1877 The Lancet  
PHYSICIAN TO THE HOSPITAL. LECTURE V. lIaemorrhage from cavities -Analysis of fourteen museum specimensfrom cases of fatal hcenaoptysis-Pathology-Signs ofhaemorrhage from puLmonaryane2crisms-Prognosis-Cases of recovery-Treatment. GENTLEMEN,-I have on the table before me fourteen specimens which I will ask you carefully to inspect, all of them, with one exception, removed from patients who had died of haemoptysis. This group fairly illustrates the pathology of that fatal accident when, as is
more » ... ent when, as is usually the case, it occurs at the period of phthisis which we have at present under consideration. Of these specimens three show large branches of the pulmonary artery, simply exposed and more or less eroded in cavities -(a) by the breaking away of the surrounding tissue in the process of excavation, or (b) by subsequent ulcerative erosion of the cavity wall. Six are examples of aneurismal dilatations, more or less typically sacculated, projecting into cavities from pulmonary vessels which are generally traversing a small portion of the cavity wall on their way further. The sacs vary in size from that of a pea to that of a large anahelled walnut; some are empty, others are partially or completely filled with laminated clot, presenting perfect pictures in miniature of sacculated aneurisms of the aorta or of other systemic vessels. In two instances the aneurismal dilatation involves the whole calibre of the vessel instead of projecting from one side of it, and are therefore of the fusiform kind. The remaining four or five specimens show lateral bulging affecting only or principally the cavity side of exposed vessels, and may therefore be described as ectasias of the pulmonary branches. If we now look to the characters of the cavities in which these aneurisms or exposed vessels are found, we see that in eleven instances the cavities are truly pulmonary, having been formed by the destruction and removal of lung-tissue. And it is important to observe that in the great majority of instances these cavities are chronic, showing a more or less distinct limiting membrane and induration of surrounding lung. In two instances, however-and in both these cases fatal hsemorrhage has ensued from erosion of exposed vessels which had not become aneurismal,-the cavities were active: in the one case, a chronic cavity undergoing active ulcerative inflammation; in the other case, a recent cavity formed by the rapid breaking down of the pulmonary tissue and the coalescence of adjacent cavities. In four cases you will observe that the aneurisms occupy bronchial cavities. In one of these the aneurism projects into the calibre of a bronchus as it is on the point of terminating in a large cavity. This case was a very remarkable one, the only one ia which any physical signs were observed which were distinctly referable to the aneurism. On examining the patient only a few hours before his unexpected death, a peculiar variety of amphoric breathing was heard on the left side, opposite the second rib and interspace, a little within the nipple line. The first third or half of the inspiration was jerking, and would be best described as interruptedly amphoric ; the remaining part of the inspiration and the expiration were equally amphoric. The only explanation of this peculiar modification of the amphoric breathinl, which RufCRt.Rd itaelf a.t the tima waa that a plug of mucus partially obstructed a large bronchus at its entrance into a cavity, so that, on the cavity becoming more expanded during the latter half of inspiration, there was room enough for air to pass in an uninterrupted current. The physical sign was, at all events, so striking as to lead me to speculate with the gentleman who was going round with me as to its cause. The patient died the next morning almost instantaneously of haemoptysis, and post mortem we found this small aneurism situated as you observe, and thus completely explaining the sound heard during life. The aneurism itself had not ruptured, but a continuation of the vessel had become exposed and eroded in the cavity, which was undergoing active ulceration. In these other two specimens there are three aneurismal sacs nestling in bronchial dilatations, as has been carefully demonstrated by my colleague, Dr. R. Thompson, who put them up. I do not think aneurism of the pulmonary artery in a bronchial dilatation has been before described ; it is certainly of rare occurrence-much more rare, indeed, than is represented by these three cases out of a collection of fourteen. In intimate pathology these aneurismal affections of the pulmonary artery differ but little from those of other vessels. Aneurism of the pulmonary artery was long disregarded as a cause of haemoptysis, although the possibility of its occurrence was suggested by Laennec in 1827, and examples were positively described by Rokitansky in 1852. The two cases (of which here are the specimens) which occurred at this hospital, and were published in the Medical Times and Gazette and the Pathological Transactions by our present consulting physicians, Dr. Cotton and Dr. Quain respectively, were the first to draw general attention to the frequency with which fatal haemoptysis arises from this cause. Atheroma of the pulmonary artery is so uncommon that this vessel has been looked upon as being almost invulnerable. It was long thought that the venosity of the blood contained in the pulmonary system was the reason this vessel so rarely , became diseased; but, as Dr. Moxon has pointed out, the very conditions which lead to the production of atheroma of the pulmonary arteries-conditions, namely, which, such as mitral obstruction, cause increased pressure of blood in the pulmonary circulation-tend to cause also increased venosity j of blood. Strain may be looked upon as the principal determining , cause of aneurism of the pulmonary artery, as it is perhaps . the most frequent cause of aneurisms elsewhere. There are , two sources of strain upon the pulmonary vessels in the I cases of phthisis in which this form of hmmoptysis most ' often occurs-first, there is heightened blood-pressure in the pulmonary circulation; and, secondly, there is local t loss of support on that side of a vessel which becomes partially exposed in a cavity. I have already pointed out that in the majority of these specimens, the cavities are chronic, and of more or less old standing. These cases ) were also for the most part one-sided cases, the opposite lung being but slightly or recently involved. In such cases , we have increased resistance to the pulmonary circulation, ! from the extensive obliteration of vessels; we also have s considerable renovation of blood volume, the patients often gaining weight and strength up to the time of their attack of bsemoptysis. After death in these cases, the right side I of the heart is commonly found to be hypertrophied to com-I pensate for the increased resistance to circulation. Any I vessels traversing the walls of these chronic cavities which I may remain pervious, have time slowly to expand on the ' exposed side. t The first part of this process of expansion consists of I a thickening of the wall of the vessel, which has been , regarded as a local hypertrophy to compensate for the , increased strain at the exposed point. That it is not, how-I ever, a hypertrophic, but an inflammatory thickening, is I clear from its being limited to that side of the vessel which is exposed, and on microscopical examination we find a , blending of the tunics in a fibro-nuclear growth, which L obscures all appearance of muscular coit. That the , thickening, too, does not compensate in any effectual way i for the increased strain is obvious, for from the earliest . period there is commencing dilatation of the vessel, which . is exaggerated in appearance by the local thickening of its L walls. Subsequently, the thickened wall, degenerating and . continuing to yield before the blood-pressure, becomes thin ! and papery, and finally rupture takes place. That the disease of the pulmonary artery in these cases Y
doi:10.1016/s0140-6736(02)49157-x fatcat:ulti3jyzvzdehcdcpdxtllzneq