lobar pneumonia as in the adult, but a bronchopneumonia, the different result being dependent upon the peculiar anatomical structure of the undeveloped lung of the infant. During the second and third years of life the pneumococcus may cause in one child a lobar pneumonia and in another a bronchopneumonia. In fact at this age not infrequently both varieties of pneumonia may be present in the same lung. Under the age of two years then most cases of primary pneumonia are of the bronchopneumonic type, and through childhood nearly all cases. The term bronchopneumonia describes a lesion rather than a disease, several quite different forms of infection being included under this head. Lobar pneumonia, as we have seen, is regularly associated with the presence of the pneumococcus, in most cases in pure cultures. In bronchopneumonia no one form of organism is always present. In primary bronchopneumonia the pneumococcus is the usual etiologic factor, in many cases in pure cultures. In secondary bronchopneumonia there is almost always mixed infection. The bronchopneumonia secondary to measles, diphtheria and other infection is usually due to the streptococcus, Loeffler's bacillus, staphylococcus, or Friedlander's bacillus. In fact, any combination of these different organisms may be found. The most frequent combination is the pneumococcus and the streptococcus, and in these mixed infections the streptococcus plays the most important part.

DOCTOR SAMUEL WEST best clears up the relations between the bronchopneumonias to one another and to their causes as follows:

(1) "That the primary and secondary bronchopneumonias have a different bacterial origin.

(2) "That secondary bronchopneumonia is for the most part due to streptococcus infection, derived from some source connected with the airtubes, throat or mouth.

(3) "That primary bronchopneumonia is of pneumococcal origin.

(4) "That pneumococcal inflammation occurs with almost equal frequency in the child and in the adult.

(5) "That pneumococcal inflammation takes a different form in each, in the adult producing massive consolidation, and in the child patches of disseminated consolidation; in other words, that there is no real pathogenic distinction between lobar pneumonia in the adult and primary lobular or bronchopneumonia in the child."

WEST further says the term bronchopneumonia would be best reserved for those inflammations of the lungs which follow antecedent affections of the bronchi, and that their exciting cause for the most part will be found to be other organisms than the pneumonic, while on the other hand, the primary bronchopneumonias of children are really croupous pneumonias varying in a disseminated and patchy form instead of a

massive consolidation.

SYMPTOMATOLOGY AND DIAGNOSIS.

BY GEORGE E. MCKEAN, M. D., DETROIT, MICHIGAN.
[PUBLISHED IN The Physician and Surgeon EXCLUSIVELY]

In the time allotted, I shall attempt only a hurried review of the symptomatology of typical cases of the two great varieties of pneumonia, namely, croupous and bronchopneumonia.

A typical case of croupous pneumonia is ushered in with a chill, generally severe, soon to be followed by a rapid rise of temperature, usually

to 103 or 105° Fahrenheit, which temperature remains quite constant until the sndden fall to normal or below of the crisis. This occurs usually from the eighth to the tenth day. In the aged and in drunkards the temperature may not be much elevated. The pulse which during the chill is small and rapid, soon becomes full and bounding, running from 100° to 120°. Later if there is much consolidation and the infection is severe, the pulse may become soft and small. The heart sounds are usually loud and clear. The second sound in the pulmonary area is accentuated. When the heart is failing the first and second sounds of the heart approach each other in character, somewhat simulating, as OSLER says, a fetal character.

Pain of a stabbing character in the side is an early symptom, usually first felt about the nipple area and sometimes under the shoulder blade. The cough is at first short, restrained, without expectoration and gives much pain. Soon the patient begins to raise a blood-tinged mucus, the tenacious "rusty sputum " so characteristic of the disease. This sputum contains leukocytes, mucus, corpuscles, red blood cells-many of them boken down, epithelia from various portions of the respiratory tract, Fraenkel's pneumococcus, Friedlander's bacillus, and in many cases the staphylococcus and streptococcus pyogenes. Later, as resolution begius, the sputum becomes more liquid. In low types of the disease the thinner, dark sputum resembling prune juice, is seen.

The respiratory symptoms are characteristic. The breathing is short and rapid, may be forty to sixty to the minute. Inspiration is short and shallow, and with expiration a short grunt is heard. Blood examination shows in nearly all cases a marked leukocytosis. The absence of this leukocytosis is said to make the prognosis much more grave.

Physical signs are as follows:

Inspection shows diminished expansion in the affected side. In contrast to pleurisy with effusion, the intercostal spaces are not obliterated. On palpating, we feel the pleural rub. After there is consolidation,

tactile fremitus is increased.

Percussion in the beginning shows no marked deviation from the normal, perhaps the note may be higher pitched over the engorged areas. With hepatization the note becomes flat and the consolidation can be easily traced by the extending dullness.

Auscultation.-At first with the restrained breathing we hear nothing unusual, but soon upon having the patient take a fuller breath, we hear the bronchovesicular breathing and at its close the fine crepitant rales. These to me always seem to come from the pleura. Later, except in cases of massive pneumonia when the bronchi are filled, the tubular breathing is heard. As resolution advances mucous rales of all varieties are heard.

Of cutaneous symptoms, the most common is labial herpes. The cheek of the side affected is often reddened.

Cerebral symptoms.—In children convulsions at the onset are common. Except in few cases and in alcoholic subjects the delirium is generally not marked.

The diagnosis is easily made from the symptoms, the sputa and the physical signs. Occasionally aspiration may be necessary to differentiate a pleurisy with effusion.

The careful man who is attending a patient suffering from some chronic affection will not often overlook an added pneumonia.

In

cases of central pneumonias the fluoroscope aids us greatly in early diag nosis and when an X-ray apparatus is available, such examination should be made of all suspected cases.

Acute tuberculopneumonic phthisis sometimes cannot be differentiated until the appearance of the tubercle bacillus and elastic tissue in the sputum.

In the typical case of bronchopneumonia, we see a child in the course of or during the convalescence from measles, whooping cough, diphtheria, la grippe or other febrile affection gradually developing a cough. The temperature again rises, respiration becomes more rapid, and the pulse is quickened. Fine subcrepitant rales are heard especially at the bases of the lungs and sibilant rhonchi all over the lungs.

There is little dullness at first, but gradually areas of comparative dullness can be made out, and later larger areas of complete hepatization can be outlined.

The temperature ranges from 102° to 104° Fahrenheit. The course of the disease is more variable than croupous pneumonia, but in favorable cases, the temperature commences to decline at about the seventh to the tenth day and falls gradually.

Dyspnea, an early symptom, gradually develops respiration running very high. In severe cases there are some signs of cyanosis. As the cyanosis progresses the cough lessens, the child's anxious efforts to breathe are given up, the lungs gradually fill, and the child dies from a paralyzed right heart.

In the primary form, the child is taken suddenly with a chill or a convulsion, temperature rises suddenly and is more constant. The physical signs are more local. This form terminates often by crisis. The whole course is much more like cropous pneumonia, and since the sputum, if any, generally contains the pneumococcus, the differential diagnosis is at times impossible.

Ordinarily, in the secondary form, this differentiation is easily made by the mode of onset and the course of the disease.

No doubt many fatal cases of so-called bronchopneumonia are tubercular. Marked dullness over the apices of the lungs, or over the bronchial glands should make us suspicious. Sometimes in the vomited matter of young children and in the sputa of older persons, elastic tissue or tubercle bacilli can be made out which of course clears up any doubt there may have been about the case.

THE MORBID ANATOMY.

BY EDMUND A. CHAPOTON, M. D., DETROIT, MICHIGAN.

PROFESSOR OF PRINCIPLES AND PRACTICE OF MEDICINE IN THE DETROIT COLL' GE OF MEDICINE.

[PUBLISHED IN The Physician and Surgeon EXCLUSIVELY}

THE morbid anatomy of the several types of pneumonia has not been increased materially of late years, except from the point of view of its origin and the opinion now prevails very generally, that microorganisms must be considered as the exciting causes of the different forms of disease which bear this name.

Although the same bacteria are often found existing benignly in the respiratory and other organs of healthy individuals, the local or general vitality of the latter, being diminished at a certain time by the predisposing causes of the disease, permits the former to become pathogenic in their action.

The organism found most commonly in croupous pneumonia, is the diplococcus pneumoniæ, but in stating this fact, we must not forget that the same pathologic results have been found in certain cases to have arisen from the action of other bacteria, such as Friedländer's and Pfeiffer's bacilli, and even from strepto- and staphylococci.

That the peculiar form of inflammation which we find in this disease is not absolutely characteristic of the diplococcus is also evident from the fact, that its colonization in other tissues, such as the peritoneum or meninges, does not produce the same character of changes.

Some difference of opinion exists as to whether the bacilli reach the lung through the blood or by aspiration through the bronchial tubes, but I believe the majority of physicians favor the latter view. Having reached. the region and found the suitable conditions for growth, their active proliferation commences and the irritation thus arising soon sets in motion the primary steps of the peculiar reaction which is to follow. Whilst they are thus multiplying, their excretions are also formed and are absorbed by their host and when the liver is no longer able to destroy the quantity of toxin in the circulating blood, we have the chill and fever or the general symptoms of the disease manifesting themselves.

We, therefore, have an infection to deal with and from this moment, we must think of the blood as containing an excess of the poison and that the latter in its course through the tissues injures them in a greater or less degree, according as they are more finely or coarsely differentiated. It is to this poison, then, much more than to the heightened temperature of the patient, that we must refer the cloudy and granular degeneration of cells, the molecular death of the tissues, which we find all through the body; to it, the slowed circulation and the faltering, stumbling heart rather than to the obstruction to the course of the blood caused by the consolidated lung and, as a corollary, it is to an antidote to this toxin that we must look for help to prevent these changes from taking place.

Which one of us who has practiced for a certain number of years, does not recall his astonishment in the times that are gone, in finding cardiac paresis promptly manifesting itself in some case of pneumonia in which the part inflamed was but egg-size in volume, whilst at the same time or shortly after, the same ominous symptom was quite absent in another patient with one or two pulmonary lobes consolidated? With the light of today, we can now read the lines of these cases in a satisfactory way. This antitoxin, however, is not yet available and I will leave any further consideration of treatment to the gentleman who is to consider that topic of our subject.

The gross anatomical changes of the lung in croupous pneumonia have been accurately described for years and I will not occupy the time of the Society in repeating them minutely, but will simply mention, as a stimulus to memory, that following the irritation of the bacilli, we find a stage of congestion or engorgement during which all the blood-vessels of the region affected are so distended with blood, that even those of the alveoli project from and occupy a portion of the lumen of the latter. The remainder of this space is occupied by air, the proliferated and castoff cells of the alveoli and the thickened condition of those remaining adherent. The lung is dark-red in color, heavier than normal and when dropped in water sinks below its surface, but not to the bottom of the vessel.

This condition gradually merges into the period of consolidation or red hepatization, during which the engorged vessels are pouring out a

fibrinous fluid, white and red blood-cells and even pure blood into the interstices of the tissues, the air-spaces and the bronchioles. This exudate is rapidly absorbed at first by the lymphatics, but eventually the task. becomes too great for them and the liquid being checked in its course solidifies, imprisoning the corpuscular elements in its fibres. The lobe is now of mahogany color and its cut surface, from its resemblance to the liver, readily suggests the name of red hepatization. The tissue is now still heavier than before and rapidly falls in water to the lowest point possible. It is airless and cannot now be insufflated as in the first phase of the disease.

During the third period, gray hepatization, so-called, and resolution, the lung loses its dark-brown appearance to become reddish-gray, from the massing of the phagocytes in the region inflamed, fatty degeneration of some of the new cells and the granular change of the fibrin fibres. Accompanying these changes is an increased amount of fluid in the parts which helps to accelerate them and soften the occluding mass, permitting its absorption, and expectoration and allowing air again to enter the alveoli. If the crisis of the disease occurs very early, the third or fifth day, much of the exudate is expectorated, as the fibrin-plugs of the lymphatic vessels do not degenerate until the seventh or eighth day, and thus its absorption cannot take place. On the other hand, when crisis occurs late, it is sometimes remarkable how little is raised, as the lymphatics dispose of far the larger portion of the croupous formation.

During the course of this third stage, we occasionally witness one of nature's mistakes in reacting to a greater degree than the occasion demands. We are all familiar with such examples elsewhere, as when a bone becomes eburnated or ivory-like from the continued thickening of the bony lamella as the result of a primary slight injury; so in the case of the attacked lung, nature marshals her host of white cells to overcome the invading bacilli. Millions of them are killed by the poisonous liquids of the region and by the bacteria themselves, but fresh ones are ever pushing forward, until they crowd themselves so badly that nutrition can no longer be brought forward to them. They likewise die and the fatty transformation of these myriad cells imparts a greenish yellow cast to the region and yellow hepatization is said then to exist.

This series of events is not necessarily generalized and therefore in the midst of the gray hepatization we may see limited regions presenting this appearance, whilst in other instances no gray hepatization is visible as the entire lobe has undergone the change. If the purulent infiltration or crowding of the leukocytes has been sufficiently intense to greatly check or arrest the blood-circulation in the trabeculæ of the lung, we may have a number of small abscesses formed; or, by the disintegration of the tissues between the latter, one or more large ones result, which either burst into the pleura causing empyema or into a bronchus inducing expectoration, or an interstitial inflammation results at the periphery and by the formation of a new fibrous tissue, they become encapsulated.

Bronchopneumonia likewise always owes its origin to the action of microorganisms and should now, like the croupous variety, be classed among the infectious diseases. Their action is first exercised upon the mucous membrane of the bronchial tree, giving rise to a catarrhal inflammation, which by continuity extends down into the finer bronchioles, producing there the first changes that interest us.