Treatment of the Edematous Patient

Treatment is first directed at halting the progression of the underlying disease. Therapies that aid in reversing the underlying pathophysiology, such as angiotensin converting enzyme inhibitors in CHF should be used when possible. A low-salt diet is critical to the success of any regimen. If these measures are unsuccessful a diuretic may be required. The clinical use of diuretics is discussed in detail in Chapter 3.

  • 1. Hypervolemic states (increased ECF volume) are associated with increased total-body sodium and commonly present with edema with or without hypertension.
  • 2. Edema is the accumulation of excess interstitial fluid and is detected by noting an indentation or “pitting” of the skin after applying pressure with the thumb or index finger on the skin of the lower extremities or presacral region.
  • 3. Edema is generated by an alteration in Starling forces that govern fluid movement across the capillary endothelium. An increase in hydrostatic pressure or a decrease in oncotic pressure favors fluid movement out of the capillary resulting in edema formation.
  • 4. The pathophysiology of ECF volume expansion is divided into 3 general categories based on the presence or absence of edema and hypertension.
  • 5. Kidney disease is the major cause of ECF volume expansion with both hypertension and edema.
  • 6. ECF volume expansion associated with hypertension and absence of edema occurs with excess concentrations of mineralocorticoids, when glucocorticoids bind to the mineralocorticoid receptor, and with genetic diseases that increase sodium reabsorption in distal nephron.
  • 7. Disorders characterized by a decreased EABV, such as CHF, nephrotic syndrome, and cirrhosis of the liver, are major causes of ECF volume expansion associated with edema in the absence of hypertension.

Sodium is the most abundant extracellular ion. As a result it determines ECF osmolality and volume. Sodium depletion means ECF volume depletion. Sodium depletion does not imply hyponatremia and conversely hyponatremia does not imply sodium depletion. The serum sodium concentration is primarily determined by changes in water metabolism (see Chapter 3). Table 2.4 illustrates the manifestations of sodium and ECF volume depletion.

When sodium excretion exceeds input, negative sodium balance and decreased ECF volume results. Given that the normal kidney can rapidly lower sodium excretion to near zero, decreased sodium intake alone never causes decreased ECF volume. Sodium depletion results from ongoing sodium losses from kidney, skin, or gastrointestinal tract. If the kidney is the source of sodium loss then urine sodium concentration exceeds 20 mEq/L and the fractional excretion of sodium (FENa) will be increased. If losses are from skin or gastrointestinal tract and the kidney is responding normally, the urine sodium concentration is less than 20 mEq/L and the FENa will be low, less than 1%.

Renal sodium losses are caused by either intrinsic kidney disease or external influences on renal function. Kidney diseases associated with sodium wasting include nonoliguric acute kidney injury, the diuretic phase of acute kidney injury, and “salt-wasting nephropathy.” Salt- wasting nephropathy occurs after relief of urinary tract obstruction, with interstitial nephritis, medullary cystic disease, or polycystic kidney disease. External factors causing natriuresis include solute diuresis from sodium bicarbonate, glucose, urea, and mannitol; diuretic administration; and mineralocorticoid deficiency as a result of primary hypoaldosteronism or decreased renin secretion.

Gastrointestinal losses are external or internal. External losses occur with diarrhea, vomiting, gastrointestinal suction, or external fistulas. Internal losses or “third spacing” result from peritonitis, pancreatitis, and small- bowel obstruction. Skin losses also are external or internal. External losses result from excessive sweating, cystic fibrosis, and adrenal insufficiency. Burns cause excessive internal and external losses.

To protect blood pressure and tissue perfusion during ECF volume depletion, a variety of compensatory mechanisms are activated. These mechanisms maintain blood pressure, minimize renal sodium excretion, and in the process, maintain ECF volume.

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