Epidemic Respiratory Disease: The pneumonias and other infections of the repiratory tract accompanying influenza and measlesOpie, Eugene L. (Eugene Lindsay)
History
Epidemic Respiratory Disease: The pneumonias and other infections of the repiratory tract accompanying influenza and measles
Weakening of the bronchial wall by the changes which have been described
will cause lasting dilatation of the bronchi. Whatever increases
pressure within the bronchi will increase the tendency to dilatation;
the bronchi being filled with mucopurulent exudate dilatation usually
appears first at the bases of the lung, since gravity increases
intrabronchial pressure here. New formation of fibrous tissue within the
wall of the bronchus, thickening of adjacent alveolar walls, and
organization of fibrin reinforce the weakened bronchial wall and limit
the dilatation which follows injury to the wall. Regeneration of
epithelium covering the dilated tube will further obscure the early
changes which have made dilatation possible. The changes which weaken
the bronchial wall permit dilatation at a time when there is no new
formation of fibrous tissue. When the bronchial lesion has persisted
several weeks, chronic pneumonia is associated with it. It has been
suggested that the contraction of newly formed fibrous tissue within the
substance of the lung might cause bronchi to be enlarged by traction
upon their walls. Newly formed connective tissue is most abundant in the
wall of the bronchiectatic cavity, and here contraction would tend to
diminish the size of the cavity.
Unresolved Bronchopneumonia
Chronic bronchopneumonia is characterized by changes similar to those
associated with chronic inflammation in other parts of the body, namely,
by thickening of the interstitial tissue of the lung, by accumulation of
mononuclear cells, by proliferation of fibrous tissue and by
organization of exuded fibrin. In a few instances these changes have
begun at the end of two weeks after onset of influenza, but they have
been little advanced until three weeks has elapsed; advanced chronic
inflammation has occurred after from four to eight weeks. Chronic
inflammation primarily affects those structures which are most severely
injured by the acute lesion and is most conspicuous in immediate
proximity to the small bronchi and bronchioles; the perivascular and
interlobular connective tissue are secondarily involved. Corresponding
to each of the lesions of the alveolar tissue which have been found with
bronchopneumonia, namely, peribronchiolar, hemorrhagic peribronchiolar,
lobular and peribronchial consolidation, there is a chronic lesion which
develops when pneumonia has failed to resolve.
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