Increase in extracellular fluid volume

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

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Causes increase in extracellular fluid volume

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

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

The main reasons for the increase in extracellular fluid

Renal sodium retention

• Cirrhosis.
• Taking medications: minoxidil, NSAIDs, estrogens, fludrocortisone.
• Heart failure, including cor pulmonale.
• Pregnancy and premenstrual edema.
• Kidney disease, especially nephrotic syndrome.

Decrease in plasma oncotic pressure

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

Increased capillary permeability

• Acute respiratory distress syndrome.
• Quincke's edema.
• Burns, trauma.
• Idiopathic edema.
• IL2 reception.
• Septic syndrome.

Iatrogenic

• Administration of excess sodium (eg, 0.9% saline intravenously)
• Symptoms of increased extracellular fluid volume

General weakness and weight gain may precede the development of edema. Dyspnea on exertion, decreased exercise tolerance, tachypnea, orthopnea, and paroxysmal nocturnal dyspnea may also be seen in the early stages of left ventricular dysfunction. Increased jugular venous pressure may cause jugular vein distension.

Early manifestations of edema include puffiness of the eyelids in the morning and a feeling of tightness in shoes by the end of the day. Marked edema is characteristic of heart failure. In ambulatory patients, edema is usually observed in the feet and shins; in patients on bed rest, in the buttocks, genitals, and back of the thighs; in women in a forced lateral position, edema develops on the chest on the corresponding side. Edema may be accompanied by a wide variety of changes, including pulmonary rales, increased central venous pressure, gallop rhythm, enlarged heart with pulmonary edema, and/or pleural effusion on chest radiography. In cirrhosis, edema is often limited to the lower extremities and is accompanied by ascites. Signs of cirrhosis also include spider angiomas, gynecomastia, palmar erythema, and testicular atrophy. In nephrotic syndrome, edema is usually diffuse, sometimes with generalized anasarca, pleural effusion, and ascites; periorbital edema is common but not always present.

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Diagnostics increase in extracellular fluid volume

Symptoms and signs, including characteristic edema, are diagnostic. Physical examination may suggest a cause. For example, the presence of edema and ascites suggests cirrhosis. Crackles and gallop rhythm suggest heart failure. Diagnostic testing typically includes serum electrolytes, blood urea nitrogen, creatinine, and other tests to identify the cause (eg, chest radiograph if heart failure is suspected). Causes of isolated lower extremity edema (eg, lymphedema, venous stasis, venous obstruction, local trauma) should be excluded.

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Treatment increase in extracellular fluid volume

In patients with heart failure, improving left ventricular function (eg, by inotropic agents or by reducing afterload) may increase sodium delivery to the kidneys and sodium excretion. Treatment of the causes of nephrotic syndrome depends on the specific renal histopathology.

Loop diuretics such as furosemide inhibit sodium reabsorption in the ascending limb of the loop of Henle. Thiazide diuretics inhibit sodium reabsorption in the distal tubule. Both thiazide and loop diuretics increase sodium and hence water excretion. Potassium loss may be a problem in some patients; K-sparing diuretics such as amiloride, triamterene, and spironolactone inhibit sodium reabsorption in the distal nephron and collecting duct. When used alone, they moderately increase sodium excretion. Triamterene or amiloride is usually combined with a thiazide diuretic to prevent K loss.

Many patients do not respond adequately to diuretics; possible causes include inadequate treatment of the cause of fluid overload, failure to adhere to sodium restriction, hypovolemia, and renal disease. Effects may be achieved by increasing the dose of the loop diuretic or by combining it with a thiazide.

After correction of excess fluid, maintenance of normal extracellular fluid levels may require sodium restriction unless the underlying cause has been completely excluded. Diets restricting sodium intake to 3 to 4 g per day are acceptable, well tolerated, and quite effective for mild to moderate extracellular fluid volume expansion in heart failure. Advanced cirrhosis and nephrotic syndrome require more severe sodium restriction (<> 1 g/day). Sodium salts are often replaced by potassium salts to facilitate restriction; however, caution is required, especially in patients taking potassium-sparing diuretics, ACE inhibitors, or those with renal disease, because of the possibility of fatal hyperkalemia.