It should be added that in the case of passive hypersemia it requires considerable increase of pressure in the capillaries to produce an oedema. It has even been stated that a simple passive hyperemia, apart from vaso-motor paralysis (producing also active hyperemia), does not lead to oedema. It has been shown that if the iliac vein of a dog be ligatured there is no oedema till the sciatic nerve is cut. The explanation of this, however, may be that on account of its anastomoses the obstruction of this vein does not raise the blood-pressure sufficiently to induce oedema, whereas a coincident vaso-motor paralysis producing dilatation of the arteries raises the blood-pressure sufficiently. Experiment proves that if a sufficient number of veins' be obstructed oedema will result without vaso-motor paralysis. Sotnitchewsky, by introducing plaster of Paris into a peripheral vein of the leg of a dog while the thigh was constricted by an elastic band, succeeded in obstructing a number of veins by the gypsum hardening in them. In this case oedema followed without the induction of vaso-motor paralysis. In passive hypersemia from thrombosis of veins there are usually many veins obstructed before cedema occurs. In the case of passive hyperamiia from heart-disease it may well be supposed that the prolonged venous engorgement will produce an extensive deterioration of the capillary wall, besides a depreciation of the blood itself. Hence valvular disease of the heart is the most frequent cause of this form of oedema.

A watery state of the blood, or Hydraemia, is frequently asserted as a cause of the so called cachectic cedemas. According to Cohnheim and his assistants a simple anaemia induced in animals by repeated blood-lettings and the replacement of the blood by a solution of common salt, is not sufficient to induce oedema. In the human subject, however, the conditions are different from those of such an acute hydremia, in respect that in chronic emaciating diseases we have a prolonged deterioration of the blood, during which the general nutrition of the tissues suffers. Under these circumstances the blood-vessels become more permeable. There is usually also in these diseases weakness of the heart, and consequently a tendency to passive hypersemia in dependent parts. A slight amount of passive hyperemia will, in the existing state of the blood and tissues, induce oedema. In accordance with these facts, the cedema is usually in the lower extremities.

The causation of the characteristic (Edema of Acute Bright's disease is much more difficult to explain. There is, indeed, in this disease a serious reduction in the specific gravity of the blood serum. It has been found reduced to 1020, or even 1013, instead of standing at 1030, which is the normal. This hydremia is induced in two different ways. There is the loss of albumen, which renders the blood directly more watery, but there is also an abnormal retention of the water in the blood, as there is a great reduction in the amount of urine secreted. These facts naturally suggest that if the oedema in Bright's disease is not due simply to the hydremia, it may be due to this in conjunction with the increased bulk of the blood, to a Hydrsemic plethora. This view has obtained much support. It has been supposed that, the entire bulk of the blood being increased, there will be increased pressure in the capillaries and increased transudation from the watery blood. This explanation, however, is not a sufficient one, as it is opposed by observations in the human subject and by experiments on animals. In the first place there are cases of absolute suppression of urine, as in hysterical females, etc., in which we must presume an exaggerated hydrsemic plethora, but without a trace of oedema, and, in the second place, an exaggerated hydrsemic plethora may be induced in animals without leading to oedema of the skin.

In some experiments by Cohnheim and Lichtheim, a hydremic plethora was induced by injecting a solution of common salt into the vessels of animals. Enormous quantities, in some cases more than three times the bulk of the blood, could be injected without killing the animal. As in other cases of transfusion, these injections did not produce any permanent rise in the blood-pressure. The most direct result was a great acceleration in the speed of the blood-current, presumably from the diminished friction of the watery blood. There was also a greatly increased transudation, and consequently, increased flow of lymph. But this was remarkably localized. There was a greatly increased flow of lymph in the thoracic duct, showing that in the viscera the transudation was increased; while the lymphatics of the limbs showed no increase, indicating -that in the skin and muscles the transudation was not increased. There was also greatly increased secretion from the salivary glands, stomach and intestine, liver, lachrymal glands, and kidneys. In these organs an oedema was developed, that is to say, in the mucous membrane and submucous tissue of the stomach and intestines, in the lymphatic glands of the mesentery, in the pancreas, kidneys, gall bladder, salivary glands; there was also ascites, but no oedema of the subcutaneous tissue. The explanation suggested for this localization of the increased transudation and the oedema is, that these organs are all normally concerned in the removal of water from the blood, and that probably their blood-vessels are unusually permeable to water. The experiments produce a great increase in the water of the blood, and the vessels give ready passage to it.

These observations and experiments may seem to throw little light on the oedema of Bright's disease, except in a negative way. But looking closely at the experiments, they show that hydrsemic plethora induces increased transudation and oedema in parts predisposed. In Bright's disease we have two elements which are awanting in these experiments. On the one hand the kidneys are inactive, and on the other there is in the blood an irritant, which, acting on the kidneys, has induced the disease in them. This irritant may be presumed to act on the skin as well as on the kidneys. As Cohnheim has pointed out, there are many facts which indicate a close relation between the skin and kidneys in Bright's disease. In scarlatina, for instance, we have an acute inflammatory hyperemia of the skin during the febrile stage. But there are, even in this stage, inflammatory changes in the kidneys, and when these phenomena advance sufficiently to induce a hydremic plethora, it is perhaps not remarkable that oedema occurs in the previously damaged skin. In the experiments above referred to, it was found that although the normal skin did not become oedematous, yet when it had been previously inflamed, as by pencilling with iodine solution, or by exposing to a strong sun, then oedema showed itself. The oedema of Bright's disease hence approaches in its pathology to inflammatory oedema.

Nervous influences sometimes play a part in the production of oedema. The most familiar examples of this are afforded by erythema nodosum, and urticaria, where nervous irritation, usually reflex, induces localized swellings, presumably oedematous, in the skin. The bites of insects, especially fleas, produce similar effects in some persons, and, in this case as in the others, there are sensations indicating irritation of the nerves. In injuries to nerve-stems, some authors have observed local oedema, and oedema sometimes follows paralysis, both paraplegic and hemiplegic, in the latter case forming a hemi-anasarca. Probably in all -these cases the nervous lesion merely induces a condition of the vessels which predisposes to oedema, and its. actual occurrence is determined by other causes. Thus in the case of urticaria and flea bites, the parts are usually subjected to rubbing, while in paralysis the position of the limbs, conspiring with vasomotor paralysis, may determine oedema by inducing passive hyperemia.

Position And Character Of The Transudation

The fluid transuded accumulates where there is room for it, and especially in places where the tissue is loose and easily stretched. The elasticity of the tissue will therefore have a considerable influence on the locality of the oedema. The oedema of Bright's disease, for instance, frequently begins in the loose subcutaneous tissue about the eyelids, and oedema in the larynx is in the loose ary-epiglottic folds.

The dropsical fluids are deficient in albumen as compared with the liquor sanguinis or inflammatory exudations, but they contain soluble salts in proportions nearly equal to these fluids.

The amount of albumen varies in different cases, being determined to some extent by the state of the blood, and the condition of the blood-pressure. It varies also very markedly according to locality. Thus the percentage of albumen is stated by Reuss to be, in the case of the pleura, 22.51; pericardium, 18.33; peritoneum, 11.14; subcutaneous tissue, 5.79; brain and cord, 1.14. Recklinghausen accounts for the larger amount of albumen in the pleura and peritoneum, as compared with the subcutaneous tissue and pia mater, by the greater richness of the former in capillaries. Some authors assert that in the pia mater there are only veins and arteries. The fluid according to its circumstances may contain bile pigment, biliary acids, fat, etc., and in Bright's disease it regularly contains urea.

Myxoedema is a term of recent introduction, which designates a condition characterized by certain alterations in the skin and elsewhere; the condition is related to atrophy or removal of the thyroid gland. (See further on).

Literature

Virchow, Hanb. d. spec. Path., i.; Arnold, Virch. Arch., lxii., 157, and lxiv., 120; Recklinghausen, Allg. Path., p. 94, etc.; Sotnitchewsky, Virch. Arch., lxxvii., 85; Cohnheim und Lichthei.m, Vii-ch. Arch., lxix., 106, and Cohnheim, Allg. Path., vol. i.; Hilton Fagge, Principles and Practice of Med., ii., 442; Runeberg (Filtration of solution of Albumen), Arch. d. Heilk., xviii., 1; Heidenhain, Hermann's Physiol., v.; Weir Mitchell, Morehouse, and Keen, Gunshot Wounds, etc.; Reuss, Deutsch. Arch. f. klin. Med., xxiv., 183; Lazarus-Barlow, Phil. Trans, of Roy. Soc, vol. 185, 1894, and (very fully) Manual of Gen. Path., 1898.