A system of practical medicine. By American authors. Vol. 3

by Unknown

⁵⁶ Thèse, Paris, 1880.

It has been noted that secondary changes of capillary embolisms are not apt to occur in the anæmic and cachectic; in the plethoric and those affected with chronic cardiac disorders the contrary is true. According to the condition of the nervous system, to its greater or less tendency to react, there will be more or fewer chances of the capillary embolisms making their existence known by an attack of suffocation (Luzzato).

PATHOLOGY AND MORBID ANATOMY.—Pulmonary embolism gives rise to different morbid lesions. The nature of these and their extent depend in great measure upon the size, situation, and character of the plug which fills the main trunk of the pulmonary artery or one or more of its divisions. The changes of tissue which take place are of course in close relationship with the length of time which has elapsed since the embolus first migrated. They are also influenced greatly by accidents or complications which have arisen. It shall be our effort first to narrate the important considerations which pertain to simple embolus, and whether it affect a large artery or only a small vessel. After speaking of the simple variety we will refer briefly to septic and fatty emboli and also to those of other nature.

The pulmonary artery may be blocked up by a clot formed in situ. This fact has been shown to be true by many writers—i.e. Lancereaux, Duguet, etc. When a thrombus is present it may be occasioned by an inflammatory condition of the artery (rare), or by a dyscrasic blood-condition, or again by localized compression in the vicinity of the coagulum, as from a tumor. We may find arterial thrombosis during pulmonary phthisis, in pneumonia, in pleurisy, and in cases of cardiac dilatation or degeneration.⁵⁷ Endocarditis of the pulmonary valve and compression of the neck by enlarged ganglia have been mentioned as causes of these thrombi.

⁵⁷ Here it is due to relative stasis of the blood.

Ordinarily, a pulmonary embolus is fixed at the point of division of the main vascular trunk. It more or less completely blocks up the calibre of the artery, and is usually situated in the midst of a soft new clot, which also covers it in front and behind. The embolus often manifests its origin from a clot contained in one of the large veins of the lower extremities. One end is rough and excavated, and fits into the coagulum we find lodged there. It is often twisted like a corkscrew, or has on its surface the mark of the valves of the vein from which it has migrated. It is white or yellow in color. If we examine the interior of an ordinary autochthonous clot, we find it softer relatively than the clot of an embolus, and, moreover, no prolongations proceed from it which fail to correspond with any vascular division. The suddenness of the accidents and the disappearance of a previous peripheric clot are strong reasons in favor of the existence of the embolus.

More emboli are carried into the right lung than into the left, on account of the larger size of the artery. The median and lower lobes are also the ones most usually affected. When the right lung is diseased the emboli are then more frequently transported on the left side. After a time an embolus goes through certain transformations. It softens at its centre, owing to degeneration of the white blood-corpuscles. The hematies disappear soon, and the fibrin also changes in structure, becoming soft and granular. This softening at the centre of the embolus must not be confounded with a purulent change which affects certain thrombi which come from or are carried to a focus of suppuration. Whenever an embolus has been a long while in the artery, a neo-membrane forms between it and the arterial wall. This neo-membrane is mainly constituted by fibrillous tissue and here and there some developed vascular twigs. As a whole, it forms a sort of cap or covering for the embolus, and finally it takes up by absorption the granular detritus which forms in the interior of the clot. We perceive from the foregoing statement that a pulmonary embolism may heal, and that the process of its cure differs in no respect from what occurs in the case of a coagulum which disappears by absorption from some other portion of the vascular system, or indeed from the surface of the serous membrane. When the embolic plug comes from a focus of suppuration or gangrene the vascular walls will probably be affected with similar alterations.

In consequence of the obstruction of the main trunk, or of the important branches of the pulmonary artery by embolic plugs, certain effects are directly produced. These are—1st, mechanical; 2d, nutritive; 3d, irritative.

Perhaps, however, before describing these effects in detail it would be well to mention certain anatomical facts with respect of the circulation of the lung which have considerable importance in view of certain morbid lesions to which we shall refer presently. It has now been proven experimentally, by the researches of Cohnheim, Litten, and Küttner, that there are no vascular communications between the pulmonary and bronchial arteries, and, further, that there are no branches coming off from the small divisions of the pulmonary artery by which a collateral circulation can be carried on when the arteries of the third order are obstructed by embolic plugs. It is also further corroborated by the investigations of the authors named that the pulmonary artery is mainly instrumental in keeping up the function of the lungs, whilst the bronchial artery is the artery of nutrition. If the latter were obstructed in any manner, gangrene of the pulmonary structure must surely follow; if the latter be ever so thoroughly closed, no death of tissue will ever result.

The mechanical effects caused by the obstruction of the main artery or of a primary division of it are much less considerable than when a smaller artery is plugged. In the first case the only observable condition is that of anæmia of pulmonary tissue. Occasionally Lancereaux has noticed atelectasis of certain lobules. The pathogeny of this condition is difficult to explain, as air enters the bronchi freely, and it should not be produced without effusion taking place. If life lasts a few hours hyperæmia and oedema of lung-tissue may be caused. The latter conditions are aided if there be existing organic disease of the heart. If, now, the smaller arteries be obstructed by embolic plugs, there is a strong tendency to the formation of hemorrhagic effusions, to which the name infarctus has been very properly given by Virchow. These infarctions vary in size from that of a small nut to that of a pullet's egg, just as they implicate one or more pulmonary lobules. They are situated at the periphery of the lung underneath the pleura. They are conoid in shape, with the apex turned toward the root of the lung. They seem like hard nuts under the surface of the lung when felt with the fingers. Their color is dark-brown or black; their cut surface is granular, even more so than the surface of a lobule solidified by broncho-pneumonia. The capillaries in and around these masses are filled with red blood-corpuscles. The same is true also of the alveoli, in which we find degenerated epithelial cells in large numbers containing granules of pigment. The connective tissue about the alveoli becomes thickened, the alveolar cavities contract, and finally the infarctions are changed into a real fibrous cicatrix, in the same way as they are transformed in other viscera of the body. Prior to this stage, however, we notice that the color of the infarction has gradually changed, and that it has become pale and yellow. This is due to the fatty degeneration of the fibrin contained in the alveoli, and the same affection of the enclosed cells. May any infarctions be restored to a condition of perfect integrity? It is more than doubtful, even if the obstructing plug of the pulmonary artery disappeared very soon, because the pulmonary parenchyma beyond the clot has suffered so much from fatty changes and hemorrhage that the vessels are unequal to their function. At times, owing to the stoppage of the nutritive action of the bronchial artery, the infarction may become a cheesy mass, which soon softens and is expectorated. This leaves a cavernous opening in the lungs. Sometimes the infarction becomes infiltrated with calcareous salts. It cannot be confounded readily with other lesions, especially pulmonary apoplexy, on account of its distinct limitations. Sometimes a lobule affected with broncho-pneumonia and hemorrhage may simulate it closely. The pathogeny or mode of production of the hemorrhage in a more or less limited area of the lung which is concomitant with an embolic plug in one of the branches of the pulmonary artery is difficult to present. This fact may be explained by the different solutions afforded by various authors as to the manner in which the apoplectic condition and the embolus are correlated. Certain writers have affirmed that the embolus itself is but a secondary phenomenon, and the surrounding hyperæmic state is the real cause of its production (Laennec). Later authorities have established that this statement is rarely true, and that the embolus always occurs first and the localized congestion follows closely afterward.