Causes of edema

Fluid enters the interstitial space as a result of blood filtration through the capillary walls; some of it returns to the bloodstream through the lymphatic capillaries and lymphatic vessels.

1. The passage of fluid from the vessels into the interstitial space (filtration) occurs under the influence of the hydrostatic pressure of the blood in the vessels and the colloid-osmotic pressure (tension) of the interstitial fluid. The hydrostatic pressure in the capillaries varies in different parts of the body. When the body is in an upright position, the pressure in the capillaries of the legs is higher due to gravity, which creates conditions for the appearance of mild leg edema by the end of the day in some people.
2. The fluid in the vessels is maintained primarily by the colloid osmotic pressure of the blood plasma and, to a lesser extent, by the pressure of the interstitial fluid.
3. The third factor that can directly influence the filtration of the liquid portion of the blood is the state of permeability of the capillary wall.

When any parameter of the described dynamic balance is disturbed, the filtration of fluid from the bloodstream increases, with its accumulation in the interstitial space and the development of edema.

Increased hydrostatic pressure of the blood and, consequently, increased filtration occur with increased venous pressure. The following conditions may be the causes of the latter.

• Local venous outflow disturbance due to venous valve insufficiency, varicose veins, and external compression of veins, venous thrombosis leads to increased venous pressure in the corresponding area, which causes blood stagnation in the microcirculatory bed and the appearance of edema. Most often, lower extremity vein thrombosis develops in diseases that require prolonged bed rest, including postoperative conditions, as well as during pregnancy.
• Systemic venous hypertension in heart failure.

A decrease in the oncotic pressure of the blood, which also increases filtration, occurs in any condition accompanied by hypoproteinemia. The following causes can lead to hypoproteinemia.

• Insufficient protein intake (starvation, inadequate nutrition).
• Digestive disorders (impaired secretion of enzymes by the pancreas, for example in chronic pancreatitis, other digestive enzymes).
• Digestive disorders with insufficient absorption of proteins (resection of a significant part of the small intestine, damage to the wall of the small intestine, gluten enteropathy, etc.).
• Disruption of albumin synthesis (liver disease).
• Significant loss of protein in the urine in nephrotic syndrome.
• Loss of protein through the intestines (exudative enteropathy)

Increased interstitial fluid pressure may occur when lymphatic outflow is impaired. When lymph outflow is delayed, water and electrolytes are reabsorbed from the interstitial tissue into the capillaries, but proteins filtered from the capillary into the interstitial fluid remain in the interstitium, which is accompanied by water retention. Similar phenomena are observed in lymphatic obstruction of any etiology.

• The so-called elephantiasis (a significant increase in the volume of the lower extremities due to lymphostasis, sometimes the scrotum and labia, accompanied by sclerosis and trophic disorders of the skin and subcutaneous tissue; less often, the term "elephantiasis" is used to describe lymphostasis of any other localization) occurs with recurrent episodes of erysipelas, in which the lymphatic vessels are affected.
• Lymphostasis with swelling of the upper limb after unilateral removal of axillary and thoracic lymph nodes due to breast cancer.
• Lymphatic edema as a result of obstruction of the lymphatic ducts by filariae (filariasis is a tropical disease). Both legs and external genitalia may be affected. The skin in the affected area becomes rough and thickened (one of the variants of elephantiasis).

Increased filtration of the liquid portion of the blood into the interstitial space occurs when the capillary wall is damaged by mechanical, thermal, chemical, or bacterial factors.

• In a local inflammatory process as a result of tissue damage (infection, ischemia, deposition of uric acid crystals in the joints), histamine, bradykinin and other factors are released, which cause vasodilation and increased permeability of capillaries, and the inflammatory exudate contains a large amount of protein, as a result of which the mechanism of tissue fluid movement is disrupted. Often, classic signs of inflammation are noted simultaneously, such as: redness, pain, local increase in temperature, dysfunction (rubor, dolor, calor, functio laesa).
• Increased capillary permeability is observed in allergic reactions. In Quincke's edema - a special form of allergic edema (manifested on the face and lips) - symptoms usually develop so quickly that a threat to life is created due to swelling of the tongue, larynx, neck (asphyxia).

In response to the changes that occur, physiological compensatory mechanisms are activated, aimed at retaining sodium and water in the body. Sodium and water retention occurs under the influence of changes in the kidneys - a decrease in glomerular filtration and an increase in tubular reabsorption. Glomerular filtration decreases as a result of vasoconstriction, which occurs when the sympathetic nervous system and the renin-angiotensin system are activated. An increase in reabsorption occurs under the influence of antidiuretic hormone (ADH).

Edema syndrome in chronic heart failure is caused by:

• increased venous pressure;
• hyperaldosteronism;
• hypersecretion of antidiuretic hormone;
• decreased renal blood flow due to venous congestion of the kidneys;
• to a lesser extent, with a decrease in the oncotic pressure of plasma (blood stagnation in the liver leads to a disruption in the synthesis of albumin in it; in addition, due to anorexia, the intake of protein with food is limited).

In kidney diseases, a long-standing pronounced edema syndrome is usually associated with high proteinuria persisting for several weeks, in which a significant amount of protein (primarily albumin) is lost, which leads to hypooncotic fluid retention, aggravated by developing hyperaldosteronism with increased renal reabsorption of sodium. This mechanism is the basis for edema in the so-called nephrotic syndrome. In the development of edema in acute nephritic syndrome [for example, at the height of typical acute glomerulonephritis], an important role is played by the vascular factor (increased permeability of the vascular wall), as well as sodium retention, leading to an increase in the circulating blood volume (CBV).

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