───────┬─────────┬───────────────────────────────┬──────┬──────┬──────
Day of │Total No.│ │ │ │
Disease│ of │ SPECIFIC GRAVITY │ Alb. │R.B.C.│Casts
│Specimens│ │ │ │
───────┼─────────┼───────┬───────┬───────┬───────┼──────┼──────┼──────
│ │1001–10│1011–20│1021–30│1031–40│ │ │
───────┼─────────┼───────┼───────┼───────┼───────┼──────┼──────┼──────
1│ 3│ │ │ 2│ 1│ 1│ │ 1
2│ 12│ │ 1│ 10│ 1│ 8│ │ 6
3│ 4│ │ │ 4│ │ 1│ 1│ 1
4│ 9│ 1│ 2│ 4│ 2│ 6│ │ 6
5│ 8│ │ 4│ 4│ │ 6│ │ 5
6│ 8│ │ 5│ 3│ │ 7│ 2│ 6
7│ 4│ │ 2│ 2│ │ 3│ │ 2
8│ 10│ │ 2│ 8│ │ 5│ 2│ 5
9│ 4│ │ 2│ 2│ │ 4│ 3│ 4
10│ 6│ │ 1│ 5│ │ 6│ 3│ 5
11│ 1│ │ 1│ │ │ 1│ │ 1
12│ 1│ │ 1│ │ │ 1│ │
13│ │ │ │ │ │ │ │
14│ │ │ │ │ │ │ │
15│ 2│ │ 2│ │ │ 1│ │ 1
───────┼─────────┼───────┼───────┼───────┼───────┼──────┼──────┼──────
Totals │ 70│ 1│ 20│ 45│ 4│ 49│ 11│ 40
───────┴─────────┴───────┴───────┴───────┴───────┴──────┴──────┴──────
Table IV includes specimens obtained at the Magee Hospital from patients
diagnosed as pneumonia. The results among these young students were very
similar to those of the previous chart, where all ages were included.
However, casts and red blood cells were more regularly noted.
From the four tables, we are able to note one or two common facts. In
acute uncomplicated influenza albuminuria occurred 57 times in 447
specimens, or 13 per cent., at the Magee Hospital. Here we dealt
entirely with the young adult. At the Mercy Hospital 88 positive results
of albumin in 344 specimens, or 26 per cent., from patients of all types
were recorded. The common total would be 781 specimens examined, and
141, or 17 per cent., showing albumin.
With the advent of pneumonia the incidence of albuminuria was increased.
At the Magee Hospital it was seen 49 times in 70 examinations, or 70 per
cent.; while at the Mercy Hospital 106 positive results were found in
133 specimens examined, a percentage of 79. The combined figures,
therefore, would show 155 out of 203, or 76 per cent.
The incidence of albuminuria for the epidemic in all its phases would
be, from our figures, 400 in 994 specimens, or 40 per cent.
Red blood cells were present in 5 per cent. of the influenza cases, and
in 11 per cent. of the pneumonias. This was always a microscopic
observation, save in the case of a slightly smoky urine. Even
microscopically the red cells were not numerous. We noted them at times
quite early in the disease in some of the severe cases which presented
epistaxis and hematemesis. Possibly one might consider the early
presence of red blood cells in the urine as a condition analogous to
those just mentioned, although we never saw anything suggesting free
hemorrhage from the kidney. It is probably better to regard the red
cells as a manifestation of an acute nephrosis of toxic origin.
Casts were found in 35 per cent. of the cases showing albuminuria. We
are inclined to feel that this observation is somewhat low, but at the
same time we have noted that in uncomplicated influenza one frequently
sees albumin without casts. We were also impressed with the fact that
casts were not as prominent a feature in the influenzal pneumonias as
they are in frank lobar pneumonia of essentially pneumococcic origin.
During the course of routine examinations several transient glycosurias
were seen. Their transient character was the outstanding feature. The
quantity of sugar was very moderate—our figures were never above 1 per
cent.—and the daily amount of urine was always within normal limits.
Acetone and diacetic acid were absent. A few observations on the blood
sugar showed a rise (.2 to .25), which readily came to normal with
treatment. Clinically these cases were not classed as diabetes mellitus,
but rather as a nervous complication of influenza, involving in some way
the carbohydrate metabolism, probably through the central nervous
system. One case of special interest, which is mentioned elsewhere, was
the association of glycosuria with almost total blindness from a very
intense optic œdema. Sugar (1 per cent.) was present on the day of
admission, while only a trace was noted on the two following days, and
from then on the urine was free from sugar. How many days the sugar had
been present before admission to the hospital we cannot say, but we
could trace the failure of vision back to almost the day of its onset,
which was three weeks previous to our first examination. The eye
symptoms were the only complaints. The patient had had a moderately
sharp attack of influenza a little over two weeks before the first sign
of failure of vision had appeared. We may add that the vision returned
slowly to normal several weeks after admission. The urine and blood
sugar were normal, on a general diet, over a period of one month while
in the hospital. Unfortunately, we have had no further record of this
patient regarding the urine, but her vision still remains normal. Cases
of this type were observed in England after the 1890 epidemic, and are
referred to in Allbutt’s “System of Medicine,” vol. i, on influenza. Our
other glycosuria cases did not present changes in the fundus of the eye.
The glycosuria and glycæmia were transient, and we feel that they do not
represent diabetes mellitus. Most of the patients of this class had long
since recovered from an attack of influenza, and came to the hospital
usually for treatment of various nervous conditions, which at times
simulated neuritis, or otherwise one saw manifestations of general
nervousness, not unlike hyperthyroidism. In all probability, we were
dealing with a hyperglycæmia associated with a hyperactive thyroid
gland. So, after all, the glycosuria, even though rare, is not
bewildering. Symptoms and signs of toxic goitre in direct relation to
the epidemic we claim to have seen, and one is justified, temporarily at
least, in having the thyroid gland father our transient glycosuria.
In relation to the positive sugar findings, we have had numerous
negative examples of almost equal interest. Furunculosis is a very
common sequel of the epidemic. It is well known that in furunculosis
there is a hyperglycæmia, but no glycosuria and no acetone or diacetic
acid in the urine. All our blood sugar readings were above the normal,
and at times unusually high. They varied from .2 to .41. This last
unusually high amount was in a young physician with recurrent
furunculosis following influenza. There was no glycosuria at any time.
Elimination of carbohydrates not only brought the blood sugar to normal
limits in the course of a week, but also assisted in the cure of the
furunculosis, but in a longer time. In all of this group we saw no
incidence of polyuria or glycosuria.
_Hematology_
There is very little evidence, as shown in the literature, that special
study on the blood during past influenzal epidemics has been made. A few
references to alterations in the count of cells have been reported for
the last epidemic (1890), but they are, as a rule, very brief
statements. Cabot notes a normal leucocyte count in two-thirds of the
cases, and a moderate increase in the rest. Several observers call
attention to the leucopenia during the height of the disease, with a
subsequent rise after the temperature has fallen to normal. According to
Rieder and Herman (American Journal of Medical Science, 1893, cv. 696),
the leucocytes were not increased in simple influenza, and only very
slightly in the pneumonia following this disease. Herman also noticed a
decline in the leucocytes in pneumonia as a fatal ending ensued. This
finding was one of the few recorded for the 1890 epidemic. Emerson
(Emerson Clinic Diagnosis, 1911, 558) found in influenza almost one-half
of the cases showing more than 10,000 leucocytes, some even reaching
25,000. He further notes that early in the disease the count may be low,
3,000 to 5,000, but it usually rose sharply, to fall again when the
temperature comes to normal. He lays stress on obtaining a leucocyte
curve for each case in order to get a true picture of what changes
occur. The past epidemic has brought out many observations on this
subject. They vary somewhat, as is to be expected, but a common factor
seems to be more or less basic—namely, a leucopenia or a normal count is
the most significant single blood picture we have of uncomplicated
influenza. Further, a leucocytosis is fairly generally, and we believe
correctly, interpreted as evidence of a secondary bacterial invasion in
this particular epidemic, and usually of the respiratory system. The
leucopenia is as much a part of the clinical picture of influenza as it
is of typhoid fever. Leucocytosis always means secondary invasion by
other organisms.
During the recent epidemic the clinical laboratory department of the
School of Medicine, University of Pittsburgh, has made 747 blood counts
on influenza cases. In most of the cases blood counts were made as a
routine, while repeated counts were done only on selected patients.
The following table indicates the leucocyte count for our series,
comprising the epidemic in all of its phases. There are a few general
points which appear striking that we may refer to at this time, and
leave until later the discussion of the minor details. One-third of the
counts, including, as they do, many cases of pneumonia, showed a
leucopenia, while 70 per cent. of the total number fell under 10,000.
This last group contains more pneumonias and other complications than
simple influenza. But 5 per cent. of the cases counted showed more than
20,000. All of these undoubtedly had pneumonia or some other
complication. Comparing this finding with our experience in the past
before the epidemic with the pneumococcic lobar pneumonia, one sees at
once that, as far as this type of clinical observation is concerned, the
two pneumonias are totally different. The writer remembers but one case
of lobar pneumonia which showed a persistent white count falling below
10,000. Certainly in this community lobar pneumonia and low leucocyte
counts were unusual combinations until the present epidemic. Further,
the evident depression of leucocytosis even where there was an actual
increase is indicated by 95 per cent. of our counts being below 20,000.
This leads us to state that the pneumococcus, although present in
practically all of our pneumonias, produced in only a small percentage
of the bloods we examined its characteristic increase. The toxic factor
of this influenzal epidemic certainly causes a marked change in the
white cells of the blood.