Laennec, and almost all subsequent pathologists, believe that bronchial dilatation is always a mechanical consequence of catarrh; that it is dependent on the accumulation of the bronchial secretion at certain points, and the powerful inspirations made during paroxysms of coughing, whereby the walls, from some unknown causes, become at one time thicker, and at another thinner, than natural. The condensation of the surrounding parenchyma is, according to their views, simply dependent on the compression exercised by the dilated bronchus, which thus becomes the primary cause of the final obliteration of the pulmonary tissue. Hence, according to Laennec, the bronchial dilatation is the primary anomaly, and the condensation of the pulmonary substance is merely a secondary change dependent on its compression by the tube.

Corrigan has recently published a theory to account for bronchial dilatation, which is directly the opposite to that of Laennec; and believing the disease to be allied, in its anatomical elements, to cirrhosis of the liver, he has given it the name of cirrhosis of the lungs. He regards the atrophy and obliteration of the parenchyma of the lung as the primary phenomenon in the development of the disease, and as occurring spontaneously, while the dilatation of the bronchi is consecutive, and is not only dependent on the tendency to fill the space thus rendered vacant, and on the expansion occurring in the act of inspiration, but also on the traction exerted on the opposite walls of the bronchial tubes, by the shrinking of the surrounding tissue.

To speak more precisely, the change that the parenchyma of the lung surrounding bronchial dilatations undergoes, consists, in extreme cases, of obsolescence and destruction of the cellular spaces, and of the contraction of the cells so as to form a cellulo-fibrous or even a callous and fibro-cartilaginous tissue, which may be either white or streaked with blackish-gray pigment, dotted or of a uniform color, and which is so intermixed with the fibrous sheath of the bronchus that the two form one continuous whole.

When we take into consideration the vast extent to which the parenchyma of the lung around a dilated bronchus is obliterated; when we reflect on the nature and the degree of this metamorphosis, which very rarely follows prolonged external pressure on a lung; and, finally, when we notice the circumstance that this metamorphosis does not always develope itself uniformly around the dilated tube, nor is most marked the nearer we approach it; we cannot help doubting if all this can be produced and explained by the mere pressure caused by the dilatation of a thin membranous bronchial tube.

In point of fact, on instituting a closer examination, we arrive at conditions of another kind, which are in themselves sufficient to explain this metamorphosis, and are of the greatest importance in reference to the genesis of bronchial dilatation.

Whichever be the form under which bronchial dilatation appears, bronchitis must be regarded as the most frequent primary cause. It acts in different ways, but not mechanically, from accumulation of mucus, according to the theory of Laennec.

In the first form of bronchial dilatation, as we have described it in a preceding page, atony and paralysis of the contractile and irritable elements of the tubes are present, dependent on chronic inflammation and blennorrhcea. The facility with which the walls undergo dilatation through the influence of the inspirations and the concussion induced by the paroxysms of cough, is proportioned to the amount of exertion re-required to throw off the secretion accumulated in the bronchial tubes. Moreover the circumstance that many of the smaller tubes are completely obstructed by the blennorrhoeal secretion, favors the above condition. This form of bronchial dilatation affects that portion of the bronchial system in which blennorrhcea occurs.

The second or saccular form of bronchial dilatation is not developed in that portion of the bronchi which is the seat of catarrh, but beyond it; it is the consequence of bronchitis in the final ramifications of the bronchi, and depends on their obstruction by the accumulation of secretion, on the tumid state of their mucous membrane, and finally on their actual obliteration. It is produced by the hinderance that is presented to the free ingress of the inspired air, and is proportional to the difficulty of breathing (Reynaud), and the prolonged length of each individual inspiration; and it is especially developed in and about the perfectly impermeable bronchial tubes. The parenchyma surrounding this portion of the bronchial system collapses, and thus produces a space which becomes filled by the dilating bronchus. The dilatation thus lies entirely, or for the most part, in a collapsed and apparently compressed portion of parenchyma; hence, the latter appears to be the primary anomaly, and the bronchial dilatation merely a resulting and consecutive morbid change. This circumstance, together with the fact that the collapsed parenchyma passes into the above-described state of complete obliteration, and thus as it were, contracts upon itself and causes additional space in the lung, closely approximates this theory to that of Corrigan.

According to him the primary affection is not bronchitis, but is a disease of the parenchyma, not so much presenting the characters of inflammation of the interstitial areolar tissue, as of a pneumonic process (of which we shall subsequently treat) insidiously extending itself from one lobule to another, and depositing a product which becomes indurated, and fused or blended, as it were, with the original tissue. The air-cells become thus obliterated and destroyed, and undergo the same change. The resulting cellulo-fibrous tissue may here, as in the first case, draw asunder the bronchial walls by the tension induced by its further contraction, and may thus contribute to the further dilatation of the bronchial sac and to the increased attenuation of its walls.

However this may be, a smaller or larger proportion of the lungs always becomes obsolete and shrivelled in proportion to the extent of the bronchial affection; indeed, when the bronchial tubes of a whole lung are thus affected, we find that all of its parenchyma is more or less obliterated, contracted to a small part of its normal volume, as if in consequence of external pressure from exudation, and drawn up in the mediastinum towards the bronchus; moreover, the cavity of the thorax is diminished, in consequence of the sinking of its walls over the cellulo-fibrous tissue surrrounding the dilated bronchial tubes.

In some rare cases a bronchial sac is entirely separated by obliteration, not only from its own branches, but also from the tube on which it was situated. It then exhibits the appearance of a perfectly closed cavity, which, in consequence of the persistent secreting activity of its lining membrane, is probably further enlarged by the accumulation of mucus. Subsequently, however, if this secreting action be suspended, the accumulated matter becomes inspissated and diminished in volume, till ultimately there is nothing left but a fibrous capsule, enclosing either a soft, fatty, calcareous mass, or a solid concretion of bone-earth.

Isolated saccular dilatations containing puriform matter may be mistaken for tuberculous cavities, especially when they are associated with pulmonary tubercles and are situated in the upper third of the superior lobes of lung, - the ordinary focus of pulmonary tuberculosis. On a closer examination we may recognize a saccular bronchial dilatation by the roundish form of the cavern and its pouches, by the smooth, uninjured, investing mucous membrane, by the absence of all signs of ulceration in the bronchial tubes entering it, by the striking difference between its contents and tuberculous pus, by the circumstance that the surrounding and contiguous obsolete parenchyma contains no tuberculous granulations, or only such as are obsolete, and by the simultaneous occurrence of similar cavities in parts of the lung, in which tuberculous excavations are not usually found. In other cases our diagnosis must be founded on general principles, as for instance, on the fact that bronchial dilatations are ordinarily found in the superficial parenchyma of the lungs towards their borders, and very rarely occur in the summit; and further, that, when the bronchial disease is very extensive, tuberculosis is incompatible with it.

In consequence of the obliteration of a large extent of lung produced by extensive bronchial dilatation, we find that this affection gives rise to a development of the right side of the heart in the form of active dilatation, stasis and dilatation of the whole venous system, cyanosis, and vicarious development of the permeable portions of the lungs, which not unfrequently leads to bronchial and pulmonary hemorrhage (haemoptoic infarctus). If the bronchial dilatation be very highly developed, it induces collapse, emaciation, a cachectic appearance, dropsy, and finally total exhaustion.

In consequence of the venosity and cyanosis to which it gives rise, it affords a very striking immunity, not only from pulmonary tubercles, but from tuberculosis in general. The fact that bronchial dilatation exerts an excluding influence on pulmonary tuberculosis has been known since the time of Laennec; and although the reasons for this influence are not understood, it has served, in recent times, as the basis of several plans for the cure of pulmonary consumption.