Increased volume of extracellular fluid

The increase in the volume of the extracellular fluid is caused by an increase in the total sodium content in the body. Usually observed with heart failure, nephrotic syndrome, cirrhosis. Clinical manifestations include weight gain, swelling, orthopnea. Diagnosis is based on clinical data. The goal of the treatment is to correct excess fluid and eliminate the cause.

[1], [2], [3], [4], [5], [6]

Causes of the increased volume of extracellular fluid

The key pathophysiological moment is an increase in the total sodium content in the body. There is an increase in osmolality, which stimulates the compensatory mechanisms that cause water retention.

The movement of fluid between the interstitial and intravascular spaces depends on the Sterling forces in the capillaries. Elevated capillary hydrostatic pressure, observed with heart failure; decreased oncotic plasma pressure observed with nephrotic syndrome; their combination, observed with cirrhosis, cause the transition of fluid into the interstitial space, which is accompanied by the development of edema. Under these conditions, the subsequent decrease in the volume of the intravascular fluid increases the renal sodium retention, which leads to the development of excess fluid.

The main causes of increased extracellular fluid

Renal retention of sodium

• Cirrhosis.
• Medications: minoxidil, NSAIDs, estrogens, fludrocortisone.
• Heart failure, including pulmonary heart.
• Pregnancy and premenstrual edema.
• Kidney disease, especially nephrotic syndrome.

Decreased oncotic plasma pressure

• Nephrotic syndrome.
• Protein-losing enteropathy.
• Decrease in albumin production (liver disease, malnutrition).

Increase in permeability of capillaries

• Acute respiratory distress syndrome.
• Edema of the Quincke.
• Burns, trauma.
• Idiopathic edema.
• Receiving IL2.
• Septic syndrome.

Iatrogenic

• The introduction of excess sodium (for example, 0.9% saline intravenously)
• Symptoms of increased extracellular fluid volume

General weakness and weight gain may precede the appearance of edema. Dispnoea during exercise, decreased exercise tolerance, tachypnea, orthopnea, paroxysmal nocturnal dyspnea can also be observed in the early stages with left ventricular dysfunction. Elevated jugular venous pressure can cause swelling of the cervical veins.

The early manifestations of edema include the swelling of the eyelids in the morning and the feeling of narrow shoes by the end of the day. Pronounced edema is characteristic of heart failure. In outpatients, edema is usually observed on the feet and legs; in patients with bed rest - on the buttocks, genitals, hamstring; in women who are in a forced position on their sides, the edema develops on the chest of the corresponding side. Swelling can be accompanied by a large number of changes, including wheezing in the lungs, increased central venous pressure, gallop rhythm, an enlarged heart with lung edema and / or pleural effusion when performing chest radiography. In cirrhosis, edema is often limited by the lower limbs and is accompanied by ascites. The signs of cirrhosis also include spidery angiomas, gynecomastia, palmar erythema, testicular atrophy. In nephrotic syndrome, edema is usually diffuse, sometimes with generalized anasarka, pleural effusion and ascites; periorbital edema is observed frequently, but not always.

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Diagnostics of the increased volume of extracellular fluid

Symptoms and signs, including characteristic swelling, are diagnostic. According to the physical examination, one can assume the reason. For example, the presence of edema and  ascites  suggests cirrhosis. The chryps and the rhythm of the gallop suggest heart failure. Typically, a diagnostic study includes the determination of serum electrolytes, blood urea nitrogen, creatinine, and other studies that can identify the cause (eg, chest radiography for suspected heart failure). It is necessary to exclude the causes of isolated edema of the lower extremities (for example, lymphostasis, venous congestion, venous obstruction, local trauma).

[11], [12], [13], [14], [15], [16]

Treatment of the increased volume of extracellular fluid

In patients with heart failure, improving the function of the left ventricle (for example, when using inotropic drugs or by reducing afterload) can increase the delivery of sodium to the kidneys and the excretion of sodium. Treatment of the causes of nephrotic syndrome depends on specific renal histopathology.

Loop diuretics, such as furosemide, inhibit the reabsorption of sodium in the ascending knee of the Henle loop. Thiazide diuretics inhibit sodium reabsorption in the distal tubules. Both thiazide and loop diuretics increase the excretion of sodium and, consequently, of water. In some patients, the problem may be the loss of potassium; K-saving diuretics, such as cacalorid, triamteren and spironolactone, inhibit reabsorption of sodium in distal departments of a nephron and collecting tubules. With monotherapy, sodium excretion is moderately increased. To prevent loss of K, a combination of triamterene or amiloride with a thiazide diuretic is usually used.

Many patients do not develop the necessary response to diuretics; possible causes include inadequate treatment of the cause of excess fluid, non-compliance with sodium intake, hypovolemia and kidney disease. The effect can be achieved by increasing the dose of the loop diuretic or when combined with a thiazide.

After correcting excess fluid, maintaining a normal level of extracellular fluid may require a restriction of sodium intake, except when completely eliminating the cause. Diets that limit the intake of sodium to 3-4 grams per day are acceptable, well tolerated and sufficiently effective with a slight or moderate increase in the volume of the extracellular fluid in heart failure. Progressing cirrhosis and nephrotic syndrome require a more significant restriction of sodium (<> 1 g / day). Sodium salts are often replaced with potassium salts in order to facilitate the restriction; however, caution is necessary in this case, especially in patients taking K-saving diuretics, ACE inhibitors suffering from kidney disease, due to the possibility of developing fatal hyperkalemia.