Swelling of the legs: effective ways to solve the problem

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Edema of the legs in chronic venous insufficiency: clinical manifestations, medical and surgical treatment

Patients with edema of the lower extremities (LE) are encountered in the practice of doctors of various specialties. Often, the appearance of edema is a sign of the development of a pathology of the venous system in a patient, in particular acute venous thrombosis or severe chronic damage to the venous bed, which can potentially lead to disability or even death of the patient. Meanwhile, the reasons for the development of LE edema are diverse, sometimes there is a combination of them, and an incorrect assessment of the clinical situation can lead to serious errors in the patient’s treatment strategy. The development of edema of the legs can be either a consequence of diseases of the vascular bed or the musculoskeletal apparatus of the NK itself, or a manifestation of some diseases of the internal organs, and sometimes even a combination of these diseases.

The causes of NK edema may be the following: 1) acute disorders of venous circulation (deep vein thrombosis – DVT); 2) chronic venous insufficiency (CVI); 3) lymphostasis (lymphedema); 4) circulatory failure (ischemic heart disease, heart defects, myocarditis, cardiomyopathy, chronic cor pulmonale); 5) kidney pathology (acute and chronic glomerulonephritis, diabetic glomerulosclerosis, systemic lupus erythematosus, nephropathy of pregnancy); 6) pathology of the liver (cirrhosis, cancer); 7) osteoarticular pathology (deforming osteoarthrosis, reactive polyarthritis); 8) idiopathic orthostatic disorders of blood outflow from NK.

The NK edema is caused by disturbances in venous and lymphatic outflow at the macrohemodynamic level, which lead to disorganization of the regional microcirculation system. CVI NK can be combined with heart failure (HF) and / or osteoarthritis, kidney disease, liver disease and other diseases.

In this regard, it must be remembered that the intensity of chronic venous edema of the LE always corresponds to the severity of pathomorphological changes in the local venous system. Ignoring this fact leads to a tactical error, when a patient with initial changes in the venous system (multiple telangiectasias, reticular varicose veins, varicose dilatation of the saphenous vein inflows, blood reflux of small length and volume, etc.) and edema of the extremities due to another pathology has no alternative recommend surgery.

Determining the type of edema is important for the diagnostic search for the causes of its development. It is necessary to pay attention to factors that will help differentiate the type of edema. Factors contributing to the development of edema are the following:

  • increase in hydrostatic pressure in capillaries;
  • decrease in oncotic pressure of blood plasma;
  • increased oncotic pressure of the interstitial fluid;
  • reduction of tissue mechanical pressure;
  • increased capillary permeability;
  • violation of the outflow of lymph.

Edema types

There are local (localized) edema associated with fluid retention in a limited area of ​​body tissues or an organ, and general (generalized) – a manifestation of the water imbalance of the body as a whole. Generalized edema includes edema in chronic heart failure, cirrhosis of the liver, nephrotic and nephritic, dropsy of pregnancy, cachexic and idiopathic, as well as resulting from chronic loss of potassium by the body during the abuse of laxatives.

Localized edema develops in the absence of general disorders of water and electrolyte metabolism and is associated with the presence of local disorders of veno- and lymphodynamics, capillary permeability and metabolism. Due to a number of anatomical and hemodynamic reasons, among which high hydrostatic pressure is of the greatest importance, the most common is LE edema, which, although not a specific nosological form in itself, usually reflects the presence of a local pathological process in the body. In most cases, NK edema develops against the background of CVI and is the main symptom of its 3rd clinical class according to the international CEAP classification. Signs of CVI NK, according to foreign and domestic literature, are available in 15-40% of the population of European countries. At the same time, in 5-8% of cases, constant edema is observed that does not have a pronounced daily dynamics.

Chronic edema in CVI LE develops against the background of a prolonged increase in intravenous pressure, resulting in a violation of the normal permeability of the venous wall and an increase in transcapillary filtration with penetration into the interstitial tissue of large molecular proteins – fibrinogen, hemoglobin fragments, fragments of blood cells, which have a high ability to fix on themselves water. In the initial stages of the development of venous edema, excess interstitial fluid is excreted through the activation of lymphatic drainage. Clinically, this period corresponds to transient (appearing in the evening and completely disappearing in the morning) edema of the lower leg and foot.

Features of the manifestation of swelling of the legs

Edema can be either on one (monolateral) or on both NKs (bilateral). Monolateral edema occurs in acute DVT, CVI LE, acute osteoarthritis, lymphedema. Bilateral edema occurs in chronic heart failure, kidney and liver diseases, dysproteinemia, and as a consequence of the use of certain drugs (hormones, calcium antagonists, etc.).

With CVI NK, the general condition may not be disturbed. Patients complain of a sharp thickening and deformation in the distal limbs of the lower leg, a feeling of heaviness in it (especially during physical exertion), numbness, sometimes shooting pains, and general fatigue. There may be complaints of sharply increased sweating of the affected limb, discoloration of the skin, recurrent exacerbation of the inflammatory process, “wetting” of the skin surface, eczema and ulcers.

With CVI NK, the first reason for visiting a doctor is often a cosmetic defect in the legs. The intensity of pain does not always correspond to the degree of expansion of the superficial veins. Pain occurs when, due to insufficiency of valves in the perforating veins, blood begins to flow from the deep veins to the superficial ones. The pressure in the veins of the legs increases, the pain gradually increases (especially when standing), swelling of the feet occurs, trophic disorders – dryness and hyperpigmentation of the skin, hair loss, muscle spasms appear at night. Diagnosis of CVI NK is based on the data of the clinical picture and the results of a special instrumental examination, allowing to confirm or exclude the local vascular genesis of edema. In order to avoid diagnostic and tactical errors, especially in elderly patients who often may have several diseases that cause edema (CVI NK and osteoarthritis or CVI NK and CHF, etc.), it is necessary to remember the presence of possible polymorbidity.

An important aspect in determining the etiology of edema, respectively, and treatment, is the differential diagnosis. Swelling of the NK with lesions of the veins of soft or moderate density, edematous skin is warm. With lymphostasis, irreversible subcutaneous seals often occur. Nephrotic edema is characterized by gradual development. Edema is localized (in addition to NK) on the face, especially in the eyelids (facial swelling is more pronounced in the morning), lower back, genitals, anterior abdominal wall. Edema quickly shifts with a change in body position. Edematous skin is dryish, soft, pale, sometimes shiny. Laboratory tests are characterized by low serum protein, proteinuria, and elevated blood lipids.

Edema in cirrhosis of the liver usually occurs in the late stage of the disease. They are manifested mainly by ascites, which is more pronounced than edema on the NK. Sometimes hydrothorax (usually right-sided) is detected. Edematous skin of NC is dense, warm.

Cachectic edema occurs with general starvation or a sharp lack of protein in food, as well as with diseases accompanied by loss of protein through the intestines (exudative forms of gastroenteritis, ulcerative colitis, lymphangiectasia with intestinal tumors).

In severe beriberi, alcoholism, edema is usually small, localized on the legs and feet, often accompanied by puffiness of the face. Swelling of the whole body is very mobile. Edematous skin of doughy consistency, dry. Characterized by general exhaustion, hypoglycemia, hypocholesterolemia, severe hypoproteinemia, hypoalbuminemia.

In cardiovascular diseases with the development of CHF, edema increases gradually. Simultaneously with the presence of edema, swelling of the jugular veins and congestive enlargement of the liver are noted, which are signs of right ventricular failure. Edematous skin with cardiac edema is quite elastic, and with distal edema it is compacted, may be rough, usually cold, cyanotic. In HF, edema is localized symmetrically, mainly on the ankles and legs in walking patients, in the tissues of the lumbar region and back in bedridden patients. Often there is massive ascites.


The NK edema caused by CVI is an absolute indication for selective complex conservative treatment, including a therapeutic and protective regimen, compression, taking phlebotropic drugs, physiotherapy and unloading exercises. An attempt at surgical intervention at the height of the development of venous edema is a gross mistake, fraught with the development of complications in the immediate period (lymphorrhea, skin necrosis) and the long-term (lipodermatodystrophy, cellulitis, lymphostasis) period.

  1. Therapeutic and protective regime includes limiting prolonged static loads and heavy lifting, eliminating the risk of leg injury and overheating of the body. In some cases, it is advisable to “hospitalize” such patients at home. At the same time, they are recommended to be predominantly in a horizontal position with the foot end of the bed raised at an angle of 15-20 °.

  2. Compression of the affected limb is carried out using bandages of limited extensibility or medical knitwear of II-III compression classes, selected individually. A good and quick decongestant effect is provided by hardware pneumocompression (15-20 procedures lasting 45-60 minutes and with a pressure of 80-100 mm Hg) with the obligatory subsequent imposition of a compression bandage.

  3. Phleboprotectors are the basis of drug therapy for edematous conditions in vein lesions, regardless of its origin (varicose veins, consequences of DVT, congenital anomalies, phlebopathies, etc.). It is very important that in this case the therapeutic effect is systemic and affects the venous system of both the NK and other anatomical regions (upper limbs, retroperitoneal space, small pelvis, etc.). Due to this, some phleboprotectors are successfully used not only in phlebological practice, but also in other areas of medicine: proctology (prevention and treatment of complications of chronic hemorrhoids), ophthalmology (rehabilitation of patients who have had thrombosis of the central retinal vein), gynecology (treatment of dysfunctional uterine bleeding, premenstrual syndrome, etc.), and recently in neurology (treatment of cerebral venous disorders).

In some cases, the anti-edematous effect of phleboprotectors can be potentiated, if necessary, by polyenzymatic preparations and diuretics. The latter should be used with great caution, since against the background of forced and prolonged diuretic therapy in patients with CVI, an increase in blood viscosity and hemocoagulation is possible, which, on the one hand, worsens microcirculation, and on the other hand, can provoke acute venous thrombosis.

It must be remembered that in cases of ineffectiveness of conservative therapy, manifested by an increase in edema or the appearance of trophic changes in the skin, surgical treatment may be used. However, an attempt at surgical intervention at the height of chronic venous edema is a gross tactical mistake, fraught with development in the immediate (lymphorrhea, skin necrosis) and late postoperative periods. Any surgical operations for post-thrombophlebitic disease are palliative, and further management of such patients without fail requires compression therapy, the use of phleboprotectors and rehabilitation therapy.

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