Fluid makes up approximately 70% of a person's body weight. About 60-70% of it is located in cells. Outside the cells is about 1/3 of the water contained in the human body, of which plasma makes up 20-25%, the rest is extracellular fluid. Thus, the body of a man weighing 70 kg contains 40 kg of water, of which 24 kg is contained in cells, 11 kg in the interstitial space, 3 kg in plasma and 2 kg in other compartments. There is a constant exchange of electrolytes and other substances involved in metabolism between the cellular and extracellular fluid. The volume, composition and distribution of fluid in the body are among its physiological constants. Interstitial fluid provides elasticity to soft tissues - turgor, usually assessed by an experienced specialist. Moreover, a small increase in the volume of interstitial fluid is not detected, while an excess of several liters contributes to the appearance of visible swelling.
Edema is a term that reflects increased fluid content in the interstitial space of tissue or in body cavities. Swelling can be local as a result of local circulatory disorders and general (generalized). Generalized edema, although it spreads over the entire surface of the body, can be more pronounced in certain areas. Thus, in heart failure, edema is located under the influence of gravity in the lower extremities. In addition, peripheral edema is often combined with the presence of effusion in the cavities (hydrothorax, hydropericardium, ascites).
The main etiological factors of peripheral edema are presented in Table 1.
Table 1. Main causes of peripheral edema
— Systolic and diastolic dysfunction of the left ventricle
— Right ventricular systolic dysfunction
— Pathology of the tricuspid valve
— Acute thrombosis or thrombophlebitis of deep veins
— Violation of venous outflow (venous obstruction)
— Chronic venous insufficiency
— Acute and chronic renal failure
— Alimentary and cachectic edema
— Scleroderma (systemic and focal);
— Edema due to arteriovenous anastomosis
Pathogenesis of edema. An increase in the volume of interstitial fluid can potentially lead to the appearance of edema, but in healthy individuals this does not occur due to the existence of a strict balance of hemodynamic forces along the capillary wall and adequate functioning of the lymphatic vessels. For the formation of generalized edema, the presence of two factors is necessary:
a change in capillary hemodynamics that promotes the movement of fluid from the vascular space into the interstitium.
retention of sodium from food or intravenous administration and water in the kidneys.
For the formation of edema, changes in one or more Starling forces are required in the direction of increased filtration, the development of which can be caused by an increase in hydrostatic pressure in the capillaries, capillary permeability or oncotic pressure of the interstitial space, or a decrease in plasma oncotic pressure. The cause of edema may be obstruction of the lymphatic vessels, as a result of which normally filtered fluid does not return to the systemic circulation (Table 1).
It is important to emphasize the role of the kidneys in the development of edema. Edema (with the exception of local edema and allergic reactions) becomes clinically obvious only when the interstitial volume increases by 2.5-3 liters. Because the normal plasma volume is only about 3 liters, patients would develop hemoconcentration and shock if plasma volume was not maintained through renal sodium and water retention. In most cases of edema, sodium and water retention in the kidneys is an appropriate compensation, thereby maintaining tissue perfusion, but also leading to an increase in the degree of edema.
Retention of sodium and water in the kidneys may be primary (as in renal failure), or secondary to a decrease in cardiac output (particularly in heart failure) or systemic vascular resistance (eg in liver cirrhosis). In the latter case, fluid retention is aimed at normalizing the effective circulating volume. Renal sodium and water retention observed in heart failure or cirrhosis is associated with a hypovolemia-induced decrease in glomerular filtration rate and, more importantly, an increase in tubular reabsorption. The latter is mediated by activation of the renin-angiotensin-aldosterone and sympathetic nervous systems, arginine-vasopressin (Fig. 1).
Fig.1. Mechanisms of Na+ and water retention and edema formation (Harrison T.R. Internal Medicine, 1997). Abbreviations: ADH – antidiuretic hormone (arginine vasopressin); BCC – circulating blood volume; GFR – glomerular filtration rate; CVP – central venous pressure.
The pathogenetic mechanisms of edema formation in various clinical situations are summarized in Table 2.
Table 2. Pathophysiology of edema (Collins RD Differential Diagnosis in Primary Care, 2007)
Complaints. Patients complain of swelling, especially of the limbs and face, causing some discomfort, possibly rapid weight gain (due to swelling).
History of the disease. A comprehensive approach is used when assessing patients with edema. It is necessary to clarify whether the patient’s weight has changed recently, since with systemic fluid retention this indicator can increase by 10% before visible edema appears. It is useful to ask the following questions:
— Is it difficult to take rings off your fingers or put them on?
— Has the belt or belt become tight?
—Have your clothes or shoes become too tight?
The rate of appearance of peripheral edema should be clarified, which makes it possible to determine the severity of the process. Thus, edema that develops suddenly requires urgent diagnosis, since it can be a serious manifestation of serious conditions. It is important to carefully collect a medical history, especially indications of previous trauma, surgery or prolonged immobilization, which increase the likelihood of venous thrombosis. In the case of a gradual onset, clarify whether there is a periodicity in the appearance of edema (for example, the appearance of edema in the legs in the evening and its disappearance in the morning) or whether it persists constantly.
Swelling accompanied by pain occurs with trauma, acute venous thrombosis, cellulite, rupture of Baker's cyst, and interfascial space syndrome. Painless swelling is usually due to systemic causes.
When collecting anamnesis, you should pay attention to the presence of concomitant symptoms of pathology of the heart, lungs, liver, kidneys or endocrinological diseases, which is important in determining further tactics for examining the patient. Thus, fever and chills are detected with lymphangitis, venous thrombosis or cellulite; chest pain, shortness of breath and orthopnea - in case of heart disease, a feeling of heaviness and abdominal distension - may be due to liver pathology with ascites, and indications in the history of recent pharyngitis or urinary tract infections allow us to focus on the renal etiology of edema. It should be noted that pretibial edema can be a sign of hypothyroidism. Edema can also appear with Itsenko-Cushing syndrome.
It is necessary to ask the patient about the medications he is taking and clarify whether the appearance of edema is related to the start of their use, since some drugs can cause edema (Table 3).
Table 3. Some drugs that may cause edema
Calcium channel blockers: dihydropyridines (nifedipine, amlodipine, felodipine), phenylalkylamines (verapamil), benzothiazepines (diltiazem);
Direct vasodilators (hydralazine, minoxidil, diazoxide);
Centrally acting drugs: clonidine, methyldopa
Sympatholytics (reserpine, guanethidine)
Non-steroidal anti-inflammatory drugs:
Non-selective cycloxygenase inhibitors
Selective cycloxygenase-2 inhibitors
Troglitazone, rosiglitazone, pioglitazone
In patients taking diuretics for the treatment of peripheral edema, the correct dosage regimen should be assessed. In addition, interview the patient in detail regarding dietary patterns, paying particular attention to dietary sodium intake, daily fluid intake, and adherence to special dietary restrictions. Thus, an increase in dietary sodium intake may play an important role in explaining the onset or increase in the severity of edema. However, in the absence of systemic disease, changes in salt or water intake by themselves usually do not cause edema, since the kidneys maintain water-salt balance in healthy people.
Edema can also appear with sodium overload due to an unbalanced diet high in salt, fasting or malnutrition (“hunger” edema), excessive use of laxatives, prolonged exposure to a certain position, obstruction of the lymphatic vessels (neoplastic process, helminthic infestations, iatrogenic), less commonly idiopathic. It should be noted that women may experience cyclic (periodic) edema, as well as during pregnancy.
Physical examination data. A comprehensive physical examination with an emphasis on pathology of the cardiovascular system, lungs, kidneys and liver is important. Pay attention to the position in which the patient is. Thus, swelling in an outpatient is detected in the legs due to prolonged standing, while in a person on bed rest - in the sacral area. Elevated levels of jugular venous pressure are usually a sign of heart failure or volume overload due to severe renal failure. In addition, the presence of ascites in the patient is determined.
It is easy to distinguish local edema from general edema when the edema is limited to one limb.
The general appearance of edema should be assessed, paying special attention to localization, symmetry, the presence of a pit on palpation that leaves a persistent impression on the skin (muscle swelling provides resistance and does not leave an indentation on the skin); soreness and changes in the skin, in particular redness and ulcers. Thus, the identification of asymmetrical edema, soreness of the calf muscles and changes in skin color, along with increased venous pressure in the jugular veins and the presence of rales in the lungs can be a diagnostic guide to the etiological factor.
Mild swelling is detected using the following test: press the skin against the underlying bone for ten seconds with three slightly spaced fingers and then run your finger over the area of compression. The feeling of a pit or "valleys between the hills" helps diagnose edema. The severity of edema is assessed by the depth of the depression remaining after pressure, on a four-point scale (in increasing order of severity from 0 to 4 points). Thus, the absence of edema corresponds to 0, mild degree of edema: the depth of the fossa after pressure is up to 2 mm - 1, moderate: the depth of the fossa is 4 mm - 2, moderately severe: the depth of the fossa - 6 mm with visible swelling - 3, and severe - 8 mm , along with a pronounced change in the shape of the limb due to edema – 4 points. If the edema is located on the legs, the level of spread to the proximal parts of the limb is recorded. It is important to emphasize that accuracy and consistency in the assessment of edema is challenging because the location of edema can vary depending on the patient's position. Thus, edema may be located on the lateral and posterior surfaces of the thighs and absent on their anterior surface.
Fatty edema has a soft consistency characteristic of adipose tissue. When pressing on the skin, there is almost no fingerprint left; palpation is painful. Such swelling is always bilateral and does not affect the feet and toes.
When examining, pay attention to the color of the skin. If hyperemia is detected, one should think about an infectious process (in particular, erysipelas, etc.) or phlebitis/thrombophlebitis; unilateral cyanosis of the limb confirms deep vein thrombosis; bilateral mild cyanosis suggests chronic heart failure, and ecchymoses on the skin may result from trauma.
Assessing the state of the peripheral and central venous system helps in diagnosing the pathogenesis of edema. Thus, unilateral edema, palpation of dense strands, or lymphadenopathy confirm proximal obstruction of venous outflow or lymphatic drainage. The presence of trophic disorders (induration, pigmentation, eczematous and ulcerative lesions) indicates a chronic process. Identification of varicose veins of the lower extremities suggests chronic venous insufficiency.
In addition, pay attention to the possible presence of signs of a systemic disease that caused edematous syndrome: spider veins, jaundice, hepatomegaly (with liver disease), hemorrhages on the face (obstruction of the superior vena cava).
Data from additional research methods. Basic screening tests allow you to confirm or exclude the suspected etiological factor of edema. Among them :
- general clinical blood and urine tests, biochemical tests (determination of electrolytes in the blood, total protein and its fractions in blood serum, bilirubin, aspartate and alanine aminotransferase, creatinine level, blood urea nitrogen, lipid spectrum indicators and blood coagulation system), allowing to assess the functional liver and kidney capacity. If hypothyroidism is suspected, determination of the level of thyroid-stimulating hormone in the blood is indicated;
— registration of an ECG is mandatory to exclude cardiovascular pathology;
— X-ray data of the chest organs allow us to exclude venous congestion, as well as cardiomegaly.
- echocardiography can detect a decrease in ejection fraction in case of chronic heart failure
- Duplex ultrasound examination of the vessels of the lower extremities helps in the diagnosis of deep vein thrombosis.
In most cases, a detailed history, physical examination, and results of basic routine laboratory tests are sufficient to diagnose peripheral edema and rarely require expensive diagnostic testing.
For swelling of the upper extremities
1. Edema of the upper extremities associated with increased venous pressure indicates superior vena cava syndrome. In cases of emergency or if there is a suspicion of obstruction of the superior vena cava, all patients are shown chest X-ray in frontal and lateral projections and computed tomography. In some clinical situations, Doppler ultrasound examination of the carotid or supraclavicular veins, possibly venography, is necessary.
2. If thrombosis of the veins of the upper extremities is suspected, duplex scanning of the veins of the upper extremities and venography are indicated.
3. If thoracic outlet syndrome is suspected, computed tomography, magnetic resonance imaging, or Doppler ultrasound may be useful.
1. Among heart diseases that can lead to edema, chronic heart failure, constrictive pericarditis, and restrictive cardiomyopathy should be noted. Mandatory diagnostic tests include chest x-ray, electrocardiography (ECG) and echocardiography.
2. Cirrhosis of the liver is considered the leading cause of liver pathology. It is recommended to determine the functional capacity of the liver (see above).
3. Renal edema:
— nephrotic syndrome: it is recommended to determine lipid metabolism and protein parameters in a 24-hour urine test.
- Glomerulonephritis or acute tubular necrosis: obtain a urine test with sediment assessment.
- preeclampsia in pregnant women: laboratory tests include determination of protein and urate in the urine, blood urea nitrogen, creatinine and bilirubin in the blood serum.
4. Other causes of edema and tests that help in diagnosis include determining: to exclude hypothyroidism - thyroid-stimulating hormone (TSH), aldosteronism - potassium content in the blood serum, Cushing's disease - daily excretion of free cortisol in the urine or conducting a test with dexamethasone, if there is insufficiency nutrition - levels of prealbumin in the blood serum, beriberi - thiamine in the blood serum or in daily urine, malabsorption - total protein in the blood serum, inflammatory bowel diseases - sigmoidoscopy, malignant neoplasms - computed tomography or magnetic resonance imaging.
Acute unilateral edema of one lower limb (see algorithm below). Causes include trauma, impaired venous drainage (venous obstruction), or inflammation.
Bilateral edema of the lower extremities.
1. If there is pain, consider lipedema, which symmetrically affects only the legs, without spreading to the feet (the swollen skin of the legs becomes like leggings), or varicose veins, if swelling is detected in the ankles and dorsum of the feet.
2. Consider taking medications as a possible reason (Table 3).
3. An increase in the level of thyroid-stimulating hormone in the blood may indicate hypothyroidism or Graves' disease.
Chronic unilateral edema may result from compression of the iliac and pelvic veins, impeding venous outflow. Phlebography, computed tomography, and magnetic resonance imaging may be useful.
The diagnostic algorithm for edema is summarized in Fig. 2.
Rice. 2. Diagnostic algorithm for peripheral edema (Cumbler E., 2011). Abbreviations: HPT – hypertension; LS – medicine; AKI - Acute renal failure; Ultrasound - duplex ultrasound examination of the veins of the extremities; cor pulmonale - pulmonary heart; ^ — increase; ^^^ - significant increase.
Chronic heart failure
As a rule, patients complain of palpitations, shortness of breath, and possibly attacks of suffocation at night. The medical history includes indications of heart pathology (angina pectoris, previous myocardial infarction, ischemic cardiomyopathy, chronic rheumatic disease).
Upon examination, bilateral swelling is determined, appearing in the evening, first in the ankle area and disappearing by the morning. The swelling gradually spreads to the upper half of the body. It is important to emphasize that the localization of edema is determined by the position of the patient’s body. In bedridden patients they are more pronounced in the presacral region. Other signs of cardiac pathology are also detected: possibly orthopnea, acrocyanosis, swelling of the jugular veins (indicating an increase in central venous pressure), congestive wheezing in the lungs, changes in heart size, rhythm disturbances or heart sounds (a third heart sound S3 is heard), an increase in size liver. It is possible to detect ascites after the appearance of edema and hepatomegaly.
Additional research methods play an important role in diagnosis. An ECG is a mandatory study: deviation of the electrical axis of the heart to the left, atrial fibrillation, heart block, Q-wave, left ventricular hypertrophy, etc. may be detected. If there are no or minimal changes in the ECG, it is less likely that the cause of peripheral edema is dysfunction left ventricle. On chest x-ray, differential signs of cardiac disease include cardiomegaly, pleural effusion, or pulmonary edema. Two-dimensional echocardiography (B-mode) allows you to assess the size of the heart cavities, the thickness of the walls of the ventricles, the condition of the valve apparatus, subvalvular structures, ventricular contractility, the presence of cavities thrombosis, etc. Using echocardiography, the type of cardiac (systolic or diastolic) dysfunction of the left ventricle is determined.
Additional information is provided by the determination of brain natriuretic peptide (BNP) or its precursor N-terminal BNUP (NT-pro BNUP) (Fig. 3). Low BNP/NT-proBNP plasma levels support a noncardiac cause of heart failure symptoms. It should be noted that an increase in the content of MNUP/NT-proMNUP in the blood plasma can also be observed with pulmonary embolism, renal failure, and pulmonary hypertension with corpulmonale.
Algorithm for diagnosing heart failure
Fig.3. An algorithm for diagnosing heart failure based on the level of natriuretic hormones in untreated patients with symptoms characteristic of heart failure.
Constrictive pericarditis/restrictive cardiomyopathy. Clinically, these conditions are sometimes difficult to distinguish from heart failure of the right ventricular type. The listed conditions can manifest with peripheral edema, increased jugular venous pressure, liver congestion and ascites.
Risk factors for constrictive pericarditis include previous chest trauma, tumors, tuberculosis, heart surgery, and radiation exposure. There is a gradual increase in symptoms of heart failure. Chest x-ray may reveal pericardial calcification (“shell heart”). On the ECG: against the background of sinus rhythm, double-humped P waves are noted; characterized by low-amplitude QRS complexes; atrial fibrillation may be detected; changes in T waves in the form of flattening or inversion in several leads. Echocardiography reveals thickening of the pericardium, fusion of the parietal and visceral layers of the pericardium, limited movement of the posterior wall of the left ventricle, as well as areas of calcification.
With restrictive cardiomyopathy, patients usually complain of shortness of breath on exertion, cardiac pain on exertion, peripheral edema, pain in the right hypochondrium, and abdominal enlargement. A history of hemochromatosis, sarcoidosis, amyloidosis, scleroderma, and radiation exposure is specified. Upon examination, swollen jugular veins can be identified. The Kussmaul symptom is characterized by increased swelling of the jugular veins during inspiration. During auscultation, you can listen to the gallop rhythm and systolic murmur. In pulmonary hypertension, characteristic auscultatory signs are determined. In the lungs, with significant congestion, wheezing is heard. Liver enlargement and ascites are detected. The ECG usually shows nonspecific changes in the ST segment and T wave, sometimes the voltage of the QRS complex is reduced, and various arrhythmias. On a chest x-ray: often normal contours of the heart in the presence of signs of venous congestion in the lungs. With echocardiography: the dimensions of the heart cavities are not changed; a characteristic sign of the disease is considered to be disturbances in the diastolic function of the left ventricle in the form of a shortening of the time of isovolumic relaxation.
Nephrotic syndrome includes a group of disorders characterized by severe proteinuria (more than 3.5 g/day), hypoproteinemia, hypoalbuminemia, hyperlipidemia and edema. The development of nephrotic syndrome is caused by acute and chronic glomerulonephritis, diabetes mellitus, renal amyloidosis, systemic lupus erythematosus, and less commonly, systemic vasculitis and neoplasms. Typically, edema, like other signs of nephrotic syndrome, develops gradually as proteinuria increases. So, first, swelling is detected in the eyelid area, more often after sleep, puffiness of the face appears and after that the swelling spreads throughout the body. The development of ascites, hydrothorax, and less commonly hydropericardium is possible. Moreover, swelling can reach anasarca. Patients have a characteristic appearance: pale, with a puffy face. Despite the pronounced pallor of patients, anemia is usually only moderate.
An important place in the diagnostic search is occupied by the determination of albumin content in blood serum, in particular the detection of hypoalbuminemia (3.5 g/day). The difficulty of collecting a 24-hour urine sample has led to the use of albumin excretion rate measurements. A commonly used surrogate measure is the urinary albumin-to-creatinine concentration ratio (ACR). Nephrotic syndrome is usually confirmed if the protein/creatinine ratio in the urine is >0.25 (in healthy people this ratio is less than 0.2, and in pathology it is within 0.2-3.5).
In urine analysis: the sediment is scanty, a small number of hyaline casts, sometimes oval fat bodies (epithelial cells filled with numerous droplets of fat) are observed. With polarized light microscopy, oval fat bodies are revealed in the form of a “Maltese cross”.
In the diagnostic search for the etiology of these changes, an important place is played by echosonography of the kidneys.
Since chronic liver diseases lead to the development of cirrhosis, patients should be checked for a history of viral hepatitis, alcohol abuse, autoimmune hepatitis, hemochromatosis, Wilson-Konovalov disease, conditions associated with alpha-1-antitrypsin deficiency, diseases of intra- and extrahepatic biliary tract.
Upon examination, bilateral edema is determined. Physical data indicating the presence of cirrhosis include: altered size and hardening of the liver and unevenness of its surface (lumpy, small wrinkled); splenomegaly and/or ascites; spider veins on the upper half of the body and face, palmar erythema, gynecomastia, dilated veins on the anterior abdominal wall (caput medusae), icterus of the sclera and jaundice. In this case, the jugular venous pressure is normal.
Dysproteinemia (hypoalbuminemia, hyperglobulinemia) is detected in the blood; prolongation of prothrombin time and increased bilirubin levels confirm dysfunction of the synthetic and metabolic functions of the liver. In this case, an increase in transaminases is possible, but they can also increase in the absence of liver cirrhosis. Transaminases may increase with venous congestion in the liver due to cardiopulmonary dysfunction. Prothrombin time is used as an indicator of liver synthetic function. Important additional information is provided by ultrasound examination of the upper half of the abdominal cavity. Thus, an enlarged spleen, dilation of the vessels of the portal system and visible collaterals indicate the presence of portal hypertension. During the examination, even a small amount of ascitic fluid can be easily detected.
General edema due to hypoproteinemia is also detected with insufficient protein intake, impaired protein absorption (malabsorption syndrome) or increased catabolism (cachexia). In the latter, along with edema, signs of the underlying disease are revealed, for example, cancer, tuberculosis, etc. Alimentary edema is not accompanied by cardio- and hepatomegaly and changes in the urine.
Swelling caused by medication. Medicines, the use of which can lead to edema, are presented in Table 3. The diagnosis is assumed if the appearance of edema coincides with the start of taking one of these medications, and other reasons for their formation are not determined. Swelling is bilateral. After discontinuation of the drug, the swelling disappears.
Idiopathic edema. The causes of idiopathic edema remain poorly understood. Synonyms for idiopathic edema are also considered cyclic edema, periodic edema, edema associated with fluid retention, and orthostatic edema. This type of edema develops in women aged 20 to 50 years (usually 30-40 years old) with a preserved menstrual cycle and who do not have pathology of the heart, liver and kidneys; more likely to be overweight. Idiopathic edema, as a rule, initially appears periodically, but not associated with the monthly (menstrual) cycle, and subsequently becomes more permanent. Moreover, the degree of fluid retention increases in the orthostatic position. Often, there is a relationship with psycho-emotional stress and concomitant misuse or abuse of diuretics or laxatives. Patients with idiopathic edema often take diuretics to reduce edema and the feeling of fullness in the limbs. However, paradoxically, swelling can become an even greater problem after diuretic therapy. Thus, in patients with idiopathic edema, diuretics can be prescribed for a period of three weeks, which often leads to the development of drug dependence, which is difficult to correct, since after discontinuation of diuretics, fluid retention usually occurs due to the rebound phenomenon, leading to a relapse of symptoms.
Idiopathic edema bilaterally, as a rule, is small and is detected on the feet and legs in the evening. Swelling of the hands and face may occur. This corresponds to an increase in weight of more than 0.7-1.4 kg per day. At the same time, the concentration of albumin in the blood serum and jugular venous pressure were within normal limits. Diagnosis is usually made based on medical history and physical examination, after excluding heart, liver, and kidney disease.
Pretibial myxedema is observed mainly in women over 40-50 years of age and is associated with thyroid pathology. During the survey, attention is paid to the presence of fatigue, cold intolerance, weight gain, paresthesia, constipation, and hair loss. A physical examination of the patient reveals dry skin, slow movements and speech, and a low timbre of the voice. Bradycardia and arterial hypotension (rarely arterial hypertension) are also often detected.
Rice. 4. Pretibial myxedema.
The diagnosis is confirmed by studying the functional status of the thyroid gland (determining thyroid-stimulating hormone and free T4 in the blood serum and the titer of antithyroid antibodies, in particular against thyroglobulin or thyroid peroxidase).
Edema in pregnant women occurs shortly before delivery and is a natural consequence of physiological processes - a slowdown in venous blood flow as a result of hormonal changes and mechanical compression of the inferior vena cava and iliac veins by the uterus, a decrease in venous tone and an increase in bcc. The general condition remains satisfactory. The appearance of peripheral edema occurs during a period when pregnancy is clinically obvious. Both limbs always swell; their increase in volume is almost equal. Swelling is localized in the lower third of the legs and is not accompanied by pain; patients may complain of a feeling of heaviness in the legs. Swelling often decreases with regular rest in a horizontal position with legs elevated.
Edema is common in patients with preeclampsia, but the development of edema is no longer considered a criterion for the diagnosis of preeclampsia.
Lymphedema is a less common form of swelling, usually of the extremities, characterized by impaired lymphatic drainage, which leads to pathological accumulation of protein-rich lymphatic fluid in the interstitial space.
Primary lymphedema. The substrate of lymphedema is aplasia, hypoplasia of the lymph nodes, or subcutaneous lymphangiectasia, which occurs as a result of impaired lymph drainage in the inguinal lymph nodes or impaired communication between the subcutaneous and retroperitoneal lymphatic systems. The disease can appear quite late, after exposure to a trigger mechanism that impedes lymphatic drainage. Depending on the time of onset of the disease, there are: congenital (10-25%), juvenile (65-80%) and slowly progressive (10%) forms. In 90% it affects women under the age of 35 (65-80% before the age of 18). In most cases, the disease is sporadic, but it is possible to identify a similar disease in relatives. As a rule, the resolving factor after which the symptoms of lymphedema increase is pregnancy or injury.
Subjective symptoms of lymphedema: pain, heaviness and fatigue in the limb. Among the objective symptoms of lymphedema of the lower extremities, one should note the characteristic cushion-like swelling of the dorsum of the foot and fingers with the development of Stemmer's symptom, pathognomonic for lymphedema (it is not possible to collect a skin fold on the back of the second toe). In the initial stages of the disease, before the development of fibrosclerotic changes in the subcutaneous tissue, the swelling is mild, and when pressed, a clearly visible hole remains. Next, the distal parts of the limb become denser, the skin thickens, and when pressed, there is no longer a hole left. As it progresses, hyperkeratosis, papillomatosis, and tissue proliferation in the form of tubercles separated by deep folds appear.
Lymphedema is not characterized by varicose veins and trophic disorders.
Secondary lymphedema (Fig. 5,6) is a consequence of acquired dysfunction of the initially normal lymphatic system. The cause of the disease can be clearly defined (tumor lesion, surgery, liposuction, radiation therapy, burns, erysipelas, filariasis, etc.). The most common cause of the development of secondary lymphedema is surgical or radiation treatment of certain types of tumors, for example, breast cancer, ovarian cancer, prostate cancer, lymphoma, etc. Therefore, in diagnosis, data from the medical history and objective examination are of leading importance (see above). With secondary lymphedema of post-infectious origin, signs of pathology of the venous system can be identified - varicose veins, trophic skin disorders.
To confirm the diagnosis, lymphoscintigraphy is performed, which makes it possible to clarify the anatomy of the lymphatic system, its patency, the dynamics of lymphatic drainage and the severity of lymphatic obstruction. If an oncological etiology of lymphedema is suspected, magnetic resonance imaging and computed tomography are used. To exclude primary deep vein thrombosis of the extremities, duplex ultrasound scanning is used.
Rice. 5. Lymphatic edema of the right lower limb. Secondary lymphedema due to cancer of the right ovary.
Rice. 6. Lymphatic edema of the right upper limb. Secondary lymphedema due to cancer of the right breast.
Chronic venous insufficiency (CVI) is a disease widespread among the adult population. Epidemiological studies have shown that the frequency of CVI ranges from 7 to 51.4%, with 62.3% in women and 21.8% in men. In the United States, chronic venous insufficiency and varicose veins are classified as “office diseases.” Today, CVI is a disease not only of people over 50 years of age.
Symptoms of the initial manifestations of CVI are varied. The most common complaints are: the presence of telangiectasias and edema, worsening in the evening; pain, cramps and pins and needles sensation in the calf muscles; loss of sensitivity and coldness of the extremities; pigment spots on the skin; constant feeling of discomfort. Thus, CVI is characterized by several syndromes: edema, pain, convulsions, trophic disorders, secondary skin lesions. Common symptoms include a feeling of heaviness in the legs (heavy legs syndrome). Risk factors for CVI include old age, female gender, obesity, pregnancy, the presence of CVI in relatives or a history of venous thrombosis.
Venous insufficiency is characterized by the development of chronic bilateral or unilateral edema, in which a depression remains in the area of edema after finger pressure. Often this form of edema is accompanied by brown deposits of hemosiderin in the lower legs and feet. Skin changes (Fig. 7, 8) can progress to the development of dermatitis and the formation of ulcers, which usually form on the medial surface of the leg in the area of the inner malleolus.
Rice. 7. Chronic venous insufficiency, initial stage of the disease: dilatation of the lateral ankle veins and corona phlebectatica - dilation of capillaries in the area of the foot and ankle. The condition is associated with an underlying disease of the large veins of the lower limb
Rice. 8. Chronic venous insufficiency, later stage: stasis dermatitis, pigmentation, eczematous changes in the skin of the leg. The photograph shows pigmentation and traces of two healed ulcers.
When deep veins are affected (post-thrombotic disease), swelling appears during the period of acute venous thrombosis, decreases somewhat after 10-12 months, but extremely rarely disappears completely. Upon examination, a visual difference in volume between the limbs is determined. Varicose veins and trophic disorders in PTFS develop 5-7 years after the development of edema. Often, with pronounced skin pigmentation, varicose syndrome is absent (Fig. 9).
Rice. 9. A patient with postthrombophlebitic disease of the left lower limb. 4 months after ankle fracture and osteosynthesis. Ultrasound of the veins of the left lower limb showed recanalized thrombosis from the popliteal vein and below with 60% patency of the popliteal vein.
When superficial veins are affected (varicose veins), swelling and trophic disorders appear during treatment of the disease 10-15 years after the appearance of the first venous nodes (Fig. 10).
Rice. 10. A 42-year-old patient with chronic venous insufficiency of the 2nd degree. Atrophy of subcutaneous tissue. A little more and there will be an ulcer if left without treatment.
The diagnosis is usually made based on clinical findings, but can be confirmed using ultrasound imaging of the veins of the extremities. With ultrasound duplex angioscanning, the patency of the veins, the nature of the blood flow, the presence or absence of reflux, and the lumen diameter of the main venous trunks are determined. In addition, to further clarify the cause of chronic venous insufficiency, radiocontrast methods such as venography can be used.
Clinical symptoms of venous thrombosis include:
- sudden appearance of unilateral swelling of the lower leg and foot or identification of asymmetry of the circumference (more than 1.5 cm) of the legs and thighs;
- pain in the foot and lower leg, worsening when walking;
- possible changes in the skin.
Patients note that within a few hours the volume of the limb has increased significantly. In the first days, the development of edema is increasing. After a few weeks, the swelling becomes permanent. Often the swelling affects both the lower leg and thigh - the so-called ileofemoral venous thrombosis (Fig. 11).
Fig. 11. Right-sided ileofemoral deep vein thrombosis, manifested by acute edema of the right lower extremity. Upon examination, the skin is hot to the touch, there is pain on palpation along the right popliteal and femoral veins. This clinical picture occurs in less than 50% of cases of deep vein thrombosis, and since a number of other diseases occur in a similar way, additional research is necessary.
Risk factors for deep vein thrombosis include: immobilization of the lower extremities; injury or surgery; oncological diseases; previous thrombosis; blood coagulation disorders in first-degree relatives; current or recent pregnancy; taking oral contraceptives.
Upon examination, swelling of the ankle or lower leg is determined; with thrombosis of the iliac vein - swelling of the entire leg. There is pain on palpation along the main veins. A positive Homans sign is the appearance of pain in the calf muscles when dorsiflexing the foot. An increase in skin temperature is detected compared to the healthy leg.
Deep vein thrombosis is often asymptomatic, which is typical for patients on bed rest. The first symptom of deep vein thrombosis may be pulmonary embolism. In patients with a femoral fracture, deep vein thrombosis may be isolated to the thigh.
It should be emphasized that the information content of a physical examination is often low. Therefore, with the acute development of edema, the use of additional examination methods is usually required. One of the methods for diagnosing thrombosis is the D-dimer test. The method is characterized by high sensitivity (96–99%), but low specificity (50%). This examination method has a high negative diagnostic value, that is, it allows one to reliably exclude deep vein thrombosis in a patient with a normal D-dimer content (<500 μg/l) (Fig. 12). However, an increased level of D-dimer is not specific for deep vein thrombosis (may be due to other reasons, in particular, malignant neoplasms, acute myocardial infarction, inflammation, pregnancy, etc.), therefore the positive diagnostic value of this method is low, and the patient requires further examination for confirmation of deep vein thrombosis.
Rice. 12. Algorithm for managing a patient with unilateral leg swelling. Abbreviations: CT – computed tomography; s/c – subcutaneously; DVT - deep vein thrombosis
If deep vein thrombosis is suspected, ultrasound examination of the veins of the lower extremities is used as a diagnostic method. As an initial screening, an ultrasound examination with compression of the proximal veins (femoral, internal femoral, popliteal) is performed. Thrombosis of these veins is excluded if their full compressibility under the influence of compression by the sensor is demonstrated. If the vein does not compress during compression, then we can confidently talk about thrombosis. Diagnosis of distal veins (veins of the lower leg) using ultrasound is difficult. If distal vein thrombosis does not spread to the proximal veins, then the risk of pulmonary embolism is very low.
If it is not possible to conduct an ultrasound examination of the veins, impedance plethysmography can be used.
The reference method for diagnosing venous thrombosis and clarifying the operation of the valve apparatus is contrast venography, which allows one to clearly determine the proximal border of the thrombus.
If the results of ultrasound or impedance plethysmography are questionable, magnetic resonance imaging is indicated.
So, peripheral edema can be a nonspecific sign of many diseases, differing in both the manifestation of the process and the potential threat to life. A thorough collection of complaints and medical history, as well as a comprehensive physical examination, along with laboratory and instrumental data, provide valuable information when carrying out differential diagnosis. It should be especially emphasized that peripheral edema is one of the manifestations of the disease, and the correct interpretation of the origin of edema allows one to choose patient management tactics.
Edema is a consequence of the accumulation of water in the tissues and serous cavities of the body (thoracic, abdominal, pericardial cavity). Swelling of tissues is accompanied by disruption of their functions. In this article we will provide a definition of edema, talk about the possible causes of its occurrence, and the principles of diagnosis and treatment.
Edema can be divided into two types: local and general.
Local are caused by a violation of the blood supply or innervation of an organ area. These include swelling due to inflammation, with impaired venous and lymphatic outflow, with damage to the nervous system, allergic and premenstrual.
General edema is associated with fluid retention in the body. They are divided into edema in heart failure, renal, in enteropathy with increased protein loss, cachectic and medicinal.
In the initial stages, general edema is peripheral in nature, that is, it affects only certain areas of the body, for example, limbs. Subsequently, the swelling spreads with the formation of extensive edema, with the accumulation of fluid in the cavities. Anasarca is formed.
Most often, water in the body begins to accumulate when there is excessive sodium retention in the kidneys. A decrease in urinary sodium excretion is associated with increased secretion of the hormone aldosterone, caused by a decrease in the intensity of blood flow in the kidneys. This process is often caused by heart failure or kidney disease. The amount of aldosterone also increases in liver diseases, which result in a decrease in its inactivation.
Edema occurs when plasma oncotic pressure decreases. It is due to the content of albumin in the blood, and to a lesser extent, globulins. This is the mechanism for the appearance of edema during fasting, nephrotic syndrome, severe liver diseases with disruption of its protein-synthetic function, enteropathies with increased protein losses through the intestines.
Edema also appears when the permeability of the walls of blood capillaries increases, with an increase in venous pressure, disturbances in the exchange of electrolytes and hormones, and with mechanical obstacles to the outflow of fluid from tissues.
An increase in venous pressure plays a role in the mechanism of development of edema in heart failure and disorders of venous outflow. The exchange of electrolytes and hormones is disrupted by kidney disease, premenstrual syndrome, and hypokalemia of various origins. Damage to the capillary walls is typical for glomerulonephritis, inflammatory and allergic edema, and damage to the nervous system.
Thus, the pathogenesis (mechanism of development) of edematous syndrome is complex. Numerous interconnected factors play a role in its appearance.
Inflammatory swelling accompanies the corresponding processes in the body. Most often they occur with phlebitis and thrombophlebitis. Their peculiarity is redness of the skin, pain on palpation, and a local increase in temperature. Inflammatory edema is most often unilateral.
Edema due to impaired venous outflow can be associated with varicose veins. They are soft, the skin is bluish and warm. Other signs of the underlying disease are also visible. Swelling with superior vena cava syndrome is located in the upper half of the body, in the face and neck.
With lymphatic edema, first one leg gradually swells, the swelling spreads to the ankles, and then higher. The swelling is dense, there is no hole left when pressing on it. In advanced cases, so-called elephantiasis occurs: significant lymphatic edema of both lower extremities.
Premenstrual edema occurs in the ankle area in the second half of the menstrual cycle. They are accompanied by headaches, sleep disturbances, increased appetite and other signs of the so-called premenstrual syndrome.
Edema in heart failure occurs gradually. They are always symmetrical. Swelling of the ankles first appears in the evening; in the morning it is absent. Swelling of the legs and then the thighs gradually appears. The skin of the legs becomes tense, cold, and bluish. When you press on the swelling, a hole remains. There is an increase in the volume of the legs. In severe cases, ascites, hydrothorax, and anasarca occur.
Renal edema can be nephritic or nephrotic. Nephritic edema appears at the early stage of acute glomerulonephritis due to a decrease in glomerular filtration. Swelling quickly occurs on the face, less often on the limbs.
Edema in nephrotic syndrome is primarily due to protein loss through the kidneys. It appears gradually, first on the face in the morning. Then swelling appears on the limbs, lower back, abdomen, and genitals. Swelling may shift with changes in body position. The skin is dry, pale, sometimes shiny. The swelling is mild.
Drug-induced edema can occur when taking nonsteroidal anti-inflammatory drugs, mineralocorticoids, sex hormones, and glucocorticosteroids. Swelling is mild and appears in the morning on the eyelids or face, as well as on the legs and feet.
General swelling becomes noticeable when at least 2 liters of fluid are retained in the body. Hidden edema is detected by daily measurement of body weight and the volume of fluid drunk and excreted.
When edema is detected, its location and conditions of occurrence are determined. Concomitant diseases are identified. A thorough examination of the patient is carried out. Minimal examinations are prescribed: general blood and urine tests, biochemical blood test, blood electrolytes, electrocardiography, chest x-ray. Based on the results of these studies, it is already possible to attribute edema to some syndrome (heart failure, nephrotic, and so on).
At the next stage of diagnosis, the cause of edema is clarified. In the presence of heart disease, echocardiography is performed, in case of kidney disease, functional tests and other special research methods are performed.
Treatment of edema depends on the cause that caused it. In many cases, diuretics are prescribed, including for differential diagnosis of the causes of fluid retention.
For edema of any origin, moderate limitation of the amount of liquid and table salt consumed is recommended.
After consultation with a doctor, in many cases it is permissible to use herbal remedies that improve kidney function (kidney tea, lingonberry leaf, bearberry and other medicinal plants). Canephron and Fitolysin can be used.
Treatment of the underlying disease that caused the swelling leads to improvement.
The main diuretics that reduce swelling are furosemide and hypothiazide. After determining the level of electrolytes in the blood, it is possible to combine them with potassium preparations: asparkam, panangin. In some cases, the doctor prescribes potassium-sparing diuretics, for example, veroshpiron.
It is important to understand that treatment of edema should only be carried out under the supervision of a physician. Self-medication can lead to serious complications both from the disease itself that caused the swelling, and to the toxic effects of inappropriately taken medications.
TVC, program “Doctor I...” on the topic “Swelling of the legs”:
Peripheral edema is a consequence of the accumulation of fluid in the intercellular space of tissues and serous cavities.
Peripheral edema occurs due to pathological conditions and diseases. Sudden swelling should be especially alarming, as it can signal serious problems in the body.
According to experts, the most common cause of edema is sodium retention in the kidneys, which in turn is associated with a decrease in the intensity of blood flow in kidney and heart diseases. Other causes of peripheral edema of the legs or arms include:
Peripheral edema also occurs as a result of:
In fact, when taking a number of medications, an adverse reaction in the form of edema may occur. Most often, swelling of the legs is observed when taking:
Attention! To determine the cause of peripheral edema, you should consult a doctor. Diagnosis of the disease is carried out on the basis of anamnesis, examination of the patient, results of clinical tests and instrumental examination.
The symptoms of peripheral edema are related to the causes of their formation. There are general clinical signs, the main ones of which are:
Among the characteristic signs of edema is the persistence of an indentation on the skin for some time after pressure.
Therapy for peripheral edema is carried out comprehensively and includes:
Dietary nutrition with a reduction in salt and liquid intake is mandatory. Drug treatment can be supplemented with herbal preparations. No less useful are contrast baths and wearing special underwear. It is also recommended to place your legs above the level of your heart when lying down.