Causes of edema

The fluid enters the interstitial space as a result of filtration of blood through the capillary walls; with some of it returned to the bloodstream through the lymphatic capillaries and the lymph vessels.

1. Transition of fluid from the vessels to the interstitial space (filtration) occurs under the influence of the hydrostatic pressure of blood in the vessels and the colloid-osmotic pressure (stress) of the interstitial fluid. The hydrostatic pressure in the capillaries varies in different parts of the body. With the vertical position of the body as a result of gravity, the pressure in the capillaries of the legs is higher, which creates the conditions for the appearance of light foot edema by the end of the day in some people.
2. The fluid in the vessels retains, primarily, the colloid-osmotic pressure of the blood plasma and, to a lesser extent, the pressure of the interstitial fluid.
3. The third factor, which directly influences the filtration of the liquid part of the blood, is the state of permeability of the capillary wall.

If any parameter of the described dynamic equilibrium is violated, the filtration of fluid from the bloodstream increases, with its accumulation in the interstitial space and the development of edema.

The increase in hydrostatic blood pressure and, consequently, the increase in filtration occur with increased venous pressure. The causes of the latter can be the following states.

• Local disturbance of venous outflow with insufficient venous valves, varicose enlargement, and vein compression from the outside, vein thrombosis leads to an increase in venous pressure in the corresponding area, which causes blood stagnation in the microcirculatory bed and the appearance of edema. The most common thrombosis of the veins of the lower extremities develops in diseases requiring prolonged bed rest, including postoperative conditions, as well as during pregnancy.
• Systemic venous hypertension in heart failure.

Reduction of the oncotic blood pressure, 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 (a violation of the secretion of enzymes by the pancreas, for example, in chronic pancreatitis, other digestive enzymes).
• Disturbance of digestion with insufficient assimilation of proteins (resection of a large part of the small intestine, damage to the wall of the small intestine, gluten enteropathy, etc.).
• Violation of albumin synthesis (liver disease).
• Significant loss of proteins in the urine with nephrotic syndrome.
• Loss of protein through the intestine (exudative enteropathy)

An increase in the pressure of the interstitial fluid can occur when the lymphatic drainage is disturbed. When lymphatic drainage is delayed, water and electrolytes are reabsorbed from the interstitial tissue into the capillaries, but the proteins filtered from the capillary to the interstitial fluid remain in the interstitium, which is accompanied by water retention. Similar phenomena are observed with lymphatic obstruction of any etiology.

• The so-called elephantiasis (a significant increase due to lymphostasis of the volume of the lower extremities, 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 in recurrent episodes of erysipelas, with which affects the lymphatic vessels.
• Lymphostasis with edema of the upper limb with unilateral removal of axillary and thoracic lymph nodes for breast cancer.
• Lymphatic edema as a result of lymphatic obstruction by filarias (filariasis is a tropical disease). In this case, both legs, external genital organs can be affected. The skin in the affected area becomes coarse, thickened (one of the variants of elephantiasis).

Increase filtration of the liquid part of the blood in the interstitial space occurs when the capillary wall is damaged by mechanical, thermal, chemical, bacterial factors.

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

In response to the changes that are occurring, physiological compensatory mechanisms are included to delay sodium and water in the body. The delay of sodium and water occurs under the influence of changes in the kidneys - reducing glomerular filtration and increasing tubular reabsorption. Glomerular filtration decreases as a result of vasoconstriction, which occurs when the sympathetic department of the nervous system and the renin-angiotensin system are activated. Increased reabsorption occurs under the influence of antidiuretic hormone (ADH).

Edema in chronic heart failure is due to:

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

In renal diseases, a long-term persistent edematous syndrome is usually associated with a large proteinuria that lasts for several weeks, at which a significant amount of protein (primarily albumin) is lost, leading to hypo-oncotic fluid retention, aggravated by developing hyperaldosteronism with increased sodium renal absorption. This mechanism forms the basis of edema in the so-called nephrotic syndrome. In the development of edema in acute syndrome [for example, in the midst of a typical acute glomerulonephritis], an important role is played by the vascular factor (increased vascular wall permeability), as well as sodium retention, which leads to an increase in circulating blood volume (BCC).

[1], [2], [3], [4], [5], [6], [7], [8], [9], [10]