may in rare instances be absent even when extensive consolidation exists and the pleura is perfectly normal. This can be accounted for in most cases by the plugging of a large bronchus. There are cases in which its absence is inexplicable.
The vocal sounds are increased in intensity and bronchophony is heard over the consolidated lung. The physical conditions of the lung which give rise to bronchophony have the same diagnostic significance as the bronchial respiration, and in all instances its occurrence, its distinctness, its temporary disappearance, and its reappearance are dependent upon precisely the same conditions as are the changes in the bronchial respiration. If the pleural cavity is partially filled with fluid, bronchophony will be indistinct or absent below the level of the fluid, while at its level the voice-sounds will be either bronchophonic or oegophonic.
During this stage the heart-sounds are transmitted to the surface over the hepatized lung with greater intensity than normal.
In children dulness is especially marked in the infra-scapular region of the affected side. Some authors44 speak of a feeling of greater solidity below than above the scapula, which can be detected before the ear can detect actual dulness on percussion. Vocal fremitus may be increased, but it is not reliable on account of the changes in the voice.
44 West.
In old age, inspection and palpation give negative results. Dulness on percussion in old age would be regarded as normal resonance in the adult; hence the percussion sound in senile pneumonia may be only relatively dull. The tubular or bronchial breathing in the second stage of senile pneumonia is more intense than in adult pneumonia. Small gurgles or mucus râles generally persist throughout this stage. Bronchophony is not well marked. On causing the aged patient to cough and expire violently, tubular breathing may be heard where it was before absent.
Stage of Gray Hepatization.—There is no abrupt transition from the second to the third stage of pneumonia, so that the physical signs of the early part of gray hepatization are the same as those of the second stage.
Inspection.—As resolution progresses, expansive motion on the affected side becomes more and more apparent.
Palpation.—On palpation the vocal fremitus will be found approaching normal, its intensity diminishing as resolution occurs.
Percussion.—Dulness on percussion becomes less and less marked, but of all the signs this is the last to disappear. Rare cases are mentioned where it has disappeared in twenty-four hours after the commencement of resolution by crisis. As the percussion sound approaches the normal, a tympanic note is again present in circumscribed spots.
Auscultation.—The bronchial respiration that was present in the second stage gives place to broncho-vesicular breathing. This soon becomes blowing, then indeterminate, and finally approximates to, and merges into, normal vesicular breathing. Bronchophony gives place to exaggerated vocal resonance in connection with the changes in the respiratory and vocal sounds. The crepitant râle returns, but is soon obscured by larger and moister crepitating sounds, "the resolving subcrepitant râle of pneumonia," called also the râle redux. Large and small mucus râles, sibilant and sonorous, accompany the subcrepitant râles, to disappear only when resolution is complete. Not infrequently the bronchial râles that are developed during the stage of resolution are of that character called consonant45 or ringing.46
45 Skoda.
46 Traube.
The physical signs of this stage are all retrogressive, and they disappear in the opposite order to that in which they appeared. In rare instances resolution is so rapid that the subcrepitant râle is not heard. In this class of cases dulness on percussion and bronchial breathing continue for some time after the crisis.
In children, bronchial breathing rarely disappears before the seventh day. It is often accompanied by the subcrepitant râle. When resolution takes place, bronchial breathing and the subcrepitant râle will disappear at the same time.
In old age, inspection, palpation, and percussion give similar results as in adult pneumonia. On auscultation coarse crepitating sounds and loud gurgles are often heard at a distance from the site of the pneumonia. The râle redux is not distinctive of or peculiar to the third stage of senile pneumonia. The sounds heard during this stage are called mucous crepitations, by which is meant liquid crepitating râles produced in tubes intermediate between the bronchioles and the larger bronchi.
If pneumonia terminates in purulent infiltration, the temperature remains high and symptoms of great prostration are developed. The bronchial breathing continues, and becomes more intense, dulness on percussion persists, and sharp, high-pitched râles resembling fine gurgles are abundant.
The occurrence of abscess or gangrene is indicated by the physical signs which attend the formation of cavities in consolidated lung-substance.
No one of the physical signs which is present in the different stages of pneumonia is sufficient for a diagnosis, but the manner and order of their occurrence, and their relation to the symptoms which mark the different stages of the disease, enable one to reach a positive diagnosis in all typical cases. The only symptom of croupous pneumonia which can be regarded as diagnosticated is the sputum.
The physical signs of pulmonary abscess in the aged are very generally wanting. Distinctly localized gurgling and cavernous respiration may, when taken in connection with the rational signs, suffice for an approximate diagnosis, but the great rarity of abscess in old age should make one cautious in its diagnosis. The sputa will greatly aid in such cases.
The physical signs of senile pneumonia are subject to greater variations than ever occur in pneumonia in the adult, and often they do not even follow the course, irregular as it is, which has just been described.
Gray hepatization or abscess may be reached without any distinctive auscultatory signs, even after repeated and careful examination. The râle redux of resolution may be absent, dulness and bronchial breathing being immediately followed by normal (senile) resonance without crepitation. This occurs most frequently in the typhoid variety.
DIFFERENTIAL DIAGNOSIS.—In typical cases of croupous pneumonia (except in childhood and old age) the diagnosis is not difficult. The prolonged chill of invasion, the rapid rise of temperature, the accelerated, panting respiration, pain, cough, characteristic sputum, increase in vocal fremitus, dulness on percussion, the crepitant râle, bronchial breathing, and bronchophony are sufficient to establish the diagnosis.
Croupous pneumonia may be confounded with acute pulmonary congestion and oedema, capillary bronchitis, pleurisy, hypostatic congestion, catarrhal pneumonia (in children), pulmonary apoplexy, meningitis, and typhoid fever.
Pneumonia begins with a chill, while pulmonary oedema has no chill. Pneumonia is a febrile disease, while in pulmonary oedema there is no rise in temperature. In pneumonia there is pain in the side; there is no pain in pulmonary oedema. The sputum in pneumonia is viscid, rusty, and microscopically pathognomonic; pulmonary oedema is accompanied by a profuse watery expectoration. Pneumonia is commonly unilateral, and can occur in any part of the lung, while pulmonary oedema is bilateral, and usually occurs in the most dependent portion of the lung. In pneumonia we have the crepitant, dry râle, while in pulmonary oedema we have subcrepitant râles, larger and more liquid than those in pneumonia. Bronchial breathing and bronchophony occur in pneumonia, and are absent in pulmonary oedema. Percussion dulness is more marked in pneumonia than in pulmonary oedema, and the diseases with which the latter condition is apt to arise will aid us very much in the diagnosis. Urinary symptoms are negative in pulmonary oedema, while in pneumonia the chlorides are diminished or absent.
The stage of resolution in pneumonia is not infrequently mistaken for general capillary bronchitis, but, though the subcrepitant râle is present in both, it is heard all over the chest in capillary bronchitis, while it is confined to a comparatively small space in pneumonia. The expectoration is muco-purulent in bronchitis, and viscid and fibrinous in pneumonia. The temperature is lower in bronchitis (100°–103°) than in pneumonia (104°–106°). Capillary bronchitis is bilateral, pneumonia usually unilateral. Capillary bronchitis does not commonly begin with a chill, like that which occurs in pneumonia, but comes on more insidiously and without pain. Capillary bronchitis gives an exaggerated percussion note, while there is dulness on percussion in pneumonia. There is bronchial breathing in pneumonia, and a feeble vesicular murmur in capillary bronchitis. In capillary bronchitis the cyanotic appearances are very much more marked than in pneumonia, and there is no perversion of the pulse-respiration ratio. The breathing is labored in capillary bronchitis, and panting in pneumonia. In capillary bronchitis there are several slight attacks of chilliness; in pneumonia there is usually only one chill, at the onset.
The chief points in making the diagnosis between pneumonia and pleurisy are the pain, sputum, and percussion note. Pneumonia is ushered in by a distinct chill, followed by a rise in temperature to 104° to 105°, while pleurisy begins with chilliness or a number of slight rigors, and the temperature is lower, rarely above 100°. The dry hacking cough of pleurisy may be accompanied by slight mucous expectoration, while in pneumonia the expectoration is characteristic. In pleurisy the breathing is catching; in pneumonia it is panting. In pleurisy the face is pale and anxious; in pneumonia the cheek bears a dull mahogany-colored flush. In pleurisy the pulse is firm, small, tense, and wiry; in pneumonia it is full and bounding. The amount of chlorides in the urine is not altered in pleurisy, but in pneumonia they are diminished or absent. The pulse-respiration ratio is not affected in pleurisy, while in pneumonia it may fall as low as 2:1. There are no critical days in pleurisy, while in pneumonia crisis occurs about the fifth or seventh day. In pleurisy with effusion there may be bulging of the intercostal spaces, and the heart may be displaced; these phenomena never occur in pneumonia. The vocal fremitus is feeble or absent in pleurisy, while in pneumonia it is much increased. In pneumonia there is dulness on percussion, while percussion over a pleuritic effusion elicits flatness, which changes with the position of the patient. In pleurisy the grazing, rubbing, or sticky friction-sound may be heard with both respiratory acts; in pneumonia we hear the crepitant râle. In pleurisy the respiratory sounds are feeble or absent, as are the vocal sounds, while bronchial breathing and bronchophony are marked in pneumonia. It may be remembered, however, that if adhesions from an old pleurisy bind the lung to the chest, vocal fremitus may be increased in pleurisy. Again, bronchophony and bronchial breathing may exist in pleurisy, but they are always diffuse, never sharp and tubular, as in pneumonia, and are usually confined to the scapular region.
Hypostatic congestion of the lungs is accompanied by copious, watery, blood-stained expectoration. In pneumonia the sputa, though bloody, are rarely watery. Pneumonia occurs anywhere in the lung, and has well-marked rational symptoms; hypostatic congestion occurs in the most dependent portion of the lung, disappears when the patient sits up, is accompanied by no rational symptoms except dyspnoea and expectoration, and usually can be traced to a long-continued recumbent posture in those who are suffering from extensive blood-changes.
It is often difficult to decide whether a child has catarrhal or croupous pneumonia. It is to be remembered that catarrhal pneumonia is always secondary, while croupous is primary. Catarrhal pneumonia usually follows a bronchitis, croupous pneumonia rarely. In catarrhal pneumonia both lungs are involved; in croupous but one, and often only a single lobe. Catarrhal pneumonia is accompanied by a catarrhal sputum, while croupous pneumonia has a viscid, rusty, fibrinous expectoration. There is no day of crisis in catarrhal pneumonia, while croupous pneumonia in children almost always ends in well-marked crisis. In catarrhal pneumonia dulness on percussion is generally confined to the posterior dorsal region, and does not extend so far forward as in lobar pneumonia. Again, the extent of the physical signs and the rapidity of their development in catarrhal pneumonia are in contrast with those of croupous.
The range of the temperature is a most valuable guide in their differential diagnosis, since not only the height of the fever is greater in croupous, but the temperature-curve is different, as seen in the accompanying tracings:
| FIG. 39. |
| Acute Lobar (croupous) Pneumonia in a Child: Recovery. |
| FIG. 40. |
| Acute Lobular (catarrhal) Pneumonia in a Child: Recovery. |
Pulmonary apoplexy is rarely met with independent of valvular disease of the heart or pyæmia. It is a non-febrile disease, while pneumonia has marked pyrexia at the onset. In pulmonary apoplexy dyspnoea is very intense and comes on abruptly; in pneumonia it comes on slowly and progressively increases. The expectoration in pulmonary apoplexy consists of small, black sooty-looking coagula, while in pneumonia the viscid fibrinous mass contains numerous cell-elements other than blood-corpuscles. In apoplexy the dulness is distinctly circumscribed, and around it moist râles are heard, while in pneumonia the area of dulness is more extended and râles are heard over the seat of the dulness. The urinary symptoms are negative in pulmonary apoplexy; in acute pneumonia the chlorides are diminished or absent. There is a peculiar acid odor to the breath—an odor like that of tincture of horseradish—in pulmonary apoplexy, never found in pneumonia.47
47 Guéneau de Mussey.
When croupous pneumonia has its seat at the apex of the lung, it may be confounded with the first stage of phthisis. But the history of a chill followed by the characteristic pneumonic symptoms will generally enable one to make the differential diagnosis. Besides, the fever in phthisis is irregular and is subject to irregular exacerbations and remissions. If the signs of consolidation persist with little or no change, if the temperature at no time falls to normal, if there are night-sweats, if emaciation is progressive,—then the case is to be regarded as one of phthisis, even though there may have been pneumonic consolidation complicating it.
In children pneumonia is so frequently accompanied by marked nervous symptoms that it may be mistaken for meningitis. Meningitis is developed insidiously; has but slight febrile symptoms (102–103° F.), which remit with comparatively great regularity; has a pulse which is often slower than normal; has no thoracic symptoms, no dyspnoea nor accelerated breathing; the face is pale and anxious; and the physical signs of pneumonia are absent.
Sometimes a latent pneumonia with typhoid symptoms is mistaken for typhus fever: especially is this the case when the latter is prevailing. I frequently saw cases where such a mistake had been made while in charge of the typhus-fever patients on Blackwell's Island during a typhus epidemic. In these cases there will be active typhoid symptoms, such as dry tongue, delirium, high temperature, etc. The countenance in this pneumonia, although the cheeks may have a purplish hue, does not exhibit that dull, heavy leaden expression so commonly seen in typhus fever. Although there may be delirium in both instances, the delirium in the former disease is of a milder type than in the latter. The characteristic pneumonic expectoration is often absent in this class of cases; therefore it cannot be relied upon as a point in the differential diagnosis. If pulmonary consolidation is a complication of typhus fever, it will not be developed until after the sixth day of the fever, the time when the eruption is visible. If no eruption is present, the pneumonic consolidation may be regarded as the primary affection, and the symptoms which simulated those of typhus fever may be regarded as secondary.
Pneumonia with typhoid symptoms is sometimes mistaken for typhoid fever. It is called typhoid pneumonia. The differential diagnosis is not difficult if one remembers that the pneumonia which complicates typhoid fever does not come on until late in the fever, and the regular history of typhoid fever precedes its development. On the other hand, when the typhoid symptoms are present from the beginning or come on at the end of the second stage of pneumonia, the physical signs of pneumonia will attend or precede the typhoid symptoms. If a patient over sixty years of age with this type of pneumonia is not seen until the second or third week of his sickness, although evidences of lung-consolidation may be found, it will be very difficult to decide whether the pneumonia is or is not complicating a typhoid fever; and under such circumstances a differential diagnosis may be impossible.
PROGNOSIS.—The mortality-rate of pneumonia is shown by the following statistics: Of 12,421 cases treated in the hospitals at Stockholm, 11 per cent. died. In the Vienna hospitals 24 per cent. died. The Basle hospital's report for thirty-two years gives 23 per cent. of deaths, Grisolle reports 59 per cent. of deaths in those over sixty years of age. In the United States medical reports from May 1, 1861, to July, 1866, of 61,202 cases which occurred among the white troops, 14,738 died, or a little more than 24 per cent.; and of 16,133 among the colored troops (for the same period) 5233 died, or nearly 33 per cent. The deaths from all other inflammatory diseases of the respiratory organs for the same period were only one-seventh as many as from pneumonia. The Confederate hospital reports give the rate of mortality from pneumonia for twenty-five months of the same period as 331/3 per cent. Of 255 cases treated in my wards in Bellevue Hospital during a period of four years, the rate of mortality was 34 per cent.
The statistics given of private practice differ remarkably from those of hospital reports, and are somewhat contradictory. Of Lebert's 205 cases, 73/10 per cent. died. Ziemssen lost only 31/3 per cent. of his cases. Bennett (mentioning, however, that no complication existed) lost none of his 105 cases. Brundes of Copenhagen lost more than 21 per cent. of his 142 cases. Wilson Fox gives to pneumonia the fifth, and Walsh the third, place among fatal diseases. The mortality-average from all the published reports to which I have had access gives 20.1 per cent. of deaths.
From such facts it must be admitted that a disease in which death occurs in 1 out of every 5 cases should be classed among the very fatal diseases. But the death-rate varies very much at different times: it is to-day the same as when Andral wrote, nearly fifty years ago. He stated that it varied from 33 to 2 per cent. There can be no doubt but that treatment somewhat influences the variations in the mortality-statistics, but not to such an extent as to account for the great differences in the reports of different observers.
The prognosis depends more upon the age of the patient than upon any other single element. In infancy the mortality is greater than in early childhood, in which period statistics give from 4 to 6 per cent. as the ratio. The period of dentition seems to influence the prognosis in children. Between the ages of forty and sixty the death-rate is from 10 to 25 per cent.; uncomplicated cases will recover. After sixty the prognosis is exceedingly grave, and the greater the age of the patient the less are the chances of recovery.
Statistics do not give pneumonia its proper place among the fatal diseases of old age. My own experience leads me to believe that it is the most fatal of all acute diseases at this period of life, for the large number of autopsies in which it has been found to be the cause of sudden death in individuals of advanced years, and the frequency with which red or gray hepatization is found at the autopsy when pulmonary disease was not suspected during life, must greatly increase the statistical rate of mortality. Many modern authorities, who have had large experience in the hospital practice of the aged, state that nearly nine-tenths of those who die over sixty-five die of pneumonia. Pneumonia is more fatal in females than in males, in the proportion of about 3 to 2.
Statistics vary in regard to the influence of seasons on the prognosis in pneumonia. In some years the proportion of deaths is far greater in summer than in either the spring or winter. And it must be acknowledged that certain as yet unknown atmospheric influences are of the utmost importance in determining the death-rate in different years. Statistics do not show that the mortality-rate is greatest during cold weather.
The prognosis is greatly influenced by the extent of the pneumonia. Double pneumonia is not often recovered from, and pneumonia of an entire lung is more dangerous than when only a single lobe is involved. In pneumonia at the apex in infancy and old age the prognosis is unfavorable. The more feeble the patient at the time of the attack, the less are his chances of recovery. Previous attacks have no influence over the prognosis.
Most authors make mention of certain diseases that complicate pneumonia. Few give condensed statements of their influence on the death-rate. In 255 cases of my own, 87 were fatal and 168 recovered. Of these 255 cases, 124 were complicated and 131 were uncomplicated. Of the complicated cases, 75 died; of the uncomplicated, 12. Of these complications, alcoholism was present in 30 cases, pleurisy in 17, Bright's disease in 13, pericarditis in 9, hypertrophy and dilatation of the heart in 3, peritonitis in 2, fibrinous bronchitis in 1, and rubeola in 1. Lebert in his statistical report on pneumonia states that he lost only 5½ per cent. of his uncomplicated cases and all of his complicated cases. Huss of Stockholm lost 6 per cent. of his uncomplicated and 20 per cent. of his complicated cases. Wilson Fox says that, according to the reports of English physicians, pneumonia complicated by endocarditis is fatal in 75 per cent. of the cases; complicated by pericarditis, in 54 per cent.; by Bright's disease, in 50 per cent.; and by alcoholism, in 25 per cent. Brundes of Copenhagen in 120 uncomplicated cases lost only 62/3 per cent., while of 22 complicated cases he lost all, or 100 per cent. Thus it is evident from my own records, as well as from those of others which I have given, that the rate of mortality in complicated pneumonia is much greater than in uncomplicated.
By a careful study of these complications it is apparent that they all exert a direct influence upon the heart, diminishing its power and crippling its action by obstructing the blood-current from the right ventricle toward the lungs. It is unnecessary to discuss these complications in detail; it is sufficient to state that weakening of the contractile power of the cardiac muscle is an essential feature of endocarditis, pericarditis, Bright's disease, and alcoholismus. In all acute infectious diseases such complications are regarded as dangerous, because they increase the liability of heart-failure when such failure is especially to be feared.
Other complications in addition to those already mentioned which increase the mortality-rate in pneumonia are chlorosis, phthisis, emphysema, laryngitis, oedema glottidis, bronchitis, pleurisy, parotitis, pregnancy, erysipelas, and rheumatism. Bronchitis, pleuritis, and jaundice do not seem to increase the mortality-rate very much, although they certainly influence it; while pregnancy, parotitis, and affections of the joints are very serious complications. Excepting small-pox and cholera, abortion is more apt to occur during the course of pneumonia than in any other acute disease.
A case of pneumonia may be called mild so long as the temperature does not rise above 104° F.; an elevation of temperature above 106° F. for two days renders the prognosis unfavorable. Wunderlich48 says that a gradual rise in temperature after the fourth day is always an unfavorable symptom. A low temperature is dangerous only when the respirations are very much accelerated.
48 In Die Eigenwärme in Krankheiten.
When the pulse is 120 or 130 for two or three days, the prognosis is bad; if the pulse reach 150 per minute, a pneumonia patient rarely recovers. An irregular and intermittent pulse, and one whose tracing exhibits dicrotism, has a most unfavorable prognosis. In children the rapidity of the pulse is not of so much importance, while in old age the pulse is seldom or never a reliable element in prognosis. A feeble, irregular, and intermitted pulse is always an unfavorable symptom.
Prune-juice expectoration is also an unfavorable sign, as it indicates extensive blood-changes or a depraved condition of the patient. If there is an entire absence of expectoration in the second or third stage of a pneumonia, or if it becomes scanty and difficult, the prognosis is unfavorable. Any sudden suppression of the expectoration, with coincident tracheal râles, in any period of the disease, indicates impending death.
In adults delirium is an unfavorable symptom, except when it occurs at the onset of the pneumonia. When delirium occurs late in one who is the subject of chronic alcoholismus, it generally indicates a fatal termination. Convulsions in children with great jactitation, and in old age subsultus tendinum and a tendency to coma, are unfavorable signs. Great exhaustion and signs of prostration, accompanied by a sunken, pallid countenance and cold, clammy perspiration, are always attended with danger. In children bronchial breathing after the seventh day, numerous subcrepitant râles, copious and persistent diarrhoea, and swelling of the veins of the hands, are unfavorable.
In old age a sudden rise or fall in temperature, apathy, somnolence, and a sallow countenance, are all symptoms indicative of great danger. Any complication renders the prognosis unfavorable, and the occurrence of pulmonary oedema or congestion in the unaffected parts of the lung is to be regarded as a forerunner of death.
Purulent infiltration, the formation of an abscess, and the development of gangrene are all attended with danger. Recovery from gangrene is very rare.
Death does not result from heart-clot, for the conditions which favor the forming of the clot precede its formation. The fibrin factors in pneumonia are increased—often 400 per cent. more than normal. The heart is so enfeebled that the right ventricle cannot empty itself; the columnæ carneæ and the chordæ tendineæ whip up the residual blood (already prepared for clotting). Heart-clot, it is well known, is the rule when the death struggle is prolonged and the cardiac contractions gradually become weaker and weaker. Such heart-failure is always the beginning of death.
In seeking for the causes of death in pneumonia, observers have taken the results of their post-mortems as a standard of their observations. One finds oedema of the lungs at the majority of his autopsies, another finds a clot in the heart in most of his fatal cases; hence the conclusion is reached that pulmonary oedema and heart-clot are causes of death in pneumonia. But it must be remembered that in every disease there is a great difference between the cause and the mode of death. If, as a result of the failure of heart-power during the last hours of life, pulmonary congestion and oedema are developed and clots are found in the heart-cavities, it ought not to be assumed that these conditions are the cause of death. Jürgensen states that in fatal cases of pneumonia oedema of the lungs is always present, and heart-clots are frequently met with.
Death may occur, then, from heart-insufficiency, from some of the complicating diseases (cardiac especially), or from asphyxia. In some cases death seems to come from the overwhelming of the system with a poison which acts primarily and principally upon the nervous system. In a few cases fatal collapse has followed an apparently regular, well-marked crisis.
TREATMENT.—The treatment of croupous pneumonia involves not only many unsettled questions in modern therapeutics, but it embraces a history of the therapeutics of inflammation. An heroic, antiphlogistic plan of one period gave place to the rational plan of another, and that in turn to the expectant plan of a later period, while to-day an antiseptic method finds many advocates.
Regarding it as a general disease with characteristic local lesions, and not a local inflammation with constitutional symptoms, its treatment must vary with the constitutional condition of the patient and the type of the disease. When uncomplicated and occurring at certain periods and in certain conditions of life, it will terminate spontaneously in recovery. But when certain complications exist and certain conditions are present, and at certain ages, it is almost necessarily fatal. Any plan of treatment in such a disease, if resorted to indiscriminately, must needs be unreliable and unsatisfactory.
Although there is no doubt that a large percentage of cases of croupous pneumonia will recover without treatment, there is also little doubt but that well-directed therapeutical efforts can save lives and render convalescence less tedious. If it is remembered in the treatment of pneumonia that the pneumonic lung no more requires treatment than do the intestinal ulcers in typhoid fever, and that we are to be governed by the patient's general condition, and not by the physical changes in the lung as indicated by the physical signs, it is evident that all those measures which have been employed for the arrest of a local inflammatory process have no place in our therapeutics. It is for this reason that venesection, which at one time had its stronghold in the treatment of pneumonia, has now fallen into disuse. A summary of the arguments against its practice seems to be conclusive, and the numerous discussions that have so often distracted the most careful and truthful observers are well expressed in the following terms:49 1st. That indiscriminate bleeding immensely increases the mortality of the disease. 2d. That it is specially fatal in old people and in young children, in patients of exhausted constitutions, and in those suffering from chronic diseases, and particularly from Bright's disease. 3d. That it is absolutely unnecessary in the majority of cases of young adults and also young children. 4th. That in the majority of cases it has no influence whatever either in cutting short the disease, in lessening its duration, or in diminishing the pyrexia, but that occasionally these results appear to follow from its use when practised early. 5th. That in the majority of cases it hinders the critical fall of temperature and delays convalescence. 6th. That in the majority of cases, as shown especially by Bennett's and Didel's data, recovery is equally if not more rapid when it is not practised as when it is resorted to. 7th. That in a few cases a moderate venesection may be necessary in the early stages to avert immediate danger of death from asphyxia.
49 Wilson Fox, Reynolds's System of Medicine.
Not only does indiscriminate bleeding increase the death-rate and have no influence over the progress, course, or severity of pneumonia, but it postpones crisis and convalescence, and in the old, young, and enfeebled is very often nothing less than a fatal procedure. In a robust, vigorous individual, in spite of the fact that a free bleeding at the very onset will temporarily relieve the urgency of some symptoms, it nevertheless diminishes by so much the chances of recovery, lessens the power to fight against the disease, and makes the patient far more pregnable to subsequent dangers and complications.
Venesection has no influence upon the temperature. It may sometimes postpone imminent death from asphyxia; and the fact that there is one condition in which bleeding may be practised is no contradiction to the foregoing statements, for venesection is then resorted to on account of conditions that must be treated independently of the coexistent pneumonia, such as sudden engorgement of the heart with blood, attended with all the signs of sudden and extensive pulmonary oedema and congestion. When the patient is vigorous and the above-mentioned emergencies exist, free bleeding gives prompt relief. In no case should more than ten ounces of blood be taken.
A careful study of the pathology of pneumonia not only leads one to the conviction that venesection must do harm, but it strongly contraindicates the employment of all those remedial agents which have been used to arrest a simple pulmonary inflammation. Hence tartar emetic, veratrum viride, aconite, and all other cardiac sedatives which at one time were used so extensively have now fallen almost entirely into disuse, as by their effects they can only add to the burden of a heart already overtaxed by the venous stasis and the lack of arterial blood. They may for a time lower the temperature and diminish the pulse-rate, but they will accomplish this at the expense of heart-power, and will almost certainly favor the earlier and more certain development of that heart-insufficiency which must be regarded as the most powerful death-producing agent in pneumonia. Dangerous collapse has frequently followed the free use of these drugs.
Veratria is claimed to be a cardiac depressant; and this fact should make us hesitate before we administer it in pneumonia. It acts promptly in slowing the pulse, but its effects are only temporary, and when used for a couple of days the larger doses that are necessary to bring about the desired results interfere with the nutrition of the patient, often causing vomiting and diarrhoea. Aconite is also a cardiac sedative, but my experience with it has convinced me that it is in all respects inferior to veratria. Digitalis, which may be regarded as a cardiac stimulant, is to be preferred to either veratria or aconite. It not only lowers the temperature, but lessens the frequency of the pulse, steadies it, and produces in the majority of cases its well-known tonic action upon the heart. Its use in children is sometimes followed by an intermittent pulse, but it is a symptom of no dangerous import.
Calomel and antimony have been almost entirely discarded from the therapeutics of pneumonia: there is no evidence that the former has any influence either upon the progress of the disease or the absorption of the pneumonic exudation. Those who advocated its use believed it to be most advantageous after the patient had been freely bled and large doses of tartar emetic had been given. The latter was also a part of the treatment where bleeding was practised. It exercises a depressant effect upon the heart, and hence, although it may diminish the frequency of the pulse and lower the temperature temporarily, it is an exceedingly dangerous relief, as it is obtained at the expense of vital power. It is absurd, with our present knowledge of the pneumonic process, to discuss what was once claimed for tartar emetic—namely, that it had the power of arresting the pneumonic process as well as preventing pulmonary congestion in the unaffected portion of lung. These drugs, while they at best afford only temporary relief, require most careful watching to guard against their dangerous and prostrating effects.
Expectorants have no place in the treatment of pneumonia, as only a very small portion of the exudative matter in the lung is removed by expectoration. If mucus or other secretions accumulate in the bronchial tubes in sufficient quantities to cause inconvenience, it is in consequence of the exhaustion and a loss of muscular power which attend the disease, for which expectorants will afford no relief.
Counter-irritation, by blisters or other irritants applied to the surface of the chest in the earlier stages of pneumonia, is of questionable utility. Occasionally, blisters may be applied during the third stage to hasten the process of resolution and promote the absorption of plastic exudation. The application of leeches, followed by a linseed poultice or some other soothing fomentation, will often relieve the pain in the side which is so urgent at the onset of a pneumonia. If extensive pulmonary oedema occurs, dry cups applied to the chest will afford relief to the dyspnoea and temporarily remove the oedema.
It has come to be a quite universal practice in this city to encase the chest in a layer of cotton batting or flannel covered with an oil-silk jacket. While this procedure has no direct influence on the course of the pneumonia, it promotes diaphoresis and protects the surface from sudden changes of temperature, and is always grateful to the patient. It is especially serviceable in children.
A pneumonic patient should be kept in bed, as nearly as possible in a horizontal position. Every appliance for promoting rest should be employed. He should be cautiously moved for the necessary examinations of the chest, and should be kept as short a time as possible in a constrained position. If there are evidences of heart-failure, the sitting posture should be avoided and talking should be prohibited. The sick-room should be large, cheerful, and well ventilated, and its temperature should range between 65° and 70° F. In acute febrile disease there is no danger of catching cold from draughts, and the idea of the laity that the moment a person is sick or has a fever he must be put in a dark, close room is one of the superstitions of ignorance. Pneumonic patients always demand air, and the cooler the more grateful it is. Pure fresh air has a marked antipyretic power. It is a good rule to allow adults to regulate the temperature of the sick-room to suit their feelings.
One of the most important things in the successful treatment of pneumonia is a carefully-regulated diet. The food should be fluid or semi-fluid and highly nutritious, such as milk, eggs, beef-tea, and concentrated meat-broths. Milk is to be preferred to all other forms of nutrition. It should be given in small quantities at short intervals.
When not contraindicated wine may always be administered with milk. Such administration of wine is not a part of the stimulating plan of treatment hereafter to be considered, but it is a means of increasing the digestive power of a feeble stomach.
If expectoration becomes difficult, it may be from a loss of muscular power in the bronchial tubes, when stimulants are indicated; or from extreme viscidity of the sputa, when alkalies will be of service. Just here it may be mentioned that alkalies and neutral salines possess a diuretic and diaphoretic power which often affords relief from the pungently hot skin, and may aid the elimination of effete material by the kidneys.
It should be remembered that in the treatment of croupous pneumonia we have to do with a self-limited, acute febrile disease, which usually runs a cyclical course.50 Routine treatment is therefore always harmful.
50 Fernet ("De la Pneumo. franche aigue," etc. Arch. gén. de Méd., 1881, pp. 5–155) has demonstrated the regular and cyclical course of pneumonia. The evolution of the malady is represented by the march of the fever and is figured by the thermometric curve.
The nervous shock which attends the ushering in of a severe croupous pneumonia is greater than in any other acute disease, unless it may be peritonitis, and the important question presents itself at its very onset, What measures shall be employed to overcome or mitigate the impression made upon the nerve-centres by the morbific agent which is operating to produce the pneumonia? The experience of the last few years leads me to the conclusion that during the developing period of the disease, when the pneumonic blow is first struck, and until the pneumonic infiltration is completed (usually for the first four days of the disease), if the patient is brought under the full influence of opium, and held in a condition of comparative comfort by hypodermic injections of morphia repeated at regular intervals, he is placed in the best condition not only for resisting the shock, but also for combating the activity of the pneumonia. Opium does not, when thus administered, interfere with a stimulating or antipyretic plan of treatment which may be demanded, but it does very greatly diminish the chances of heart-failure, cases often recovering under its use which from age and condition of life seemed hopeless. Then the great relief and comfort which it gives to the sufferer in the first four days of his struggles are sufficient to commend it, especially in those cases where pain is severe and the restlessness of the patient is exhausting.
After the pneumonic infiltration is completed opium should be administered with great caution, for paralysis of the bronchi (which it induces), and the consequent accumulation of secretion in the bronchial tubes, may greatly increase the already existing difficulty of respiration.
In all severe types of croupous pneumonia there are two prominent sources of danger: heart-insufficiency and high temperature. There are consequently two prominent indications for treatment—viz. to sustain the heart and reduce temperature.
A large proportion of deaths from pneumonia result directly or indirectly from heart-failure. Alcoholic stimulants, judiciously employed, are the most efficient means which we possess for sustaining a flagging heart, but their indiscriminate use is more dangerous than indiscriminate venesection. It may be that only a few ounces of brandy will be required to carry a pneumonia patient through a critical period, or it may be that its free administration will be required to save life. In the old and feeble, and in those who have been accustomed to the use of alcohol, stimulants may be indicated from the commencement of the attack, and their free use required throughout the whole course of the disease. Each case demands careful study. In no other disease is so much discretion and judgment required in the administration of stimulants as in croupous pneumonia. The pulse, being the indicator of the condition of the heart, must be carefully studied. A frequent, feeble, irregular, or intermittent pulse always indicates heart-insufficiency. The quantity of stimulants to be administered in any case must be determined by their effect upon the pulse. It is advisable to commence their use in small quantities, and carefully watch their effects. If the effect is beneficial, a favorable result will follow within a few hours, and then the quantity to be administered can be increased according to the necessities of each case. It is seldom necessary to give more than six or eight ounces of brandy in twenty-four hours, yet if the necessity of the case demands it may be given in much larger quantity, twelve or twenty-four ounces often being required in twenty-four hours. A dicrotic pulse is a certain indication for the administration of stimulants.
The period immediately following the crisis is the one in which stimulants are usually most serviceable. Delirium is a symptom which calls for their administration, whether it is due to asthenia, pyrexia, or is an expression of blood-poisoning. When muscular tremor and subsultus tendinum are present, alcohol may usually be freely given. A critical collapse in the aged and weak, attended by great prostration and a subnormal temperature, is a condition in which alcohol shows its best effects, and the amount of asthenia will determine the amount of stimulation required.
It has been claimed that carbonate of ammonium in large doses stimulates the heart and prevents the formation of heart-clots by its action on the blood. The cause of heart-clot is the heart-failure, and there is no evidence that carbonate of ammonium prevents the coagulation of the blood when the blood-current is slowed. Besides, large doses of carbonate of ammonium irritate the stomach, and on this account interfere with nutrition, and thus diminish the chances of recovery. As a diffusible stimulant it is inferior to champagne. Moreover, champagne can be administered for a much longer period without causing gastric disturbances.
Camphor and musk have been highly recommended as cardiac stimulants, but they are inferior to alcohol.
Digitalis of late years has been extensively used to counteract heart-insufficiency, but it is very uncertain in its action in the heart-insufficiency of pneumonia, and has seemed to me more frequently to do harm than good. The nervous element of the heart-failure contraindicates its use.
The second important indication in the treatment of croupous pneumonia is to lower the temperature. The plan of applying cold compresses to the chest in pneumonia, though far from being a new one, still has its strongest advocates in the modern school of therapeutics. It is proposed to apply thick compresses wet in ice-water over the seat of the inflammation, changed every five minutes. Some use the Esmarch ice-bag for the same purpose. Patients who were moribund have, it is said, been revived by immersion in a cold bath. The advocates of this treatment claim that the temperature is lowered; that the patient experiences a feeling of relief during the bath; that the pain, dyspnoea, pulse-rate, restlessness, and severity of the attack are all ameliorated; and that the duration of the disease has been cut short by the continued use of cold baths or cold packs.51
51 Rules for the employment of cold as an antipyretic in pneumonia:
Cold Bath.—As soon as the axillary temperature in the evening rises above 103° F., place the patient at full length in a bath with a temperature of 70° F. or 80° F. Gradually lower the temperature of the bath by the addition of cold water or ice until the temperature of the patient begins to fall. It may be necessary to lower the temperature of the bath to 60° F. before the temperature of the patient is affected. After the temperature begins to fall, thermometrical observations must be taken every two or three minutes; the rectal temperature only can be relied upon. If the temperature falls rapidly—that is, two or three degrees in five or six minutes—as soon as the fall reaches 102° F. the patient should be removed from the bath; if it falls slowly, as soon as it reaches 101° F. he should be removed and immediately placed in bed. The patient should never be kept in the bath until the temperature reaches the normal, for it continues to fall for some time after his removal from the bath, and he may pass from a condition of fever into a state of collapse. The duration of the bath should rarely exceed fifteen minutes. While the patient is in the bath cold should be applied to the head by means of a sponge or by an ice-bag.
In the young, the feeble, and the aged the duration of the bath should never exceed five minutes. Once commenced, the baths must be persisted in until the crisis is reached.
Cold Pack.—This is much less effective than the bath, but if the patient is too feeble to be moved it may be employed. The patient should be wrapped in a sheet wrung out of tepid water, and over this a sheet should be applied wrung out of ice-cold water; the latter may be removed as often as it becomes warm. Its application and removal may be continued until the desired fall in temperature shall be obtained.
Cold Compresses.—The method of applying cold compresses in pneumonia is as follows: A cloth of some thickness is to be wrung from ice-cold water and applied every five minutes to the affected side, or an ice-bag is employed instead of the compresses. It is claimed for this method that it not only relieves the local symptoms, but lowers the temperature and hastens the day of crisis.
If cold is to be applied to the chest, either moist or dry, all the disadvantages arising from repeated exposure and frequent changes of temperature can be avoided by the use of the rubber coil, and it should always be employed in preference to wet compresses.
The experience of American practitioners, so far as I have learned, is against this plan of treatment. It is found that under it pneumonia is more liable to extend; that the shock of the cold to the surface causes a nervous depression from which the old and feeble do not rally; that although a reduction of temperature may be effected, heart-insufficiency is more rapidly reached and is more difficult to overcome. Besides, the statistical results of this plan of treatment are decidedly against its use. The above statements do not prohibit cold sponging of the limbs and face if it is grateful to the patient.
If the high temperature in pneumonia is due to rapid tissue-metamorphosis, the result of the action of some morbific agent in the blood, it follows that we must look for an antipyretic which can check this rapid tissue-change. It is claimed with reason that the sulphate of quinia is a sedative to the arterial system, and has a stimulating effect, sui generis, upon the capillary circulation; that it can arrest cell-development, and also check the amoeboid movements of the white corpuscles. Theoretically, therefore, it is a remedy par excellence for the lowering of the temperature in this disease; and clinically and empirically it has been found to reduce temperature more permanently and with greater certainty than any other agent. None of the objections brought against the other antipyretics can be urged against this one, for it possesses the twofold power of reducing temperature and sustaining the heart-power from its action on the nervous system. To act antipyretically, quinia must be given in large doses. From twenty to forty grains must be given within two hours, or the whole quantity may be given at a single dose. The greatest reduction of temperature will be reached in about seven hours after the quinia is taken.52
52 When quinia is employed as an antipyretic in pneumonia it must be given in large doses. The administration of two grains every two hours, or a larger quantity administered in divided doses within a period of twenty-four hours, will not act as an antipyretic; but from twenty to forty grains must be administered within a period of two hours. If the stomach is irritable, ten grains may be given every half hour until the desired quantity has been administered. Usually in from four to six hours after the antipyretic dose has been taken the fall of temperature will begin, and in about twelve hours it will reach its minimum height; then it will remain stationary from twelve to twenty-four hours. After the temperature has once been reduced by the quinia, its administration may be discontinued until the temperature shall again rise to 105°. As a rule, the temperature does not reach as high a point as before the quinia was administered. This mode of administering quinia rarely produces any symptom of cinchonism other than transient deafness after the first dose. In a large proportion of cases the temperature by this method can readily be kept below 103° F.
In Ringer and Gill's experiments with quinia on temperature it took at least twenty grains to produce a fall of a degree. From fifty to eighty minutes were required before the fall occurred, and the effects lasted from forty-five minutes to three hours. Ringer states that in pneumonia the quinia does not readily pass out with the urine, but is delayed in the system for a considerable time.
Lately, antipyrine has been brought before the profession as a valuable and powerful antipyretic. I have used it in both private and hospital practice, and have found it a prompt and efficient means of reducing temperature. It has not seemed to me, however, to have any other beneficial effect either in mitigating the severity or shortening the course of the disease. In two cases its use was followed by collapse, which in one case terminated fatally. My experience has seemed to bear out the belief that this drug is a decided cardiac depressant, and I should for this reason consider it much less desirable as an antipyretic than quinia.
During convalescence tonics and restoratives—iron, quinia, the mineral acids, cod-liver oil, or strychnia—should be administered, and the highest degree of nutrition should be maintained. If bronchitis complicates pneumonia, it may be treated with muriate of ammonium, ipecacuanha, and senega. If severe gastric catarrh occurs, hot fomentations may be applied to the abdomen, and calomel, followed by a saline purgative, may be administered.
Diarrhoea is rarely so severe as to require treatment; five grains of Dover's powder usually suffices to control it.
In the delirium which occurs in alcoholic patients small doses of the tartrate of antimony and potassium are said to be useful. I have controlled this form of delirium best with small doses of hydrate of chloral.
By some, camphor, musk, and turpentine are recommended during the stage of gray hepatization, but it seems to me that the requirements are far better fulfilled by alcoholic stimulants.
In the first stage of senile pneumonia an emetic, when not specially contraindicated, is given in the Salpétrière Hospital. The physicians of the Montpellier General Hospital regard ipecacuanha as an heroic remedy in senile pneumonia. The English regard nitrate of potassium as the most efficacious, while the Germans prefer hydrochlorate of ammonium. Antipyretics are rarely necessary in senile pneumonia; the most important thing is to sustain the heart by stimulants and concentrated fluid nutriment combined with iron and quinia. In senile pneumonia the diarrhoea occurring with the typhoid form must be promptly checked by vegetable astringents.
In children, as in old age, leeches and blisters should never be used. The whole chest should be enveloped in a linseed-meal poultice, to which some anodyne may be added (opium, aconite, or belladonna) if there is severe pain.
In asthenic pneumonia, in addition to the nutritious diet, burgundy, port wine, or brandy should be used, and stimulant embrocations should be applied to the chest. In children the state of the bowels must be most carefully watched. Stimulating expectorants are more frequently necessary than at any other period of life.
In conclusion, I would urge that all remedial measures which tend to paralyze the heart should be excluded from the treatment of pneumonia, and great care should be exercised not to over-stimulate the heart, for over-stimulation often results in paralysis. It must always be remembered that in the milder cases there is necessity for no treatment except a regulated diet and attention to those general hygienic measures which have already been referred to.
I shall not attempt to discuss the treatment of the complications which may occur in the course of a pneumonia, for it is impossible to even mention every contingency that may arise. The rule is to treat the pneumonia so long as it is the controlling disease, and the complication when it shall have become the most prominent and dangerous element in any given case. In prolonged convalescence it is of the utmost advantage that the pneumonic patient shall have a change of scene and climate.
Antiseptics.—The use of antiseptics in the treatment of pneumonia has as yet given no definite results. I have employed hypodermically phenic acid after Declat's method in several well-marked cases of simple pneumonia, without being able to determine that the temperature or course of the disease was at all influenced by its use.
F. Schwarz53 states that the very favorable results which he has obtained in croupous pneumonia can only be due to one thing—i.e. the specific action of iodine, which renders inert the exciting cause of the disease, which he regards as an organism, and that its efficacy is limited exclusively to the very early stage of the pneumonia. He believes that its action in acute lobar pneumonia is the same as Von Willebrandt claimed for it in typhus, typhoid, and in malarial fevers. He even states that he regards iodine as a genuine specific in pure uncomplicated croupous pneumonia if employed within twenty-four or thirty-six hours after the ushering-in chill, that hinders its development and arrests its progress.
53 Deutsche medicinische Wochenschrift, January, 1881, No. 2.
After using benzoate of soda in diphtheria, scarlet and puerperal fever—drachm ij in the twenty-four hours—E. B. Cady54 states that when an epidemic of pneumonia visited his town in Wisconsin he had equally good results from the similar use of this salt in pneumonia, cases recovering which had a temperature of 106° F. and 107° F.
54 N.Y. Med. Record, 1880, July, 3, "Benzoate of Soda in Pneumonia."
Orth55 has recently written an interesting account of the treatment of pneumonia (lobar) with iodine.
55 Allg. med. Centr. Zeitschr., Berlin, 1881, i. p. 181.
T. H. Buckler strongly recommends its treatment with salicylate of sodium and fresh lemon-juice.56
56 Phila. Med. News, 1882, xl. p. 652.
Phenic acid, boracic acid, and the salicylates are highly recommended by many as the best drugs in the antiseptic treatment.