An Important Reason Why Edema Should Never Be Ignored, part 1

Edema is one of the most common clinical signs that patients encounter, yet at the same time one of the most underestimated. Most often it is perceived as an everyday occurrence: “sat too long,” “it’s hot,” “uncomfortable shoes,” “age,” or “drank too much water.” Over time, a person gets used to the fact that the legs become heavier by the evening, sock marks remain on the skin, and the face looks puffier in the morning than before.

The problem is that edema is not a cosmetic feature and not a separate condition, but a marker of a disturbance in the internal fluid balance. Under normal conditions, the body regulates with precision in what volume and in which compartment water should be located. When this system fails, one of the first signals is swelling.

Edema is often ignored also because it can develop gradually, not be accompanied by pain, and temporarily disappear after rest, creating an illusion of well-being. However, even “mild” functional edema means that the body is finding it harder to manage the distribution and elimination of fluid. In some cases this is only a temporary shift, but often it is the first sign of systemic overload of the heart, kidneys, vascular, or hormonal systems.

What edema is in simple terms

From a physiological point of view, edema is an excessive accumulation of fluid in the intercellular (interstitial) space of tissues. It is not adipose tissue and not “excess weight” in the classical sense, but water that has left the vascular bed and remained in the tissues.

Edema can differ in density. In medicine, a simple test is used: if you press with a finger on an edematous area (for example, the anterior surface of the shin over the bone), sometimes an indentation — a “pit” — remains. In typical “water” edema, this pit persists for approximately 10 seconds to several minutes, and then gradually disappears. Such edema is called pitting. If, however, after pressing the skin immediately returns to its original position and no indentation appears, the edema is considered non-pitting (dense).

Normally, fluid continuously circulates between vessels and cells. It leaves the capillaries to deliver oxygen and nutrients, and then must return back — through the venous limb of the capillaries and the lymphatic system — for subsequent elimination by the kidneys.

Edema forms in two cases:

• When the rate of fluid leaving the vessels exceeds the body’s ability to return it to the bloodstream;
• When the body begins to retain sodium and water systemically.

It is also important to distinguish:

• Increase in body mass due to adipose tissue: the process is slow, body size remains relatively stable throughout the day;
• Increase in volume due to fluid retention: volumes change quickly, weight can fluctuate within 1–3 kg over a few days, and the severity of symptoms depends on the time of day and body position.

Edema can be local (limited to one area, for example, the lower leg) or systemic (affecting the face, limbs, and body cavities). The mere presence of edema does not indicate a specific diagnosis, but it always reflects a disturbance in the balance between intake, distribution, and elimination of fluid.

How fluid is normally regulated in the body

Fluid balance is the result of coordinated work of several systems. All water in the body is distributed between three main compartments: inside the vessels, inside the cells, and in the intercellular space. Exchange between them follows strict physicochemical laws, primarily hydrostatic and osmotic pressure.

For this circulation to function without disruption, key mechanisms are involved:

• Cardiovascular system: The heart provides blood flow dynamics and maintains the pressure necessary for fluid filtration. When blood flow slows down (especially venous), pressure in the capillaries increases, literally “pushing” water into the tissues;
• Vascular wall: Acts as a semi-permeable barrier. It must be permeable enough for nutrients, but maintain integrity to prevent uncontrolled “leakage” of plasma;
• Plasma proteins (Albumin): Create oncotic pressure, which, like a magnet, holds water inside the vessels and prevents it from leaving into the tissues;
• Kidneys: The main excretory organ regulating the overall volume of sodium and water. Even minimal shifts in filtration or reabsorption change fluid volume in all compartments;
• Lymphatic system: Performs a drainage function, collecting excess fluid and protein molecules that could not return directly to the veins;
• Neurohumoral regulation: Hormones (aldosterone, vasopressin, natriuretic peptides) regulate vascular tone and kidney function, allowing the body to adapt to changes in temperature, physical activity, or body position.

Edema develops when one or more of these systems fail to cope with the load. Further understanding of the cause of swelling depends on the level at which the failure has occurred.

Main mechanisms of edema formation

Despite the wide variety of clinical situations, edema forms through a limited number of basic mechanisms. This is critically important to understand: the same external symptom may look identical but have completely different underlying causes. That is why there is no universal way to “get rid of excess water” — treatment must target the specific disrupted mechanism.

Increased hydrostatic pressure

This mechanism is directly related to the mechanical pressure of blood on the vessel walls. When venous outflow slows down (due to weakness of the heart muscle or venous insufficiency), blood stagnates, and pressure inside the capillaries increases. Under this physical force, water is literally “pushed” into the surrounding tissues.

Clinical features: Such edema directly depends on gravity. It is localized in the lower extremities, worsens in the evening after prolonged standing, and significantly decreases or disappears after a night’s rest.

Decreased oncotic pressure

Oncotic pressure is created by plasma proteins, primarily albumin. Protein acts like a sponge: it holds water inside the vascular bed. If protein levels decrease (due to liver disease, where it is synthesized, or loss through the kidneys), this retaining force weakens, and fluid freely moves into the tissues even at normal pressure.

Clinical features: This type of edema does not depend on body position. It is usually soft, “mobile,” spreads throughout the body, and is often accompanied by generalized soft swelling of the face and torso.

Increased vascular permeability (Membrane mechanism)

Normally, the vascular wall acts as a selective filter. However, during inflammation, anaphylactic/allergic reactions, or exposure to toxins, the pores in this “mesh” expand. As a result, not only water but also large protein molecules move into the intercellular space, drawing even more fluid with them.

Clinical features: Such edema develops rapidly and can be either localized or systemic (for example, in severe allergic reactions). It may appear in a limited area or involve multiple regions (such as the face, lips, or tongue) and is often accompanied by redness or itching. It is not related to an overall excess of fluid in the body but rather to a problem with the “heaviness” of specific vessels.

Osmotic retention of sodium and water

Sodium is the main “magnet” for water in the extracellular space. When the kidneys, for various reasons (hormonal imbalance, renal pathology), begin to retain sodium, it inevitably draws water with it to maintain the required salt concentration. The total circulating blood volume increases, and excess fluid is distributed into the tissues.

Clinical features: Systemic edema that is often noticeable in the morning. Characterized by sharp fluctuations in body weight (up to 1–2 kg per day) and pronounced sensitivity to salt intake.

Impaired lymphatic drainage (Lymphedema)

The lymphatic system acts as the body’s “drainage pump.” It returns to the bloodstream those proteins and fluid that could not re-enter the veins directly. If lymphatic pathways are compressed, damaged, or overloaded, tissues begin to “accumulate” fluid.

Clinical features: Edema develops gradually, is dense (pitting is prolonged or absent), often asymmetric, and poorly responds to standard diuretics or short-term rest.

Why mechanisms are rarely isolated

In real clinical practice, “pure” mechanisms are rare. The body is a system of feedback loops, so a disturbance at one level quickly involves others.

Examples of cascade reactions:

• Heart failure: Begins with increased venous pressure (hydrostatic mechanism), but due to reduced renal perfusion, hormonal sodium retention is activated (osmotic mechanism);
• Liver disease: Reduced protein synthesis (oncotic pressure) leads to fluid leakage into tissues. This decreases intravascular volume, and the kidneys, perceiving this as a deficit, begin to retain sodium (osmotic mechanism).

That is why attempting to treat edema from only one perspective, for example using only diuretics, is often ineffective or even dangerous. Diuretics reduce fluid volume but cannot repair venous valves, restore plasma protein levels, or correct lymphatic drainage.

Understanding where edema is localized is the first step in identifying the “broken” mechanism. In medicine, it is essential to distinguish between local disturbances in a specific area and systemic dysfunctions affecting vital organ systems.

Local edema

Local edema is limited to one area or part of the body. In these cases, the total volume of water in the body may remain normal, and the problem lies in impaired local outflow or vascular damage. The key feature of such edema is asymmetry.

• Venous insufficiency: When venous valves fail, blood stagnates in the lower extremities under the influence of gravity. Pressure in the capillaries increases, and fluid moves into the tissues. Such edema is localized in the ankles and lower legs, worsens in the evening, and significantly decreases after rest with the legs elevated;
• Lymphedema (lymphostasis): Occurs when lymphatic drainage fails to remove proteins and fluid from the intercellular space. Edema in lymphedema is usually dense, often asymmetric (one leg noticeably larger than the other), and poorly responds to body position or diuretics;
• Inflammatory and traumatic edema: In trauma or infection, the vascular wall becomes “leaky” (permeability increases) to allow immune cells to reach the affected area. Fluid follows. Such edema is always accompanied by pain, redness, or local increase in temperature;
• Deep vein thrombosis: When a clot forms in deep veins, venous outflow is sharply impaired, pressure in the venous system increases, and fluid begins to move into surrounding tissues. Edema usually develops in one leg and is accompanied by a feeling of tightness, pain, or increased skin temperature;
• Baker’s cyst: This is an accumulation of fluid in the popliteal area associated with knee joint pathology. When enlarged or ruptured, fluid may spread into the lower leg tissues, causing local edema that can resemble venous thrombosis;
• Soft tissue cellulitis: Bacterial inflammation of the skin and subcutaneous tissue leads to increased vascular permeability and fluid influx into tissues. Edema is accompanied by pronounced redness, tenderness, and local warmth.

Systemic edema associated with organ function

Systemic edema affects multiple areas of the body simultaneously and indicates that the body’s regulatory systems are not coping with the load.

Heart (cardiac edema)

When the heart loses its pumping function, blood begins to stagnate in the veins (“a queue” at the entrance to the heart). Pressure in the vessels increases, and the kidneys, receiving less blood, mistakenly begin to retain sodium and water in an attempt to raise pressure. Such changes often develop against the background of prolonged cardiac overload, for example in chronic high blood pressure.

• Typical presentation: Initially appears in the feet and lower legs, is symmetrical, worsens in the evening. In advanced stages, it may spread higher and be accompanied by shortness of breath;

Kidneys (renal edema)

The kidneys directly regulate salt balance. In pathology, sodium is retained systemically, drawing water into all tissues.

• Typical presentation: Unlike cardiac edema, renal edema “prefers” loose tissue. It appears in the morning on the face and eyelids (“bags” under the eyes), is soft and doughy to the touch, and may shift downward by evening;

Liver (hepatic edema)

The liver synthesizes albumin — the main protein that holds water inside the vessels. When liver function declines, oncotic pressure decreases, and fluid literally leaks out of the vessels into tissues and body cavities.

• Typical presentation: Often accompanied by abdominal enlargement due to fluid accumulation in the abdominal cavity (ascites) and generalized soft tissue swelling;

Thyroid gland (myxedema)

This is a special, atypical type of edema. In hypothyroidism, complex sugars (glycosaminoglycans) accumulate in the intercellular space. They turn tissue fluid into a viscous gel.

• Typical presentation: The edema is very dense, meaning that if you press on the anterior surface of the shin, no pit forms. This is “myxedematous” edema that requires correction of the hormonal background rather than removal of water.

Externally, edema in the leg in heart failure and hypothyroidism may look similar, but their pathophysiology is fundamentally different. The use of diuretics in myxedema (thyroid-related edema) will be ineffective, while in venous insufficiency it will only serve as a temporary “crutch” that can lead to dehydration and blood thickening without addressing valve dysfunction.

Systemic edema associated with hormonal factors

Hormones rarely act as the sole cause of edema, but they create the physiological background in which fluid retention becomes clinically apparent. The hormonal system directly affects kidney filtration, vascular tone, and the hydrophilicity (ability to attract water) of tissues themselves. This is why hormonal edema is unstable, cyclical, and often depends on external factors such as diet or stress levels.

Estrogens and progesterone

Estrogens have a pronounced ability to retain sodium and water and increase capillary permeability. This leads to fluid leaving the vessels more easily and returning less efficiently.

• Clinical features: Characteristic worsening of edema in the second phase of the cycle (PMS) or during pregnancy, when estrogen effects are not balanced by sufficient progesterone. Edema may affect the face, breasts, and lower legs and fluctuate noticeably from day to day;

Cortisol (stress hormone)

Cortisol affects water-salt balance through cross-interaction with aldosterone receptors. During chronic stress or glucocorticoid use, the body begins to “store” sodium.

• Clinical features: A feeling of general “fullness” and puffiness develops. Such edema is often accompanied by changes in well-being, sleep disturbances, and cravings for salty food;

Aldosterone and RAAS

The renin–angiotensin–aldosterone system (RAAS) is the main “control panel” of fluid volume. Aldosterone signals the kidneys to return sodium from primary urine back into the blood.

• Clinical features: With hyperactivity of this system, edema becomes systemic and symmetrical. It is highly sensitive to salt intake: even small amounts of sodium chloride can cause noticeable fluid retention the next day;

Insulin and insulin resistance

Insulin is a powerful stimulator of sodium reabsorption in the renal tubules. With elevated insulin levels (even when blood glucose is normal), the kidneys operate in a “water-conserving” mode.

• Clinical features: Evening swelling and a sharp increase in edema after consumption of simple carbohydrates (sweets, refined flour). In patients with insulin resistance, edema is often the result of a “carbohydrate rebound”;

Androgens and antiandrogen therapy

Androgens themselves rarely cause edema directly, but they influence it indirectly through metabolism and vascular tone.

• Special case: During antiandrogen therapy, the hormonal balance may shift toward relative estrogen predominance. This alters fluid regulation at the tissue level. Edema develops gradually, is symmetrical, and often does not respond to standard diuretic therapy because the issue lies in receptor sensitivity rather than excess fluid intake.

The main difficulty is that hormones rarely create edema “from scratch” but rather reveal existing weak points. If a person has mild venous insufficiency, hormonal changes will make it clinically apparent. If the kidneys are already functioning at their limit, hormones will push the situation into visible edema. That is why such symptoms require a comprehensive assessment — not only hormone levels but also the condition of target organs (vessels and kidneys).