═══════════════════════════════════════════════╤═══════════════════════
Day of Pneumonia on Which Death Occurred │ No. of Cases
───────────────────────────────────────────────┼───────────────────────
Second │ 2
Third │ 4
Fourth │ 7
Fifth │ 6
Sixth │ 7
Seventh │ 3
Eighth │ 1
Tenth │ 1
Twentieth │ 1
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To a certain degree we were able to analyze the types of the lesions as
they occurred in the different stages and progress of the pulmonary
inflammation. Briefly, these were as follows: the earliest stage of
congestion following rapidly upon the infection from the bronchi was
followed by (1) inflammatory œdema, (2) hemorrhage, (3) cellular exudate
(a. mononuclear cells, b. leucocytes, c. interstitial infiltration) and
(4) resolution or organization, abscess, infarct and gangrene. The
majority of our cases died during the stages of congestion, hemorrhage
or early purulent infiltration. In the early stages the amount of fibrin
was small or entirely absent, later, with the appearance of leucocytes,
some fibrin was present.
For the estimation of the time elapsing between the onset of the
pneumonia and death we are dependent upon the clinician. This is often
quite difficult to do, in as much as with a primary respiratory disease,
such as epidemic influenza represents, it is very difficult to determine
the time when there is a transition from the inflammatory process of the
upper respiratory tubes to that of the pulmonary tissue. In many of the
cases where from the onset there was intense prostration and every
evidence of marked intoxication the clinical manifestations of localized
processes taking place in the respiratory system were very much in the
background and often of insidious progress. In four of our cases it
appeared as if the pulmonary manifestations had made their appearance
with the first sudden and severe onset of the influenza. On the other
hand, also, the clinical signs and symptoms of lung involvement were
different from those of frank lobar pneumonia. We would, from our
experience at the autopsy table, say that where in the cases of epidemic
pneumonia there are present the signs of pulmonary consolidation like
those of true lobar pneumonia, that there has been an antecedent period
of a pulmonary lesion which passed unrecognized by the clinician. To
more clearly state the case, whereas in lobar pneumonia the stage of
congestion preceding the stage of red hepatization gives rise to no
signs whereby the clinician can indicate the time of its onset or
determine the time when it has passed into the succeeding stage, and
moreover, the stage of congestion is of short duration to be measured in
a period of a few hours, this stage in epidemic influenza though equally
indefinite in its clinical manifestations is much prolonged, lasting not
only a period of hours but even a period of several days. It is this
pulmonary state which is difficult or even impossible to recognize in
the living. All gradations of it occur and the clinician can only
broadly suggest from all the evidence at hand, the period when
inflammation with definite exudate began in the lung. In as much as the
total length of illness of a number of cases was only three, four and
five days, whereas there was nothing at the onset to suggest pulmonary
involvement, we can estimate approximately, at least, the duration of
the lung condition. This makes it possible to give a relative estimate
of the character of the lesions present at different periods of time.
The outstanding finding, as we will discuss again, was that a distinct
and peculiar pulmonary reaction was primarily imposed upon the lung,
which made its appearance at periods different from those of frank lobar
pneumonia.
We were repeatedly surprised at finding death to have occurred during
the stage of acute congestion with some hemorrhage and inflammatory
œdema of lung and in the absence of any sign of grey hepatization or
purulent infiltration. In many of these cases the involved areas of lung
though heavy and œdematous, were still partly air-containing and the
amount of lung involvement was insufficient, on the basis of mechanical
interference, in accounting for the severity of the clinical symptoms
and the fatal outcome. This must have impressed everyone dealing with
the autopsies during the acute epidemic. It immediately suggests that in
some cases at least the pulmonary lesion, in as far as incapacitating
the external respiratory system, was not the sole or even the important
cause of death, but that a condition of intoxication, borne out by the
evidence of damage in muscles, blood and kidney is a large factor of
danger in this disease.
We shall briefly describe the important pulmonary findings as we have
met with them in the successive stages of influenza-pneumonia. This, we
hope, will make clear the interpretation of the pathology of the lung
lesion of the epidemic as it came under our observation.
The earliest pulmonary lesion which we encountered was one of
congestion, inflammatory œdema and hemorrhage. These three conditions
were usually present at the same time and were found in the height of
intensity in all of the cases dying within the first four days of
illness. During this early period these manifestations of inflammation
were not accompanied by definite red or grey hepatization as might
ordinarily be expected. The lesions varied greatly in their intensity,
the œdema always being very prominent, while the hemorrhage varied from
a diffuse infiltration of the involved lobe or added to this, was
localized in massive collections four or five cm. in diameter and
commonly occupying the central portions of the lobes. We have seen
several hemorrhages lying in close proximity to each other with their
borders coalescing and leading to a larger central involvement. In the
regions where the hemorrhage and inflammatory œdema were diffuse, air
was still present within the lung tissue, sometimes to an extent
permitting the lung tissue to float on water but more often in quantity
sufficient only to suspend the tissue at various depths. On pressure the
fine air bubbles were recognized amidst the blood-stained fluid. Acute
compensatory emphysema often occupied the anterior borders of the lobes
or formed interstitial blebs beneath the pleura. The quantity of fluid,
inflammatory œdema and hemorrhage, contained within these bulky lobes
was often very surprising. A lobe when compressed would leak fluid with
the ease that it could be obtained from a sponge. Out of the lower lobe
on one occasion we pressed 700 c.c. of limpid blood-stained exudate. The
acute emphysema which may make its appearance suddenly, is