Mechanism of inflammatory edema

Depending on the causes and mechanism of development, such types of edema as cardiac (stagnant), renal, cachexic, toxic, endocrine, neurogenic, inflammatory, allergic are distinguished.

Heart, or stagnant, swelling. It arises as a result of heart failure caused by myocardial damage (myocarditis, infarction) or endocardium (endocarditis, decompensated defects).

Insufficiency of the left side of the heart (heart attack,decompensated defects of the valvular apparatus) leads to venous stasis, increase of pressure in the system of the small circle of blood circulation. Stagnation of blood in the vessels of the lungs develops. Stagnant phenomena in the pulmonary vessels are accompanied by hypoxia, a decrease in lung tissue resistance, propensity to develop opportunistic microflora, pneumonia. Acute failure of muscle contractions of the left side of the heart leads to severe pulmonary edema, asphyxia, and death.

Insufficiency of the functional activity of the righthalf of the heart (myocarditis, myocarditis, decompensated vice) is accompanied by increased pressure, venous congestion in the system of a large circulatory system. Edema in animals in this case is found on the body parts lying below the heart area - in the subcutaneous tissue of the abdomen, thoracic and pelvic limbs, podgrudka.

Chronically flowing right-sided cardiacInsufficiency is accompanied by hypoxia of parenchymal organs, development of dystrophic changes. This is one of the reasons for the development of cirrhosis, portal hypertension, dropsy of the abdominal cavity (ascites).

Hypotension due to cardiacdeficiency, reflexively involves the renin-angiotensin-aldosterone mechanism of water retention in the response. The resulting hypervolemia aggravates the severity of the process, contributing to a large accumulation of transudate in tissues.

The cause of congestive edema in addition to cardiacInsufficiency can be thrombosis of veins, violation of outflow of intercellular fluid through lymphatic collectors. The hydrodynamic pressure in the veins, the capillary network increases, the vessels expand, the outflow of interstitial fluid stops. Transudation in the focus of stagnation is promoted by the resulting hypoxia and acidosis, due to the development of which the permeability of membranes significantly increases, entailing the release of not only the liquid but also the plasma protein. Transudate, squeezing lymphatic ducts, prevents lymphatic drainage.

Renal edema. Its development is due to two factors. The first factor is the diffuse lesion of the glomerular apparatus by the inflammatory process (glomerulonephritis), as a result the filtration capacity of the kidneys sharply decreases. The resulting circulatory disturbance stimulates the secretion of renin. The entire system - renin-angiotensin-aldosterone-antidiuretic hormone - is activated. Sodium, water, urea are retained in the body. The permeability of the capillary walls increases. The combination of difficult urinary excretion, hypernatremia, hypervolemia and high permeability of the vascular wall leads to the development of nephrotic edema.

The second factor determining the development of renaledema, - primary lesion of the renal tubules. Acutely and chronically occurring nephroses are characterized by the release of a large amount of protein, mainly finely dispersed albumin (albuminuria) by the kidneys. Developing hyponionia facilitates the movement of fluid from the bloodstream into the tissues. Hypoonkia and accompanying hypovolemia, irritating osmo- and volumoreceptors, reflexively stimulate increased release of aldosterone and sodium and water retention in the body, which aggravates the development of nephrotic edema.

In diseased animals, renal edema can be observedin the abdomen, podgorudka, sacrum, larynx. Especially clearly manifested puffiness of renal origin in the eyelid, often in dogs and pigs. This is explained by the fact that these areas are rich in loose fiber, which readily adsorbs electrolytes.

Cachectic edema. Occur as a result of alimentaryinsufficiency, especially lean protein nutrition, chronic severe diseases with a predominance of catabolism (malignant tumor, lesions of the gastrointestinal tract, chronic anemia, etc.). The leading factor in the pathogenesis of cachexic, including hungry, edema is hypoproteinemia. Reducing the concentration of proteins in the blood leads to a drop in the oncotic pressure, so that the fluid is not retained in the lumen of the vessels and moves into the tissues. The development of cachexia edema is promoted by:

decrease in the protein-forming function of the liver;

cardiovascular insufficiency, leading to an increase in venous pressure;

a decrease in the tone of the walls of the vessels of a centrogenic origin and, as a result, a violation of their trophism;

increased consumption of water by starving animals.

Cachexia is accompanied by swelling of tissues, mucous membranes and serous membranes, accumulation of transudate in various cavities.

Toxic edema. Most often observed in animals after bites of venomous snakes, bees, other stinging insects. The causes of such edema can also be poisoning by fighting toxic substances (phosgene, diphosgene), chlorine, ammonia. Inhalation of gaseous toxins leads to pulmonary edema, and the defeat of the skin with mustard gas, lewisite, croton oil, other toxic substances leads to its edema. Some infectious diseases (anthrax, etc.), characterized by intoxication, are also accompanied by swelling of the tissues.

In the genesis of toxic edema the main significanceincrease the permeability of the vascular wall, hyperonkia in connection with cell alteration and hyperosmia. Transsudation is facilitated by vasoactive substances, such as histamine, serotonin, bradykinin, prostaglandins, released by damaged cellular elements. Perhaps a reflex influence on the vasomotors, accompanied by dilatation of the capillary network, increased vascular permeability. Toxic edema is local, their boundaries are determined by the effect of the etiological factor.

Endocrine swelling. The most common edema of endocrine originare found in animals suffering from hypothyroidism of the thyroid gland. Deficiency of thyroid hormones leads to violations of protein, fat, carbohydrate and water-salt metabolism. The pathology of glycoprotein metabolism leads to the accumulation of mucin in the tissues, a mucus-like substance that binds the water, and to the appearance of myxedema-mucous edema. It is well expressed in cattle in the submandibular region. When pressing on the edematous tissue there is no fossa, in contrast, for example, from cardiac or renal edema, when the depression of the finger is not replenished for a long time.

Neurogenic edema. Appear as a result of a disturbance of the nervoustrophies of tissues and vessels, nervous reflex regulation of water metabolism. The dominant role in the development of edema of neurogenic origin has an increased permeability of the vascular wall and a disorder of metabolic processes in tissues with impaired innervation. Swelling of the mucous membranes, skin can be observed in neuralgia, in particular the trigeminal nerve, damage or compression of nerve trunks.

Inflammatory swelling. Occur under the influence of tissue alteration. They differ from other forms of edema by a sharp increase in the permeability of histohematological barriers. This increase is due to the numerous inflammatory mediators released by the damaged cells. Primary importance is attached to such mediators as biogenic amines (histamine, serotonin), lysosomal hydrolases, prostaglandins, leukotrienes, adenosinephosphoric acids (ATP, ADP, AMP), peroxide oxidation products of lipids, etc. The inflammatory fluid contains at least 3- 5% protein and is called exudate. Exudation is caused by increased filtration, diffusion, strengthening of microvesicular transport. These processes are combined with a decrease in fluid resorption, as increased venous pressure.

Inflammatory edema accompanies many animal diseases of an infectious and non-contagious origin.

Allergic edema. Develops in sensitized animals inresponse to re-hit the allergen. It is manifested by hyperergic inflammation in the form of urticaria, allergic rash, sharp edema at the site of antigen administration with the development of hypersensitivity of immediate or delayed type. In addition to mediators of inflammation in the development of edema of allergic origin, great importance is attached to the formation of immune complexes that have cytotoxicity.

The consequences of edema depend on localization,duration and severity. The prolonged accumulation of fluid in the tissues reduces the possibility of nutrients entering the cell elements, subjecting them to squeezing. The structure and function of the affected tissues and organs are disturbed. Pulmonary edema leads to asphyxia, edema of the pericardial cavity - to cardiac tamponade, ascites disrupts the function of the abdominal cavity organs.