═══════╤════╤════════════════════════════╤════════════╤══════════════════════
AUTOPSY│AGE.│ RIGHT LUNG. │ TYPE OF │ LEFT LUNG.
NUMBER.│ │ │ LESION. │
───────┼────┼──────┬─────────────────────┼────────────┼────────┬─────────────
│ │WEIGHT│INVOLVEMENT OF LOBES.│ │ WEIGHT │ INVOLVEMENT
│ │ OF │ │ │OF LUNG.│ OF LOBES.
│ │LUNG. │ │ │ │
───────┼────┼──────┼──────┬───────┬──────┼────────────┼────────┼──────┬──────
│ │ │UPPER.│MIDDLE.│LOWER.│ │ │UPPER.│LOWER.
───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼──────
741│ 18│720 G.│ + │ + │ ++ │Lobar S. & │ 850 G.│ + │ ++
│ │ │ │ │ │ H. │ │ │
───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼──────
743│ 20│825 G.│ + │ + │ + │Lobular S. &│ 1375 G.│ +++ │ +++
│ │ │ │ │ │ H. │ │ │
│ │ │ │ │ │ │ │ │
───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼──────
744│ 30│900 G.│ + │ – │ ++ │Lobar and │ 900 G.│ ++ │ ++
│ │ │ │ │ │ Lobular S.│ │ │
│ │ │ │ │ │ & H. │ │ │
───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼──────
745│ 18│575 G.│ + │ – │ ++ │Lobular S. &│ 480 G.│ – │ ++
│ │ │ │ │ │ H. │ │ │
───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼──────
746│ 21│900 G.│ + │ ++ │ +++ │Lobar S. & │ 650 G.│ + │ +++
│ │ │ │ │ │ H. │ │ │
───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼──────
747│ 27│ 1510│ +++ │ ++ │ +++ │Lobar S. & │ 1000 G.│ +++ │ +++
│ │ G.│ │ │ │ H. │ │ │
───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼──────
748│ 22│900 G.│ + │ + │ +++ │Lobar and │ 1250 G.│ + │ +++
│ │ │ │ │ │ Lobular S.│ │ │
│ │ │ │ │ │ & H. │ │ │
───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼──────
749│ 23│ 1480│ ++ │ ++ │ +++ │Lobar S. & │ 1250 G.│ ++ │ +++
│ │ G.│ │ │ │ H. Slight │ │ │
│ │ │ │ │ │ Purulent. │ │ │
───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼──────
750│ 24│ 1200│ +++ │ + │ +++ │Lobar and │ 825 G.│ + │ +++
│ │ G.│ │ │ │ Lobular. │ │ │
│ │ │ │ │ │ Early │ │ │
│ │ │ │ │ │ Purulent. │ │ │
───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼──────
751│ 22│ 1250│ – │ – │ +++ │Lobar │ 610 G.│ ± │ ±
│ │ G.│ │ │ │ Purulent. │ │ │
───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼──────
752│ 27│ 1125│ +++ │ + │ +++ │Lobar S. & │ 775 G.│ ± │ +++
│ │ G.│ │ │ │ H. │ │ │
───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼──────
756│ 22│ 1000│ ++ │ ++ │ ++ │Lobar S. & │ 820 G.│ +++ │ ++
│ │ G.│ │ │ │ H. Slight │ │ │
│ │ │ │ │ │ Purulent. │ │ │
───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼──────
757│ 21│815 G.│ ++ │ – │ ++ │Lobular S. &│ 1075 G.│ +++ │ +++
│ │ │ │ │ │ H. │ │ │
│ │ │ │ │ │ │ │ │
───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼──────
758│ 22│ 1150│ +++ │ + │ + │Lobar │ 1400 G.│ +++ │ +++
│ │ G.│ │ │ │ Purulent │ │ │
───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼──────
761│ 21│ 1250│ +++ │ ++ │ +++ │Lobar S. & │ 550 G.│ + │ +
│ │ G.│ │ │ │ H. and │ │ │
│ │ │ │ │ │ Lobular │ │ │
│ │ │ │ │ │ Purulent. │ │ │
───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼──────
762│ 21│680 G.│ + │ + │ + │Lobular S. &│ 750 G.│ + │ +++
│ │ │ │ │ │ H. │ │ │
│ │ │ │ │ │ │ │ │
───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼──────
763│ 22│920 G.│ + │ – │ + │B. P. and │ 540 G.│ – │ +
│ │ │ │ │ │ Lobar S. &│ │ │
│ │ │ │ │ │ H. │ │ │
───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼──────
764│ 23│725 G.│ – │ + │ + │Lobular S. &│ 550 G.│ + │ +
│ │ │ │ │ │ H. │ │ │
───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼──────
765│ 25│ 1100│ ++ │ – │ ++ │Lobar S. & │ 1400 G.│ – │ +++
│ │ G.│ │ │ │ H. │ │ │
│ │ │ │ │ │ │ │ │
───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼──────
767│ 25│ 1075│ + │ +++ │ +++ │Lobar and │ 850 G.│ – │ ++
│ │ G.│ │ │ │ Lobular S.│ │ │
│ │ │ │ │ │ & H. and │ │ │
│ │ │ │ │ │ Lobular │ │ │
│ │ │ │ │ │ Purulent. │ │ │
───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼──────
770│ 21│900 G.│ ++ │ ++ │ ++ │Lobar S. & │ 750 G.│ ++ │ ++
│ │ │ │ │ │ H. and │ │ │
│ │ │ │ │ │ Lobular │ │ │
│ │ │ │ │ │ Purulent. │ │ │
───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼──────
773│ 22│ 2050│ +++ │ ++ │ +++ │Lobar S. & │ 780 G.│ – │ +++
│ │ G.│ │ │ │ H. and │ │ │
│ │ │ │ │ │ Purulent. │ │ │
───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼──────
778│ 22│ 1100│ ++ │ + │ ++ │Interstitial│ 975 G.│ ++ │ ++
│ │ G.│ │ │ │ Pneumonia.│ │ │
───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼──────
781│ 21│ 1000│ +++ │ ++ │ +++ │Lobar S. & │ 540 G.│ + │ +++
│ │ G.│ │ │ │ H. │ │ │
│ │ │ │ │ │ │ │ │
───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼──────
782│ 18│650 G.│ + │ – │ ++ │Lobular S. &│ 875 G.│ ++ │ +++
│ │ │ │ │ │ H. Slight │ │ │
│ │ │ │ │ │ Purulent. │ │ │
───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼──────
783│ 21│ 1250│ +++ │ +++ │ +++ │Lobar S. & │ 580 G.│ + │ ++
│ │ G.│ │ │ │ H. │ │ │
───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼──────
784│ 21│ 1590│ +++ │ +++ │ +++ │Lobar │ 1400 G.│ +++ │ +++
│ │ G.│ │ │ │ Purulent. │ │ │
│ │ │ │ │ │ │ │ │
───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼──────
786│ 20│ 1100│ ++ │ +++ │ +++ │Lobar S. & │ 700 G.│ – │ ++
│ │ G.│ │ │ │ H. Slight │ │ │
│ │ │ │ │ │ Lobular │ │ │
│ │ │ │ │ │ Purulent. │ │ │
───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼──────
787│ 21│750 G.│ ++ │ – │ ++ │Lobular S. &│ 1125 G.│ +++ │ +++
│ │ │ │ │ │ H. │ │ │
───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼──────
791│ 21│775 G.│ + │ ++ │ ++ │Lobular S. &│ 1050 G.│ ++ │ +++
│ │ │ │ │ │ H. and │ │ │
│ │ │ │ │ │ Purulent. │ │ │
───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼──────
792│ 21│ 1050│ + │ + │ +++ │Lobar and │ 950 G.│ + │ ++
│ │ G.│ │ │ │ Lobular S.│ │ │
│ │ │ │ │ │ & H. │ │ │
───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼──────
793│ 18│500 G.│ – │ – │ + │Slight │ 435 G.│ - │ +
│ │ │ │ │ │ Lobular S.│ │ │
│ │ │ │ │ │ & H. │ │ │
───────┴────┴──────┴──────┴───────┴──────┴────────────┴────────┴──────┴──────
═══════╤════════════╤════════════╤════════════╤══════════
AUTOPSY│ TYPE OF │ PLEURA. │ ABSCESS OF │ DAY OF
NUMBER.│ LESION. │ │ LUNG. │ DISEASE.
───────┼────────────┼──────┬─────┼────────────┼──────────
│ │ │ │ │
│ │ │ │ │
│ │ │ │ │
───────┼────────────┼──────┼─────┼────────────┼──────────
│ │RIGHT.│LEFT.│ │
───────┼────────────┼──────┼─────┼────────────┼──────────
741│Lobar S. & │S.F. │S.F. │ │ 3d.
│ H. │ │ │ │
───────┼────────────┼──────┼─────┼────────────┼──────────
743│Lobar S. & │F. │S.F. │ │ 5th
│ H. Early │ │ │ │
│ P. │ │ │ │
───────┼────────────┼──────┼─────┼────────────┼──────────
744│Lobar S. & │S.F. │S.F. │ │ 7th
│ H. │ │ │ │
│ │ │ │ │
───────┼────────────┼──────┼─────┼────────────┼──────────
745│B.P. with │S.F. │– │ + │ 10th
│ Necrosis. │ │ │ │
───────┼────────────┼──────┼─────┼────────────┼──────────
746│Lobar S. & │– │– │ │ 5th
│ H. │ │ │ │
───────┼────────────┼──────┼─────┼────────────┼──────────
747│Lobar S. & │S.F. │– │ │ 6th
│ H. │ │ │ │
───────┼────────────┼──────┼─────┼────────────┼──────────
748│Lobar S. & │– │– │ │ 4th
│ H. and │ │ │ │
│ B.P. │ │ │ │
───────┼────────────┼──────┼─────┼────────────┼──────────
749│Lobar S. & │F. │– │ │ 4th
│ H. Slight │ │ │ │
│ P. │ │ │ │
───────┼────────────┼──────┼─────┼────────────┼──────────
750│Lobar and │F. │F. │ │ 9th
│ Lobular. │ │ │ │
│ Early P. │ │ │ │
│ │ │ │ │
───────┼────────────┼──────┼─────┼────────────┼──────────
751│B.P. slight.│S.F. │– │ │ 7th
│ │ │ │ │
───────┼────────────┼──────┼─────┼────────────┼──────────
752│B.P. and │F. │S.F. │ │ 13th
│ Lobar P. │ │ │ │
───────┼────────────┼──────┼─────┼────────────┼──────────
756│Lobar and │F. │S.F. │ │ 8th
│ Lobular S.│ │ │ │
│ & H. │ │ │ │
───────┼────────────┼──────┼─────┼────────────┼──────────
757│Lobar S. & │F. │F. │ │ 6th
│ H. and │ │ │ │
│ Purulent. │ │ │ │
───────┼────────────┼──────┼─────┼────────────┼──────────
758│Lobar │F. │F. │ │ 14th
│ Purulent. │ │ │ │
───────┼────────────┼──────┼─────┼────────────┼──────────
761│Lobular S. &│– │– │ │ 7th
│ H. │ │ │ │
│ │ │ │ │
│ │ │ │ │
───────┼────────────┼──────┼─────┼────────────┼──────────
762│Lobar S. & │S.F. │S.F. │ │ 10th
│ H. and │ │ │ │
│ Lobular P.│ │ │ │
───────┼────────────┼──────┼─────┼────────────┼──────────
763│B.P. │F.P. │– │ │ 11th
│ │ │ │ │
│ │ │ │ │
───────┼────────────┼──────┼─────┼────────────┼──────────
764│B.P. │– │– │ │ 9th
│ │ │ │ │
───────┼────────────┼──────┼─────┼────────────┼──────────
765│Lobar S. & │– │– │ │ 9th
│ H. and │ │ │ │
│ Early P. │ │ │ │
───────┼────────────┼──────┼─────┼────────────┼──────────
767│Lobar S. & │– │F. │ │ 10th
│ H. Lobular│ │ │ │
│ P. │ │ │ │
│ │ │ │ │
│ │ │ │ │
───────┼────────────┼──────┼─────┼────────────┼──────────
770│Lobar S. & │S.F. │F. │ + │ 11th
│ H. Lobular│ │ │ │
│ P. │ │ │ │
│ │ │ │ │
───────┼────────────┼──────┼─────┼────────────┼──────────
773│Lobar S. & │F. │F. │ │ 20th
│ H. Lobular│ │ │ │recurrence
│ P. │ │ │ │
───────┼────────────┼──────┼─────┼────────────┼──────────
778│Interstitial│S.F. │S.F. │ │ 23d
│ Pneumonia.│ │ │ │
───────┼────────────┼──────┼─────┼────────────┼──────────
781│Lobar S. & │S.F. │S.F. │ + │ 5th
│ H. │ │ │ │
│ Purulent. │ │ │ │
───────┼────────────┼──────┼─────┼────────────┼──────────
782│Lobar S. & │F. │F. │ │ 8th
│ H. and │ │ │ │
│ Early P. │ │ │ │
───────┼────────────┼──────┼─────┼────────────┼──────────
783│Lobar S. & │S.F. │S.F. │ │ 8th
│ H. │ │ │ │
───────┼────────────┼──────┼─────┼────────────┼──────────
784│Lobar S. & │S.F. │S.F. │ │ 8th
│ H. and │ │ │ │
│ Purulent. │ │ │ │
───────┼────────────┼──────┼─────┼────────────┼──────────
786│Lobar S. & │S.F. │– │ │ 4th
│ H. and │ │ │ │
│ Early P. │ │ │ │
│ │ │ │ │
───────┼────────────┼──────┼─────┼────────────┼──────────
787│Lobar S. & │S.F. │S.F. │ │ 8th
│ H. │ │ │ │
───────┼────────────┼──────┼─────┼────────────┼──────────
791│Lobar S. & │F. │S.F. │ │ 6th
│ H. and │ │ │ │
│ Slight P. │ │ │ │
───────┼────────────┼──────┼─────┼────────────┼──────────
792│Lobar and │S.F. │S.F. │ │ 6th
│ Lobular S.│ │ │ │
│ & H. │ │ │ │
───────┼────────────┼──────┼─────┼────────────┼──────────
793│Slight │– │F. │ Strep. │ 10th
│ Lobular │ │ │Bacteriemia.│
│ Purulent. │ │ │ │
───────┴────────────┴──────┴─────┴────────────┴──────────
S—Serous. H—Hemorrhagic. P—Purulent. B.P.—Broncho-pneumonia.
S.F.—Serofibrinous. F.—Fibrinous. F.P.—Fibrinopurulent.
It was very evident that the smaller bronchi and bronchioles were much
more readily involved in a severe inflammatory reaction than the larger
tubes. A purulent inflammation was not uncommonly found in the
bronchioles of the lung when a pneumonic state with leucocytic
infiltration was present. Even where such purulent infiltration of the
walls of the bronchioles was readily demonstrable the trachea and main
bronchi were devoid of this intense reaction. These purulent
inflammations were not uniformly distributed in the bronchioles of the
lung, but only occurred in those regions where the parenchymatous
tissues were in themselves involved in a purulent reaction. It was
difficult to find the evidence whether the purulent bronchitis preceded
or followed the presence of a purulent pneumonia. The intimacy of the
lung tissues with those of the small bronchioles makes it impossible for
one or other of these structures to escape when one of them is
implicated in a purulent reaction. It is equally important to appreciate
that to a considerable extent the lung tissue surrounding the small
bronchioles becomes involved by a direct radial extension through the
walls of the thin respiratory tubes. Such extension laterally is
assisted by the free lymphatic communication lying about the bronchioles
and stretching into the lung parenchyma. Purulent processes of the small
air tubes always showed a similar reaction in the interstitial tissues
of the neighboring air sacs.
Our material did not permit of following the bronchial reactions to
their conclusion. In some instances we have found that where abscesses
developed within the lung the contiguous bronchi and bronchioles either
became eroded or suffered intense suppurative inflammatory lesions on
their inner surface. The manner in which repair of the more common
inflammatory processes of the bronchi is accomplished could not be
demonstrated in the cases dying during the acute stage. In one case an
organizing bronchitis was associated with an organizing lobular
pneumonia. In this instance the connective tissues were proliferating
freely from the inner wall of the bronchi, there being no evidence of a
basement membrane at the point where the connective tissue was growing.
The development of the connective tissue appeared to be spontaneous and
was not taking place within an unresolved fibrinous exudate. In as much
as the fibrosing process was largely scattered through all of the lobes,
the numerical involvement of the respiratory tubes was quite great. In
this instance the amount of obstruction which was imposed upon the
respiratory tissues by the fibrosing pneumonia and bronchitis was
sufficient to cause considerable distress and dyspnœa during the last
few days of the patient’s life. The amount of dyspnœa was out of
proportion to the clinical manifestations of pulmonary involvement, and
from a clinical point of view it was difficult to arrive at a conclusion
of the nature of the lung lesion.
Undoubtedly during the subsidence of the inflammatory process within the
bronchi the gradual restitution of the tissues with little or no
fibrosis is accompanied by a reproduction of the lining membrane arising
from the epithelial remnants in the small mucous crypts. In a few cases
lately coming to autopsy where the patients had suffered an influenza
five or six weeks previously, the mucosa of the trachea and bronchi had
assumed its normal appearance and was fully clothed by a normal
epithelial covering.
_Lung—Early Stage_
We have just discussed the importance of the inflammation of the trachea
and bronchi in the cases of influenza. It is our belief that every case
of influenza has some tracheitis, and a great many have both tracheitis
and bronchitis. This is true in the absence of localizing signs and
symptoms, as was evident even in these cases in which the simple
influenza passed into its more severe type with its pulmonary lesions.
In many of these instances clinical evidences of an inflammatory
reaction in the respiratory tubes were wanting, while the reactions
observed at autopsy were often astounding.
Just as we feel that simple influenza and inflammation of the
respiratory tubes go hand in hand, or better that these respiratory
localizations are the all-important ones in every case of simple
influenza, so, too, we are of the belief that the pulmonary lesions bear
the same relation to all cases of severe and fatal epidemic influenza.
We hold that no case comes to his death through acute epidemic influenza
without having a lesion in the lung. The pulmonary condition, therefore,
is of first importance and its analysis is imperative for a proper
understanding of this disease. There has been divided opinion as to the
part played by the pulmonary lesion in epidemic influenza, some holding
that it is to be looked upon as a part of the disease and others that it
must be viewed as a complicating lesion. Complications of various kinds
are very common, and there are a number of conditions arising in the
lung (abscess, gangrene, necrosis) which must be viewed as
complications. There is, however, a type of pneumonia, and here I use
the term in its broad sense, which is not in truth a complication but
merely a wider extent of involvement of the respiratory tract by the
same virus which is always present to cause lesions in the respiratory
tubes. The reaction within the lungs is distinctive and differs from the
pneumonias which are met with under other conditions and with various
bacterial agencies. Nor are our findings in this matter unique for this
epidemic. They have been described and discussed in the past. True it is
that, like in the epidemic which has just passed us, the incidence of
clinical and pathological pneumonia varied quite widely in different
communities, so, too, the reports of past epidemics do not give a
uniform description of a pulmonary lesion. Where, however, the analysis
has been made during the four weeks’ period of the acute epidemic and
where the descriptions have been recorded by painstaking observers, the
similarity with our present findings is very striking. I would refer in
particular to one report made in 1893 in Petrograd by Kuskow. His report
deals with 40 carefully studied cases in which records both macroscopic
and microscopic were accurately made.
One of the great difficulties in placing an accurate interpretation upon
the pulmonary findings lies in the fact that true pneumonia as seen in
epidemic influenza in man has not been reproduced in animals.
Furthermore, as the majority of the fatal human cases of epidemic
influenza with their associated pneumonias present a mixed infection of
the lung tissues, it is difficult, if not impossible, to indicate the
lesions which have resulted through the activity of one of these as
against those induced by the other bacteria present. In our own
carefully studied cases wherein bacteriological cultures were taken from
every lung there was not a single instance in which the influenza
bacillus was present in pure culture. This is more fully commented upon
in the studies by Dr. Holman, but the point we wish to make here is the
difficulty in arriving at a conclusion in our material as to the actual
effects induced by any one type of organism. As it is fully discussed by
Dr. Holman we are convinced of the importance of the influenza bacillus
in this epidemic. We also appreciate that pneumonia lesions in animals
have been induced by a variety of materials gained from influenza
patients, but yet in view of the abnormal manner of producing such
lesions these are hardly comparable to those in man. We may well expect
severe œdema, inflammation and hemorrhage, if in guinea pigs, rabbits
and monkeys we introduce by intra-tracheal insufflation large quantities
of fluid suspensions of bacteria. And thus we find positive results
obtained by the use of a filtrable virus, streptococci, influenza
bacilli and other organisms. The lung is a sensitive tissue which quite
readily responds to a variety of irritants. In many respects some of
these lesions simulate those in influenza, but still we are far from the
conclusion that the disease, influenza, with all its manifestations has
been actually reproduced.
The pathology of the pulmonary lesions in acute epidemic influenza is so
distinctive that except for the late purulent stage which may resemble
types of reinfected and unresolved pneumonia the condition cannot be
confused with the stages of frank lobar pneumonia. We appreciate that
this is a very positive statement, and that opposition will be taken by
those who resting their opinion upon individual factors may claim that a
clear distinction from other forms of pneumonia is not available. We,
however, base our opinion not upon a single feature, but upon the
combined pathological complex observed in many individual cases. These
features are mainly those seen in the type of the lesion, the character
of the distribution, extent of involvement and the multiple stages so
commonly present at one time in different portions of the lung. The type
lesion that has become so well known in pneumococcus lobar pneumonia has
its distinctive stages which for teaching purposes are divided into the
stage of (1) congestion, (2) red hepatization, (3) gray hepatization and
(4) resolution. In dealing with lobar pneumonia from the standpoint of
illustrating these stages the majority of teachers annually confess
their inability to present for the student’s study the stage of
congestion. The student is impressed that the congestive stage of lobar
pneumonia is very transient and rapidly passes into the stage of red
hepatization. Patients do not die with pneumococcus pneumonia in the
stage of congestion. And this is also largely true of the stage of red
hepatization, which is but rarely seen at the autopsy table. This
community (Pittsburgh) gives its large quota to the mortality statistics
of pneumococcus pneumonia, but it is most unusual to meet with a
specimen of red hepatization except for the borders of the advancing
gray area. And, furthermore, red hepatization even when found in the
unusual cases shows remarkably little of this character when seen under
the microscope. True it is that a certain number of red blood cells will
be found in the alveoli and a certain degree of congestion will occupy
the alveolar walls, but its extent is far less than what we may have
hoped to demonstrate to others. So that broadly speaking the intensely
congested lung with or without red hepatization is unusual in our frank
lobar pneumonia. This was quite the reverse in our cases of acute
epidemic influenza-pneumonia. Furthermore lobar pneumonia in the great
majority of instances illustrates a distribution distinctive for the
name. Massive lobar, or pneumococcus pneumonia is found to occupy one or
more lobes or parts of lobes. The involved lobe is fairly uniform in the
stage of the inflammatory process. If it is in the early gray stage,
this will be seen with equal intensity in the different areas of the
lobe. Patches of pneumonia in different stages within the same lobe are
not to be found, while this finding is not uncommon in the pneumonias of
acute epidemic influenza. And lastly, the frequency with which an
inflammatory œdema occupied the lungs in the cases of influenza was in
quite striking contrast with the dry fibrinous lesion of common
pneumonia. This wet state of the lung was but a stage in the
inflammatory process varying in its extent in the different periods, but
nevertheless inducing a character in the early pulmonary lesions which
was quite foreign to our usual finding. This wet state also assisted in
modifying the subsequent picture so that when the lung assumed its gray
appearance it was rather of a slimy character than of the firm dry
nature. In this late gray stage the slimy lung somewhat resembled the
appearance of unresolved pneumonia where this condition had been brought
about by a new infection upon the original cause of the pneumonia.
It is incorrect in influenza pneumonia to speak of the lesions as lobar
pneumonia or broncho-pneumonia if by these terms we have in mind the
pathological characters observed in the pneumococcic pneumonia with its
lobar or bronchial distribution. Influenza-pneumonia appeared with both
lobar and lobular characteristics. Nearly every case had both types of
lesions present, but the nature of the inflammatory process is so
decidedly different from that of the ordinary endemic pneumonia that a
confusion in the interpretation is likely to arise and in fact has
already raised a considerable polemic. Influenza-pneumonia is commonly
lobar, lobular or bronchial in distribution. It is, however, not of the
characters that are associated with the lesions designated under these
terms. When, therefore, we here use the word “lobar” we mean lobar _in
distribution_ but not lobar in type. As will be seen from our table, it
was usual to have multiple lobes involved. But the lesions, not only in
the different lobes varied in their character and distribution, but even
within the same lobe a variety of types was present.