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.