Types of edema

Classification by etiology

Depending on the cause of the disease (etiology), the following main types of edema are distinguished:

• Cardiac;
• Renal (this group is strictly subdivided into two fundamentally different types: nephrotic and nephritic);
• Cachectic (in clinical practice, they are often called "hunger" edema);
• Hepatic;
• Angioneurotic;
• Allergic;
• Toxic and a number of other forms.

Each of these types has its own specific pattern of development, but is subject to the general laws of pathogenesis.

General mechanisms: hormones and the lymphatic system

Systemic hormonal regulation of the water-electrolyte balance plays a huge role in the progression of any edema syndrome. The key trigger in this process is hypovolemia — a pathological decrease in the volume of circulating blood. It triggers the following neurohumoral cascade:

1. In response to a decrease in blood volume, the secretion of aldosterone increases sharply. This hormone causes massive sodium retention in the body, leading to the development of hypernatremia.
2. Concurrently, the production of antidiuretic hormone (ADH) increases. The main task of ADH is water retention, which ultimately leads to the formation of hypervolemia.

In addition to hormonal imbalance, dynamic lymphatic insufficiency inevitably develops in the tissues. Its mechanism is caused by physical factors: due to the massive exit of water from blood vessels into the interstitial space, a sharply increased volume of lymph is formed. Lymphatic vessels simply cannot cope with adequate drainage of such a colossal amount of fluid, which exacerbates the edema.

Cachectic ("hunger") edema

This type of edema manifests in stage III of general or protein malnutrition (cachexia). Under conditions of severe nutrient deficiency, the body is forced to use its own structural proteins to meet basic energy needs. The catabolism process proceeds in a strictly sequential manner: blood plasma proteins (predominantly albumins) are consumed first, followed by tissue proteins, including the most important protein structures of vascular membranes.

The pathogenesis of cachectic edema has a complex mixed nature and unfolds in stages:

1. Oncotic factor (is the leading one): Develops first. Due to the consumption of albumins, pronounced hypoproteinemia (blood hypoonquia) occurs. Plasma oncotic pressure drops, and fluid rushes into the tissues.
2. Osmotic factor: Activated secondarily. The loss of fluid into the tissues causes hypovolemia, which immediately activates the aldosterone–ADH system.
3. Membranogenic factor: Arises due to the breakdown of proteins in the vascular wall itself, which critically increases its permeability to the fluid part of the blood.
4. Hydrodynamic factor: Joins in terminal states (e.g., during the development of hunger syncope or cachectic coma), when severe cardiovascular failure increases against the background of general exhaustion.

Nephritic edema

Etiologically, nephritic edema is inextricably linked with the early stage of acute diffuse glomerulonephritis — a severe disease based on an infectious-allergic lesion of the renal glomeruli.

The pathogenesis of nephritic edema has a completely different sequence of mechanism activation:

1. Membranogenic factor: In this case, it is the starting factor. There is a generalized lesion of capillaries, which leads to a sharp increase in the permeability of microvascular walls throughout the body.
2. Activation of the RAAS: Due to the inflammatory process in the glomeruli, renal blood flow decreases. This immediately activates the renin–angiotensin–aldosterone system, causing pathological retention of Na^+ and H_2O ions.
3. Hypervolemia: A drop in the glomerular filtration rate leads to a sharp decrease in urine formation. As a result, the volume of circulating blood increases pathologically.
4. Oncotic factor: Progressive blood hypoonquia develops. In nephritic edema, it is caused by three reasons simultaneously:
5. Dilution of plasma proteins due to developed hypervolemia;
6. Moderate proteinuria (loss of protein in the urine);
7. Exit of protein from the vascular bed into the tissues through damaged capillary walls.

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Pathogenesis of cardiac edema
• Nephrotic edema (differences from nephritic)
• Hepatic edema
• Mechanisms of allergic and angioneurotic edema development
• Toxic edema

Other topics in the section "Morphology of Metabolic Disorders — Dystrophies"

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