§ 2. THROMBOSIS AND EMBOLISM.

Thrombosis is a particular case of blood-coagulation, and exhibits as the latter does the essentials of the dissolutional process. The following description of artificially-produced thrombosis indicates the nature and conditions of the phenomenon :

'The mesentery of a frog is exposed and subject to microscopic examination. A vessel of some size, an artery or vein, is chosen, and its wall in some way injured, as by twitching it slightly with forceps, or by placing a small crystal of common salt near it. Very soon white blood-corpuscles begin to adhere at the injured part. As the blood passes over it successive layers of white corpuscles adhere, and a growing clump of them is formed. Along with the white. corpuscles a stray red one may be insinuated, or there may be several red ones. The clump so formed, be it wholly white or partly mixed with red corpuscles, may be carried off, in which case a new one begins to form, but the clump may remain fixed and be continuously enlarged by successive depositions of corpuscles from the circulating blood. In course of time a change occurs in the appearance of the clump, the white corpuscles lose their individual outline to a great extent, and the clump gathers itself together into a grey granular mass, in which neither by acetic acid nor by staining are the majority of the white corpuscles to be discovered. It has, indeed, very much the characters of fibrine which has been obtained by whipping the blood outside the body. The clump of

white corpuscles, in fact, by the disintegration of the corpuscles and the attraction of the fibrinogen from the blood plasma, has converted itself into a fibrinous coagulum.'

Thrombosis as here typically portrayed is accompanied, we may safely say, by a disintegration of matter. In an assemblage of leucocytes or bloodplaques (the latter are thought by some observers to be the chief agents in the construction of a thrombus), the protoplasm of the individual cells coheres in spheroidal forms. When thrombosis results, this protoplasm is subjected to radical rearrangement, moving from the former centres of aggregation so that the spheres are obliterated (chap. i. § 2).

The known causes of this morbid change prove in many cases, and imply in others, an absorption of energy from the outer surroundings. It is most plainly shown in thrombosis induced experimentally, as when foreign bodies are introduced into veins. But less so when apparently set up solely by the stagnation of blood in vessels, in the apices of the ventricles, in the auricles, or about the columnæ carneæ. Here thrombi are probably due indirectly to stagnation and directly to the structural and functional alteration to which stagnation gives rise in the endothelium.

When thrombi grow by the accretion of layer upon layer of corpuscles, as in aneurismal coagulation, and as in the extension of thrombi from the uterine to the iliac veins, the surface of the coagulum plays the part of a foreign body in transferring a molecular motion to the circulating corpuscles sufficient to

overthrow the balance of their inherent forces and effect their continuous deposition.

Where thrombi form at the mouths of wounded vessels, upon valves that have suffered inflammation, as in endocarditis and phlebitis, upon tumours protruding into vessels, or upon the walls of atheromatous arteries, the conditions sustain the inference that a passage of molecular energy from the immediate investment of the blood is the cause of the coagulation. In these cases, as in cases of inflammation, the remote origin of the changes in surrounding structures, upon which thrombi so commonly depend, is not in all instances certainly known. Nevertheless, in numerous instances, the starting-point in the series of causes is indubitably among the forces externally incident. If in endocarditis the qualitative change in the living membrane of the heart is the immediate forerunner of thrombosis, the inflammation of the endocardium we find related to some impurity of the blood, and the cause or causes of this impurity may generally be traced to some form of external energy. This is the case with endocarditis from rheumatism, measles, and scarlet fever.

The remote antecedents of thrombosis sequential to aneurism, phlebitis, and atheroma, may, in part, be traced to the conditions of the individual life. Efficient causes of aneurism are found in atheromatous disease and increased arterial pressure. The frequency of aneurism among those whose occupation entails great stress being put upon the heart and vessels, shows us that the absorption of energy in undue functional exercise is an important factor. Soldiers,

ironworkers, and others who perform severe manual labour, are the chief sufferers from aneurism. And atheroma itself may possibly be related to the same causes. Its common seats are those points in the arterial system where friction of the blood is most felt, as at the arch of the aorta, at the bifurcations of arteries, in the pulmonary artery when the right ventricle is hypertrophied. There are also unknown factors in the production of atheroma.

Of phlebitis, its associations with the specific fevers, pyæmia, and gout, may be alluded to as indicating its connection with external incident forces.

The remaining qualities of the dissolutional process can be inferred of thrombosis, since it is but a variety of blood-coagulation in which the change from a definite, coherent heterogeneity to an indefinite, incoherent homogeneity, was perceived, indeed, to obtain.

The softening, putrefaction, and desiccation to which thrombotic coagula are liable exemplify dissolution carried a step further; and so does the socalled organisation of thrombi. In the process of becoming organised the substance of a thrombus is not an active participant; it is dead matter and cannot give origin to a new formation. Its rôle is a passive one; the fibrinous substance is disintegrated and resorbed by the wandering cells from neighbouring structures. These cells uniting to form, with young vessels from the vasa vasorum, a granulated tissue, a cicatricial mass having the characters of connective tissue is developed.

Particles detached from the substance of a throm

bus may be carried into different divisions of the arterial system and, becoming arrested in arteries or capillaries, give rise to embolism. This involves transformations recognisable as dissolutions. Emboli have also, of course, other sources of origin, as neoplasms, vegetations, fat, pigment, &c. They may bring about inflammation and irritation of vessels, and in the brain the phenomena of apoplexy; but these results we shall pass over, being here interested only in the infarctions which embolism occasions.

Infarction is a common consequence of the plugging of end-arteries, and may be either hæmorrhagic, in which case the wedge-shaped piece of tissue possesses the general lineaments and attributes of a blood-clot; or the infarction may be necrotic, in which case the metamorphosis is a species of coagulation-necrosis; a solid homogeneous mass is substituted for the normal structure. In both of these effects of an embolus the individualities of the tissue elements are sooner or later completely effaced by the redistribution of matter; the mass exhibiting no marks of organisation.

The conditions under which necrotic infarction occurs have suggested that stoppage of nutritive supply is the proximate cause of the death of the tissue. Can local or systemic death from starvation be harmonised with the doctrine of dissolution, which requires an absorption in excess of outside forces? Dissolution from innutrition implies a deficiency of ingested energy, since food is the source of organismal power.

The answer is, that, failing due nourishment, the