Peripheral edema

E.N. Amosova. Corresponding Member. AMS of Ukraine, Dr. med. Sci., Professor, Head. Department of Hospital Therapy №1

L.L. Sidorov. Cand. honey. Sci., Associate Professor, Department of Hospital Therapy No. 1

National Medical University. A.A. Bogomolets

Edema is an increase in extravascular(interstitial) component of the extracellular fluid. Peripheral edema is characterized by a visible and palpable pathological accumulation of free fluid in the subcutaneous connective tissue.

In a number of cases, for example, with cardiac edema,accumulation of fluid occurs also in cells. Peripheral edema becomes noticeable after increasing the amount of fluid in the interstitial tissue by an average of 5-7 liters. This is preceded by so-called hidden edema, detected only indirect methods (measurement of body weight in dynamics, including after taking diuretics).

Special forms of edema are ascites and hydrothorax, i.e. accumulation of excess fluid in the abdominal and pleural cavities. Significant edema of the whole body is called anasarka.

Depending on the etiology and pathogenesis, swelling can be general (generalized) and local.

The main causes of peripheral edema:

4. Other hypoproteinemic conditions (exudative enteropathy, malabsorption syndrome, alimentary and cachectic edema).

7. Taking medications.

- Acute thrombosis or thrombophlebitis of deep veins;

- violation of venous outflow (venous obstruction);

chronic venous insufficiency.

3. Fatty edema (lipoidema).

- angioedema (edema of Quincke);

scleroderma (systemic and focal);

- swelling on the soil of arteriovenous anastomosis.

Decrease in the minute volume of the heart withcoronary and non-coronary heart diseases by reducing the irritation of the aortic baroreceptors and renal blood flow leads to the activation of the sympathetic part of the autonomic nervous system and neurohumoral regulatory systems (Fig. 1), which initially plays a compensatory role and is aimed at maintaining the stroke volume of the heart. However, over time, cardiac output decreases and swelling develops due to increased hydrostatic pressure in the capillaries above the level of colloid osmotic pressure.

Increased hydrostatic pressure in the vessels andcolloid osmotic (oncotic) pressure of the interstitial fluid facilitates the movement of water from the arteriolar part of the capillaries into the tissues. With patency of lymphatic canals, this process is accompanied by an increase in lymphatic drainage. With increasing oncotic pressure of the plasma and / or hydrostatic pressure of the interstitial fluid (the so-called tissue stress), it, on the contrary, passes from the tissues to the capillaries in their venous part, and also enters the vascular bed through the lymphatic system. The magnitude of the oncotic pressure is determined by the concentration of the protein, which in the blood plasma is much higher than in the tissues, since the wall of the capillaries is normally impermeable to protein molecules.

The concentration of electrolytes, especially Na +,has a significant effect on the total amount of fluid in both the vessels and in the intercellular tissue. The delay of Na + by the kidneys simultaneously leads to an increase in the volume of circulating plasma and tissue fluid. In the pathogenesis of edema, the increase in the permeability of the wall of capillaries under the influence of chemical, infectious, immune, thermal and other factors is also important, which leads to the release of proteins from the blood into the tissues, as well as impaired patency of lymphatic vessels. In some cases, the mechanism of edema development remains unclear.

With local disturbance of venous outflow of bloodthe hydrostatic pressure in the capillaries rises sharply proximally to the site of the obstruction, which causes an increased transfer of fluid from them to the interstitial space. Similar pathogenesis has local lymphatic edema due to impaired lymphatic drainage. Local accumulation of liquid is promoted by an increase in the protein content in it. In hypoproteinemic conditions, a decrease in the oncotic pressure of the blood plasma causes an intensified transfer of intravascular fluid into the tissue with the development of hypovolemia and the inclusion of renal and humoral mechanisms of Na + and water retention. As long as the expressed hypoalbuminemia persists, Na + and water can not remain in the vascular bed, and therefore the stimulus for their kidney delay continues to act. Pathogenetic factors of edema in cirrhosis of the liver, in addition to hypoalbuminemia, are portal hypertension and impaired intrahepatic lymphatic drainage, which cause excessive accumulation of fluid in the abdominal cavity (ascites).

Differential and diagnostic features of various types of edema

Cardiac edema is formed in sheltered places,corresponding to the largest value of the hydrostatic pressure. They first appear in the area of ​​the ankles and at first disappear in the morning after sleep. Gradually, swelling spreads to the upper half of the trunk. Since the localization of such edema depends on the position of the body, in bedridden patients they are more pronounced in the region of the sacrum or on the corresponding side with constant lying on one side.

Very characteristic of cardiac edema isthe presence of other manifestations of heart failure and its cause - heart disease. The first include cyanosis, dyspnea and tachycardia, which increase with exercise, gallop rhythm, congestive wheezing in the lungs, hepatomegaly. Especially valuable distinctive features are cardiomegaly and an increase in central venous pressure (clinically manifested by cervical vein swelling). Ascites appear after the development of edema and enlargement of the liver.

For edema that occur as a result of reducedoncotic pressure, the most characteristic absence of a pronounced dependence on the position of the body and a low content of total protein or albumin in the blood serum. These include edema with nephrotic syndrome, with severe liver disease, "hungry" and cachectic.

The most frequent causes of nephroticsyndrome are acute and chronic glomerulonephritis, diabetic glomerulosclerosis, amyloidosis of the kidneys, more rare - systemic vasculitis, neoplasms. Like all hypoproteinemic edema, they first appear in places of accumulation of loose connective tissue, especially in the eyelid, more often after sleep, then cause a puffiness of the face and only then spread throughout the body. Patients are pale and anemic. Of decisive importance are laboratory data. Determined massive proteinuria, hypoproteinemia, dysproteinemia and in a number of patients - hypercholesterolemia.

General hypoproteinemic edema is observedalso with insufficient intake of protein with food, a violation of its absorption in the intestine (malabsorption syndrome) or increased catabolism (cachexia). Alimentary swelling is not accompanied by cardio- and hepatomegaly and changes in the urine. With an increase in the amount of food they eat, they can build up, which is due to an increase in the intake of salt in the body, causing a fluid retention. With cachectic edema, the symptoms of a major disease, for example, a malignant tumor or tuberculosis, are clearly pronounced.

For edema with cirrhosis of the liver, ascites are characteristic,which precedes peripheral edema, as well as other signs of portal hypertension (enlargement of the liver, spleen, port-caval anastomoses) and liver damage (jaundice, "spider veins", etc.). In contrast to heart failure, cervical veins in these patients are not swollen, central venous pressure, as well as the size and function of the heart are practically unchanged

For myxedema, there is a general swelling in whichpressing on the skin does not leave a trace. Skin rough, rough, dense. To diagnose the disease, signs such as weight gain, inhibition, delayed speech and movements, drowsiness, fatigue, low voice, hair loss, and a tendency to bradycardia and arterial hypotension (occasionally there may be hypertension) can diagnose the disease. The diagnosis is confirmed by the results of determining the level of thyroid hormones in the blood.

The cause of edema can also be a number ofdrugs that promote kidney retention Na + and water: hormonal (glucocorticosteroids, estrogens, progesterone, testosterone); antihypertensive (hydralazine, rauwolfia alkaloids, guanethidine); calcium channel blockers (dihydropyridine derivatives); non-steroidal anti-inflammatory drugs (diclofenac, indomethacin, etc.); antidepressants (MAO inhibitors).

Angioedema (angioedema) - quicklydeveloping local edema of the skin, subcutaneous tissue and (or) mucous membranes in combination with hives or without it. It is most often a manifestation of type I allergic reaction and develops as a manifestation of sensitization to medicines (more often antibiotics), food products and venom of stinging insects (wasps, bees and hornets). It can develop due to direct non-immune histamine-releasing action of non-steroidal anti-inflammatory drugs, angiotensin-converting enzyme inhibitors and dextrans. In some cases, the cause of edema remains unknown (Idiopathic Quincke's Edema). Angioedema may develop on any part of the body, most often on the face and limbs. The danger to life is the swelling of the larynx and the asphyxia caused by it.

Periorbital edema and erythema (symptom of "glasses")are characteristic for dermatomyositis. This disease reveals a variety of skin changes: papular, bullous, petechial rashes, telangiectasias, foci of pigmentation, depigmentation and hyperkeratosis. Edema of the face and extremities is usually localized over the affected muscles, has a doughy or dense consistency. Diagnosis is made on the basis of typical skin changes, progressive weakness in the symmetrical sections of the proximal muscles of the extremities, increasing levels of serum muscle enzymes and creatinine.

Sudden appearance of edema in one of the lowerlimbs are characteristic of deep vein thrombosis. The cause of the violation of venous outflow may be the compression of these vessels from the outside by a tumor or lymph nodes.

Venous edema can also be caused bychronic venous insufficiency on the basis of varicose veins or postthrombophlebitic insolvency (postthrombophlebitic syndrome) and other causes.

With thrombosis or compression of the pelvic veins, edemaspread to both lower limbs, and when the obstruction is localized at the level of the inferior vena cava - also on the skin of the abdomen and the lumbar region. Other manifestations of this so-called syndrome of the inferior vena cava are the expansion of collaterals in the abdominal region, and if the blood flow is more proximal to the place where the hepatic veins fall, also ascites and the head of the jellyfish.

In the syndrome of the superior vena cava,significant edema and cyanosis of the upper half of the trunk, face, occiput, neck ("Stokes collar"), upper limbs, which are more pronounced in the horizontal position of the patient. The causes of this syndrome are lung cancer, tuberculosis, aortic aneurysm, mediastinitis, mediastinal tumor, lymphoproliferative diseases, thrombophlebitis.

Features of local venous edema arecyanosis of the skin and enhancement of its superficial venous pattern ("venous stars"), as well as a reduction in edema with an elevated limb position. Confirm the diagnosis and establish the localization of obstruction or failure of venous blood flow allows Doppler ultrasound examination of veins and impedance plethysmography, and in disputable cases - phlebography.

Lymphatic edema caused by stagnation of lymph,in most cases, unilateral, edematous tissue dense to the touch, painless when pressed, the skin over it thickened ("pig skin"). With the elevated position of the limb, puffiness decreases more slowly than with venous edema, and the pressure trail persists longer.