3d. Gravitation in weak states of the circulation must be looked upon as a cause of venous congestion. This is seen in the examples of hypostatic congestion and œdema seen in the lungs and other internal organs in low conditions and in the advanced stages of debilitating diseases, and in certain cases of stocking of the limbs in horses.
4th. Valvular insufficiency of the left heart and tumors or aneurisms interfering with circulation through the aorta, cause passive congestion of the pulmonary veins and œdema of the lung.
5th. Tumors and diseases of the liver determine passive congestion of the portal system and ascites.
6th. Passive congestion is very liable to take place in an organ the functions of which are impaired as in a paralyzed part. In this the hyperæmia may start in the capillaries and extend to the veins or even to the arteries.
Symptoms and results. If on a mucous membrane or white skin the color becomes dark red, or violet (cyanotic) with evident distension of the capillaries and veins, the latter of which may stand out as knots or cords, there is an appearance of swelling or enlargement and sometimes coldness of the part. Soon the watery part of the blood transudes in excess, constituting dropsy, with increased swelling and pitting on pressure. On the mucous surfaces it determines an abundant serous secretion. The color is deepened by the escape from the vessels of red globules as well as white. The transudation contains little albumen and only exceptionally fibrine. In connection with the marked deoxidation and high carbonization of the blood, the nutrition of the part is largely arrested together with the functions, secretory, motor or otherwise. The imperfectly nourished vessels may give way, leading to hæmorrhage, or nutrition may be definitely arrested producing moist gangrene or ulceration. Sometimes a thrombus is formed in a congested vein. The changes in the affected organs depend much on the degree and duration of the hyperæmia. If slight and lasting it causes permanent induration and thickening, from connective tissue hyperplasia as frequently seen in the hind limbs of the horse. In case of blood transudations the altered coloring matter gives the various shades of gray, brown or black. If long continued the organ may shrink and atrophy occur from defective nutrition and contraction of the fibrous hyperplasia.
In making post mortem examinations mistakes may be made through the occurrence of changes after death. Thus a hvperæmia which was quite considerable during life may virtually disappear through the contraction of the arterial and capillary coats forcing the blood on into the veins. A minute point of extravasation here and there may be the only macroscopic lesion left. Again a marked venous and capillary hvperæmia in a dependent part of the body or of an organ may be entirely due to hypostatic conditions, the blood having settled into the lowest part of the vessels since the death of the animal. To avoid this source of error one must always carefully note the position of the carcass after death. Under other circumstances the superficial veins and capillaries may fill up with blood through the occurrence of decomposition and the evolution of gases in the internal cavities, which empty the splanchnic and parietal vessels by compression.
Treatment. The general principles of treatment may be stated thus: 1st. Remove the cause of the hyperæmia if possible, especially any mechanical cause; 2d. Secure the influence of gravitation in favor of the return of blood to the heart; though not so available in animals as in man, it is of great value in congestions of the head, ears, tail, and to a less extent of other parts; 3d. Correct any fault of blood pressure, excess or deficiency, which may act so as to cause active or passive hyperæmia; 4th. Establish derivation by cupping, leeches, fomentations, pediluvia, sinapisms, etc.; 5th. Apply cold, astringents, bandages, to empty the hyperæmic vessels, or kneading, rubbing, or electricity, to hasten the flow of blood; 6th. To improve the quality of the blood and general health, in plethora by low diet, purgatives and diuretics, in anæmic or debilitated conditions by iron, bitters, nourishing food, fresh air, sunshine and exercise.
It is especially important to check passive congestion in febrile diseases, and mechanical congestion at an early stage of its progress (Roberts).
INFLAMMATION. PHLOGOSIS. PHLEGMASIA.
Definitions. Relations to active hyperæmia. Redness. Heat. Pain. Swelling. Forms: in vascular tissues: in nonvascular. Changes in tissue elements. Death of cells. Cloudy swelling. Granular degeneration. Cell proliferation. Karyokinesis. Embryonic cells. Amœboid functions. Migration of leucocytes. Red cells escaping. Changes in innervation. Vaso-motor disorders. Fever. Changes in circulation. Contraction of capillaries, dilatation, rapid flow, tardy flow, stasis, oscillations, thrombus, collecting of white globules in periphery of current, migration of leucocytes, blood plates, and red globules, massing of red globules, exudation, softening of the capillary walls, nutrient artery more rigid and transmits more blood, heart contracts more forcibly, increase of fibrine, increase of waste products. Buffy coat, physiological causes. Microbes. Ptomaines. Toxins. Chemiotaxis. Phagocytosis. Polynuclear and mononuclear leucocytes. Exudates, unlike dropsies. Mucous exudate. Serous exudate. Fibrinous exudate. Blood exudations. Croupous exudation. Chyliform exudate. Results and Products. Resolution. Delitescence. Metastasis. New formations. Suppuration. Pus microbes. Pus. Healing by 1st intention. Healing by 2nd intention, granulation. Granule corpuscles. Interstitial neoplasia. Degenerations in lymph. Fatty degeneration, melanotic. Softening. Ulceration. Gangrene.