Part 5

This can be described as showing a sudden rise to 102–104, at which point it is maintained for a few days, and subsides by lysis in a few days more. A typical chart is as follows:

CHART I ]

Or the temperature might fall one or two degrees for a day or so after the first rise, and then go up again for one or two more days, and subside by lysis as is shown in Chart II.

CHART II ]

This would occur without our being able to find any lung lesion unless we accept the acute œdema or wet lung as a complication, and this we were rarely able to recognize by any definite physical signs in the chest. Cyanosis frequently accompanied this second rise of temperature, and was later interpreted as being associated with the so-called wet lung. When the temperature remained up longer than five days it could safely be concluded that lung involvement must be present.

The Pulse and Respirations

The pulse was invariably slow, or rather out of proportion to the temperature. Even when the patient seemed very ill the pulse remained from 84 to 96, and of surprisingly good quality. This was noted also when some of the more severe pulmonary involvements or some complications arose. The pulse frequently did not become rapid until shortly before death. The respirations in an uncomplicated case also remained about normal. The rate was not accelerated until lung complications arose, and then a gradually increasing rate was often the first herald of oncoming danger and a sign of grave prognostic import. The relation of the pulse phenomena toward the end of a fatal case was most remarkable. The respiratory rate was accelerated, as has been noted above, but the pulse rate frequently remained unchanged, being characteristically slow. In a patient seen in consultation with Dr. Lester H. Botkin, of Duquesne, Pa., death took place while we were in the sick room. It was a case of apparently uncomplicated influenza of seven days’ duration. The respirations were rapid and the pulse was only 96. In the last five minutes of life the heart beats as observed with the stethoscope never varied, until they suddenly ceased; during the same time the respiratory efforts were only three agonal ones, the last being a minute or so before the last heart beat. There were no physical signs of consolidation at any time recognized in this case, but we feel that the lung, had we seen it at autopsy, would in all likelihood have shown the peculiar hemorrhagic and œdematous character so often observed in the fatal cases.

There were, of course, marked exceptions to the description of slow pulse and later rapid respirations observed. In some the pulse rate and respirations increased, together with or without definite signs of a grave complication.

Cyanosis

This was recognized early in the epidemic. It was sometimes preceded by a peculiar flushing of the face, such as accompanies belladonna poisoning. It might be noticed in the very first days of the attack. The cyanosis was looked upon as being a very early symptom of lung involvement. With our later knowledge from autopsies, and especially as shown by Dr. Klotz, we feel it was surely an accompaniment of, or may even have preceded, the changes in the lung which have been designated as œdematous, “wet” or cyanotic. At the earliest appearance of the cyanosis we were frequently unable to find any change in the physical signs of the chest. Of course, the indefinite signs of an acute bronchitis were present, and in some cases an additional “impaired resonance” was noted over one or both lower lobes, but when this was definitely present other more definite signs soon followed, and our case was shifted suddenly from Group I, i. e., without apparent lung involvement, to Group II, i. e., with definite lung involvement. This cyanosis was noticed first in the face, and frequently was marked on the dorsal surface of the hands. It was not unlike the cyanosis which may sometimes be seen when large doses of certain coal tar derivatives are taken. In fact, the question arose whether in the epidemic of 1889 and 1890, when the coal tar derivatives were prescribed with such freedom and with accompanying cyanosis and apparently such deleterious effects, the cyanosis may not after all have been due more largely to the infection than to the medication. After that epidemic it was said: “Influenza has slain its thousands, but the coal tar products have slain their tens of thousands.” There was no gross hæmaturia or hæmoglobinuria present in these cases, although a few red blood cells were seen microscopically. There was, however, epistaxis, sometimes early in the disease or later associated with the cyanosis. In a few cases there was hæmoptysis, which we regard as always arising in cases where the wet or hemorrhagic lung was present. Cyanosis in disease of the lungs, and especially in the terminal stage of lobar pneumonia, is a familiar and common occurrence, but the cyanosis observed in this epidemic seemed quite different from the ordinary. The points of difference were these: (a) it came early in the disease; (b) it seemed to be more generally present when very little lung involvement could be demonstrated physically, and was just as likely to disappear when more definite chest signs were demonstrable; (c) it was not associated with embarrassment of respiration; (d) it had no relation with a demonstrable circulatory disturbance. The pulse did not become rapid; the quality of the pulse did not change; the right heart was not dilated, as is so frequently the case in the terminal stage of a lobar pneumonia when cyanosis appears; (e) and finally there was no associated œdema of the lungs, or at least that œdema of the lungs which occurs in the later stage of lobar pneumonia, when the pulse becomes rapid, when there is rapid and labored respiration, when the right heart dilates, when there is cold perspiration, and when the signs of impending death are plainly evident. The cyanosis of influenzal pneumonia seemed to be due to an entirely different cause or combination of conditions from those present in lobar or pneumococcic pneumonia. The cyanosis of influenzal pneumonia was, therefore, most confusing, and became all the more so when it was recognized that it did not yield to the respiratory and circulatory stimulants usually employed when cyanosis is present. The inhalation of oxygen was resorted to rather routinely early in the epidemic. It seemed to temporarily influence the cyanosis, but the results were not permanent, and the outcome of the cases did not seem to be different from those in which oxygen inhalations were not used.

The blood pressure in those cases in which cyanosis was observed was invariably low. This seemed to be due to the infection, for in several private patients not belonging to this group of patients with previously known high blood pressures the blood pressure was observed as much lower throughout the course of the infection.

Leucopenia

The peculiar behavior of the white blood corpuscles will be discussed more fully in another paper of this series. Our remarks will deal more particularly with the clinical observations and interpretations. The leucocytes fell below the normal from the very onset of the disease; they varied very little regardless of great changes in temperature; they did not always increase, or if they did increase at all it was comparatively little, even in an extensive invasion of the lungs or in severe complications. Concerning the leucopenia we have no explanation to suggest, save that it is a clinical characteristic of the disease. Our first thought was that the infection came on so suddenly and profoundly there was no time for a leucocyte reaction. But when we recall other diseases associated with a leucopenia, notably typhoid fever, which does not come on with such suddenness, our explanation for the leucopenia of influenza does not seem to hold. The leucopenia must be simply a peculiar toxic blood reaction characteristic of the Pfeiffer bacillus invasion. Such an explanation has long been accepted in the Eberth bacillus infection.

Asthenia

A condition which was frequently noted by the patient was an indescribable weakness and prostration which appeared early, sometimes before any other symptoms were noted or before any elevation of temperature. The young soldier was in apparent perfect condition when he arose in the early morning. During the “setting up” exercises he did not feel so fit, and a few hours later appeared extremely weak. When his condition was called to the attention of the medical officers he was found to have a slight elevation of temperature and was sent to his bed.

In former epidemics, as also in this one, marked prostration was recognized as coming at the height of the disease and remaining persistently during convalescence. But it does not seem to be recorded as among the first symptoms.

Influenza with Lung Involvement

Of the group with lung involvement much may be written from a clinical standpoint, and much confusion may be brought about. Especially is this so if one has no definite idea of the pathology present, or if one enters into a discussion of the character of the infection—a point upon which there is as yet no unanimity of opinion. From the many reports which have been put forth from the base hospitals of the various cantonments, and also from the reports coming from civilian practice, it is evident that scarcely any two groups of laboratory men or any two individuals of those separate groups have the same idea as to the bacteriology and the pathology peculiar to this epidemic.

As long as there is this confusion and element of doubt in the minds of those to whom we are accustomed to look, the clinician must necessarily speak with considerable hesitancy, especially when he attempts to interpret the physical signs observed. In our own group the observations of Klotz, Guthrie, Holman and others have given us an interpretation of our clinical findings which, at present at least, is more or less satisfactory. We shall definitely keep in mind their observations and conclusions as we go on with the description of the physical signs of the chest in cases having lung involvement.

In the description of this group it will readily be seen that the lower respiratory tract stood the brunt of the infection. Of the 153 soldiers under our care, 60, or about 40 per cent., were recognized as having pneumonia. Of these, 34 had undoubted demonstrable signs, while 26 were questionable, and yet from the temperature and other symptoms we concluded there was a pneumonia. Of the 394 civilians, 189, or about 50 per cent., had pneumonia. Of this group there were again some 28 or 30 in which the diagnosis was doubtful, according to the ordinary way of making a diagnosis, but we felt sure from the temperature course that more than a simple influenza was present. In the description of the physical findings of the chest in these influenzas with lung involvement it will be readily seen why the diagnosis must sometimes be in doubt.

Before referring to the physical signs it might be well to describe the condition and general appearance of the patient when the lungs became involved. The patient who had been progressing with an apparently simple influenza, with no chest signs except those of bronchitis or tracheitis, occasionally slightly cyanotic, became more cyanotic, the elevation of temperature continued longer than three to seven days, or if it came to the normal began to rise again, his respirations gradually increased and the pain in the chest became well localized. One could safely assume that the patient had developed a lesion in the chest. This could not always be localized during the first few hours or on the first day. The evidence of increased bronchial disturbance was frequently recognized, and later impairment of resonance and diminished breath sounds associated with “a few crackles” were noted. This, so far as we can tell, may have been the only evidence of the stage of œdema or “wet lung.” After this, as the disease advanced, definitely increased vocal fremitus and rather definite tubular breathing with greater impairment of resonance were noticed. These signs were usually observed first at the apex of the left lower lobe, and from here they extended forward along the inter-lobar sulcus, or downward along the spinal column. If the lesion was noticed first on the left side, in a day or two it was found more or less definitely in the right lower lobe also. It seemed to occur more frequently first in the body of the right lobe, instead of in the apex of the lobe as on the left side. In both lobes it might spread to contiguous areas and form a massive consolidation, or it might be found in small separate areas, some of which would clear up in a day, while others would persist.

The expectoration was frothy, containing either blood or masses of yellowish, greenish purulent material floating in a watery sanguiolent or clear fluid, or enmeshed in frothy mucus. The amount of expectoration in some cases was enormous, but as a rule it was scanty. It was thick and ropy at times and distinctly annoying to the patient.

At this stage the physical signs were very much in accord with those of broncho-pneumonia. In a few hours sometimes, or in a day, the small areas of consolidation became confluent and massive consolidation was formed. It appeared as though the whole lobe would in time become solid, as in a true lobar pneumonia. Or the original areas may apparently have cleared and other areas involved, became the centers of massive consolidations. In many cases both lower lobes were thus similarly affected, and one had the physical signs of a double lobar pneumonia. However, nearly always a small angle of the lobe remained clear, thus differing from the entire lobe involvement characteristic of a true croupous pneumonia. Other signs, such as the absence of vesicular breathing and presence of the crepitant râle, moist râles of all sizes to very coarse râles, could be noted. As in certain stages of a complete consolidation, the lung might be dry; no râles present, but definite tubular breathing present. This in a day or two, or after a longer time, might give the signs of resolution. The stage of resolution, however, was almost invariably prolonged, sometimes extending over weeks. With these variable lung signs were often mingled the signs of a fibrinous or serofibrinous pleurisy, which occasionally but remarkably infrequently went on to effusion or empyæma.

As stated above, the demonstrable pathology was in the lower lobe, and more frequently in the left than in the right, only occasionally in the middle lobe, and never, we might say, in the upper lobes. The very earliest definite signs were found at the apex of the left lower lobe.

This observation seems to be entirely contradictory to that of the pathologist, who found in 65 per cent. of all cases coming to autopsy a lesion in all the lobes of the lungs (Klotz). The only explanation we can give which seems at all satisfactory to us is that the pathology in the upper and middle lobes must not have been sufficient, or must have been of such a nature that it did not yield the physical signs, i. e., definite impaired percussion resonance, increased vocal fremitus and tubular breathing, with varying shades of moist râles—signs upon which we insisted before we were willing to state definitely that there is a demonstrable pneumonia present.

In this description it has been attempted to follow the order of invasion in a lung which seemed to go through the entire course of the disease. There were, necessarily, all degrees of the process, some cases showing few signs and yet being remarkably ill, and others all of the signs with very little other evidence of serious illness.

We were continually impressed with the notion that the pathology in the lung, at least the pathology demonstrable physically, did not tell the whole story of the case, and that the outcome depended as much or possibly more upon a general infection or toxæmia of which the recognized condition in the respiratory system was only a small part. We were particularly impressed with this in the success or failure following the application of any therapeutic measures. It was quite a common remark, therefore, in the wards of the hospital among those associated in the work that “the patient died too quickly to permit of the succession of the various stages of pneumonia”; or, in the autopsy room, that if the patient had lived long enough he would have had demonstrable, well-recognized pathology of the lung, instead of the cyanotic, wet, spongy lung which was found.

The temperature course in the pulmonary cases was characterized by its irregularities, and by its being entirely out of harmony with the extent and severity of the lung invasion in so far as it could be interpreted by the physical signs. The temperature as described in a simple influenza might not come to the normal in the time of three to seven days, and might even go higher, with no demonstrable chest signs, but with every other evidence of lung involvement. Later the temperature might come down by lysis, which was the usual way, and the chest signs gradually or suddenly become evident. The temperature might remain normal throughout the rest of the course, and a lobe or even both lower lobes of the lungs be as solid as in a true lobar pneumonia. Occasionally the temperature fell by crisis, but there was no associated change in the physical signs of the chest. In short, the temperature seemed to run a course entirely independent of the physical signs in the chest. In two remarkable cases seen in consultation on two consecutive days the physicians in charge declared that no signs of consolidation could be found, though all other evidences of pneumonia were present. In the 12 hours which had elapsed from the time the last examination was made the temperature fell by crisis. At the consultation, to the surprise of the family physicians, we found both lower lobes consolidated, it having occurred apparently with the crisis. Both patients were healthy-looking, robust, young men, and both recovered with delayed resolution. In the convalescence of such cases, if the patient got up too soon or if any other indiscretion took place, a relighting of the lung occurred. From the above description it can be readily seen that a diagnosis of the conditions in the chest in influenzal pneumonia was frequently impossible, because one had to abandon all his previous ideas of pneumonia, in so far as onset, crisis, blood picture, sputum, temperature, respiratory and circulatory phenomena, physical signs and prognosis were concerned.