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Acute bronchitis and tracheitis 26
Subacute bronchitis and tracheitis 1
Acute mucopurulent tracheitis 5
Acute purulent bronchitis 2
Acute mucopurulent bronchitis 7
Ulcers of trachea 1
Acute bronchiectasis 1
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Thus whereas we have indicated that the inflammation of the trachea and
of the large bronchi is of a peculiar kind and remains confined to the
tissue lying inwardly from the cartilage rings, we found that where
these structures give place to a loose muscle tissue with a more
extensive lymphatic drainage the zone of inflammation is not so limited,
but proceeds outwardly into the neighboring tissues. We often use the
terms bronchus and bronchioles very freely without clearly
distinguishing any real difference. In a study of the inflammatory
reactions of the respiratory tubes in epidemic influenza (as well as in
other infections) it is best to accept the anatomical definition that
the bronchioles not only represent the minute tubules passing to the
alveoli, but also those small air passages which devoid of cartilage,
mucous glands and heavy connective tissue stroma are in close relation
to the parenchymatous tissues of the lung. These soft muscular tubes
possess blood and lymphatic vessels which freely communicate with the
blood vessels of the lung alveoli. It is in association with these
distant tubes that concomitant inflammatory reactions are found in the
alveoli and in the bronchial tubes.
Desquamation of the epithelial lining is to be found in every size of
bronchial tube where the infection has caused an acute inflammatory
reaction. Throughout the pulmonary tissues where the lung is found in
some stage of influenzal pneumonia the bronchial tubes, both large and
small, are either entirely denuded of the mucosa or show only remnants
attached to irregular areas. In the smaller passages dense clusters of
desquamated cells are sometimes found within the lumen and indicate the
accumulation of a desquamated epithelium obtained from portions of the
tubular system in deeper portions of the lung. In the early stages, this
desquamation is accompanied by a serous exudate and a certain amount of
hemorrhage. Later we find masses of leucocytes which fill up the tube,
and though appearing to arise from these structures have in fact largely
come from the lung alveoli. Like the larger bronchial tubes the distant
ramifications show relatively little cellular reaction in their walls in
the early period. It is only when the neighboring lung tissues are
extensively implicated in a purulent inflammation that we find a similar
exudate occupying the tissues of the bronchioles. Polymorphonuclear
leucocytes are equally distributed through the region of the basement
membrane, submucosa, muscular coat and outer connective tissue layer.
Some grades of degeneration may occupy the inner surface wherein the
basement membrane first shows a homogeneous swelling and later a
granular degeneration. In a few instances where the small bronchioles
have communicated with regions with abscess formation an ulcerating
surface occupied the inner boundary.
The evidence in the smaller bronchial tubes, both those with cartilage
and those without, that an inflammatory reaction of some degree may
occupy the muscular coat is of importance. We have found reactions of
inflammation in the muscular coat varying from a mild œdema and cellular
exudate to an intense polymorphonuclear leucocyte involvement. In the
latter the muscle fibers showed evidence of degenerative change and
suggested an acute weakening of this layer. We lay particular importance
upon this finding as indicating a causative factor in the development of
acute bronchiectasis as was met with in one of our cases. In this
particular instance the bronchi passing to the lower lobes of each lung
were unusually dilated and could be followed, in the gross, to their
distant extremities. The dilatation was more or less uniform and no
large pouches or cavities had developed. A mucopurulent exudate was
found occupying these dilated tubes. Others have likewise observed the
development of acute bronchiectasis under these conditions. Goodpasture
and Burnett found that as early as the second to the fourth day one of
the striking appearances was the gaping dilated condition of the
infundibula, and the tendency to dilatation of the air passages was
manifested in a bronchiectasis in 4 out of 30 cases. Boggs as well as
Lord have reported upon chronic bronchiectasis associated with the B.
influenzæ and there appeared to be evidence that a certain percentage of
cases recovering from influenza permanently develop irregular
dilatations of the bronchial tubes.
The recognition of inflamed bronchi or bronchioles was never difficult.
In the gross the presence of the abnormal exudate and the intense
injection of the mucosal surfaces always attracted attention to the
inflammatory state. Furthermore where the mucosa had been desquamated
the surface of these tubes was found to be quite granular if closely
observed. With moderate magnification by means of a hand lens the
granular appearance was shown to be due to the engorged vessels. Much
easier, of course, was the recognition of the inflammatory reaction by
the microscope. The importance, however, of the bronchitis and
bronchiolitis lay in the amount of involvement which had occurred in the
neighboring tissues. As we, however, indicated elsewhere, we do not
doubt that many of the cases of three-day fever have a state of
tracheitis and bronchitis equal to that which we have observed in many
of our cases. Whether the inflammatory reaction progressed beyond the
firmer bronchial tubes to the softer and more vascular structures would
be difficult to say where our evidence rests upon the clinical findings
alone. It is, however, probable that a certain number of the severe and
sharp attacks of influenza not only cause a tracheitis and bronchitis of
the larger tubes, but also extend more deeply into the smaller
ramifications tending to simulate the reactions which we have above
described. When we ask ourselves, however, how distantly must the
infection invade the smaller bronchial tubes before involving the
parenchymatous tissues of the lung we are at a loss to enunciate a
general rule. It is more than probable that there are modifying
influences which determine whether the bronchitis with a certain amount
of its bronchiolitis will progress to a true pneumonia or will remain
localized to these tubular systems. I can well appreciate that in the
event that a bronchitis has an inflammatory reaction accompanied by much
serous exudate there is great danger of flooding the neighboring alveoli
with this inflammatory fluid and of carrying the large numbers of the
micro-organisms within the tubes to the air sacs of the lung. Under
these conditions the virus has an unusual ability to develop the disease
from one localized in the air passages to that of a true pneumonia. It
is probable that the peculiar early acute reaction which is present in
the air passages in epidemic influenza is responsible for the extensive
involvement of the lung in the severe and dangerous form of
inflammation.