Fluid Volume Excess (Hypervolemia)

FLUID VOLUME EXCESS (HYPERVOLEMIA)

Fluid volume excess (FVE) refers to an isotonic expansion of the ECF caused by the abnormal retention of water and sodium in approximately the same proportions in which they normally exist in the ECF. It is always secondary to an increase in the total body sodium content, which, in turn, leads to an increase in total body water. Because there is isotonic retention of body substances, the serum sodium concentration remains essentially normal.

Pathophysiology

FVE may be related to simple fluid overload or diminished func-tion of the homeostatic mechanisms responsible for regulating fluid balance. Contributing factors can include heart failure, renal failure, and cirrhosis of the liver. Another contributing factor is consumption of excessive amounts of table or other sodium salts. Excessive administration of sodium-containing fluids in a patient with impaired regulatory mechanisms may predispose him or her to a serious FVE as well (Beck, 2000).

Clinical Manifestations

Clinical manifestations of FVE stem from expansion of the ECF and include edema, distended neck veins, and crackles (abnormal lung sounds). Other manifestations include tachycardia; in-creased blood pressure, pulse pressure, and central venous pres-sure; increased weight; increased urine output; and shortness of breath and wheezing.

Assessment and Diagnostic Findings

Laboratory data useful in diagnosing FVE include BUN and hematocrit levels. In FVE, both of these values may be decreased because of plasma dilution. Other causes for abnormalities in these values include low protein intake and anemia. In chronic renal failure, both serum osmolality and the sodium level are de-creased due to excessive retention of water. The urine sodium level is increased if the kidneys are attempting to excrete excess volume. Chest x-rays may reveal pulmonary congestion. Hyper-volemia occurs when aldosterone is chronically stimulated (ie, cir-rhosis, heart failure, and nephrotic syndrome). Urine sodium levels, therefore, will not rise in these conditions.

Medical Management

Management of FVE is directed at the causes. When the fluid ex-cess is related to excessive administration of sodium-containing fluids, discontinuing the infusion may be all that is needed. Symp-tomatic treatment consists of administering diuretics and re-stricting fluids and sodium.

PHARMACOLOGIC THERAPY

Diuretics are prescribed when dietary restriction of sodium alone is insufficient to reduce edema by inhibiting the reabsorption of sodium and water by the kidneys. The choice of diuretic is based on the severity of the hypervolemic state, the degree of impair-ment of renal function, and the potency of the diuretic. Thiazide diuretics block sodium reabsorption in the distal tubule, where only 5% to 10% of filtered sodium is reabsorbed. Loop diuretics, such as furosemide (Lasix), bumetanide (Bumex), or torsemide (Demadex), can cause a greater loss of both sodium and water be-cause they block sodium reabsorption in the ascending limb ofthe loop of Henle, where 20% to 30% of filtered sodium is nor-mally reabsorbed. Generally, thiazide diuretics, such as hydro-chlorothiazide (HydroDIURIL), trichlormethiazide (Diurese), and methyclothiazide (Enduron), are prescribed for mild to mod-erate hypervolemia and loop diuretics for severe hypervolemia.

Electrolyte imbalances may result from the effect of the di-uretic. Hypokalemia can occur with all diuretics except those that work in the last distal tubule of the nephrons (eg, spironolac-tone). Potassium supplements can be prescribed to avoid this complication. Hyperkalemia can occur with diuretics that work in the last distal tubule, especially in patients with decreased renal function. Hyponatremia occurs with diuresis due to increased re-lease of ADH secondary to reduction in circulating volume. De-creased magnesium levels occur with administration of loop and thiazide diuretics due to decreased reabsorption and increased ex-cretion of magnesium by the kidney.

Azotemia (increased nitrogen levels in the blood) can occur with FVE when urea and creatinine are not excreted due to de-creased perfusion by the kidneys and decreased excretion of wastes. High uric acid levels (hyperuricemia) can also occur from increased reabsorption and decreased excretion of uric acid by the kidneys.

HEMODIALYSIS

When renal function is so severely impaired that pharmacologic agents cannot act efficiently, other modalities are considered to remove sodium and fluid from the body. Hemodialysis or peri-toneal dialysis may be used to remove nitrogenous wastes and control potassium and acid–base balance, and to remove sodium and fluid. Continuous renal replacement therapy may also be considered.

NUTRITIONAL THERAPY

Treatment of FVE usually involves dietary restriction of sodium. An average daily diet not restricted in sodium contains 6 to 15 g of salt, whereas low-sodium diets can range from a mild restric-tion to as little as 250 mg of sodium per day, depending on the patient’s needs. A mild sodium-restricted diet allows only light salting of food (about half the amount as usual) in cooking and at the table, and no addition of salt to commercially prepared foods that are already seasoned. Of course, foods high in sodium must be avoided. It is the sodium salt, sodium chloride, rather than sodium itself that contributes to edema. Therefore, patients need to read food labels carefully to determine salt content.

Because about half of ingested sodium is in the form of sea-soning, seasoning substitutes can play a major role in decreasing sodium intake. Lemon juice, onions, and garlic are excellent sub-stitute flavorings, although some patients prefer salt substitutes. Most salt substitutes contain potassium and must therefore be used cautiously by patients taking potassium-sparing diuretics (eg, spironolactone, triamterene, amiloride). They should not be used at all in conditions associated with potassium retention, such as advanced renal disease. Salt substitutes containing ammonium chloride can be harmful to patients with liver damage.

In some communities, the drinking water may contain too much sodium for a sodium-restricted diet. Depending on its source, water may contain as little as 1 mg or more than 1,500 mg per quart. Patients may need to use distilled water when the local water supply is very high in sodium. Also, patients on sodium-restricted diets should be cautioned to avoid water soft-eners that add sodium to water in exchange for other ions, such as calcium.

Nursing Management

To assess for FVE, the nurse measures intake and output at reg-ular intervals to identify excessive fluid retention. The patient is weighed daily and acute weight gain is noted. An acute weight gain of 0.9 kg (about 2 lb) represents a gain of approximately 1 L of fluid. The nurse also needs to assess breath sounds at regular intervals in at-risk patients, particularly when parenteral fluids are being administered. The nurse monitors the degree of edema in the most dependent parts of the body, such as the feet and ankles in ambulatory patients and the sacral region in bedridden pa-tients. The degree of pitting edema is assessed, and the extent of peripheral edema is monitored by measuring the circumference of the extremity with a tape marked in millimeters.

PREVENTING FVE

Specific interventions vary somewhat with the underlying condi-tion and the degree of FVE. Most patients, however, require sodium-restricted diets in some form, and adherence to the pre-scribed diet is encouraged. The patient is instructed to avoid over-the-counter medications without first checking with a health care provider because these substances may contain sodium. When fluid retention persists despite adherence to a prescribed diet, hidden sources of sodium, such as the water supply or use of water soft-eners, should be considered.

DETECTING AND CONTROLLING FVE

Detecting FVE is of primary importance before the condition be-comes critical. Interventions include promoting rest, restricting sodium intake, monitoring parenteral fluid therapy, and admin-istering appropriate medications.

Some patients benefit from regular rest periods, as bed rest favors diuresis of edema fluid. The mechanism is probably related to diminished venous pooling and the subsequent increase in ef-fective circulating blood volume and renal perfusion. Sodium and fluid restriction should be instituted as indicated. Because most pa-tients with FVE require diuretics, the patient’s response to these agents is monitored. The rate of parenteral fluids and the patient’s response to these fluids are also closely monitored. If dyspnea or orthopnea is present, the patient is placed in a semi-Fowler’s posi-tion to promote lung expansion. The patient is turned and posi-tioned at regular intervals because edematous tissue is more prone to skin breakdown than normal tissue.

Because conditions predisposing to FVE are likely to be chronic, the patient is taught to monitor his or her response to therapy by documenting fluid intake and output and body weight changes. The importance of adhering to the treatment regimen is emphasized.

TEACHING PATIENTS ABOUT EDEMA

Because edema is a common manifestation of FVE, patients need to recognize its symptoms and importance. The nurse gives spe-cial attention to edema when teaching patients with FVE. Edema can occur from increased capillary fluid pressure, decreased cap-illary oncotic pressure, or increased interstitial oncotic pressure, thus expanding the interstitial fluid compartment. Edema can be localized (eg, in the ankle, as in rheumatoid arthritis) or general-ized (as in cardiac and renal failure). Severe generalized edema is called anasarca.

Edema occurs when there is a change in the capillary mem-brane, increasing the formation of interstitial fluid or decreasing the removal of interstitial fluid. Sodium retention is a frequent cause of the increased extracellular fluid volume. Burns and infection are examples of conditions associated with increased inter-stitial fluid volume. Obstruction to lymphatic outflow, a plasma albumin level less than 1.5 to 2 g/dL, or a decrease in plasma on-cotic pressure contributes to increased interstitial fluid volume. The kidneys retain sodium and water when there is decreased ex-tracellular volume as a result of decreased cardiac output from heart failure. A thorough medication history is necessary to iden-tify any medications that may cause edema, such as nonsteroidal anti-inflammatory drugs (NSAIDs), estrogens, corticosteroids, or antihypertensives.

Ascites is a form of edema in which fluid accumulates in the peritoneal cavity; it results from nephrotic syndrome or cirrhosis. Patients commonly report shortness of breath and a sense of pres-sure because of pressure on the diaphragm.

Edema usually affects dependent areas. It can be seen in the ankles, sacrum, scrotum, or the periorbital region of the face. Pitting edema is so named because a pit forms after a finger is pressed into edematous tissue. In pulmonary edema, the amount of fluid in the pulmonary interstitium and the alveoli increases. Manifestations include shortness of breath, increased respiratory rate, diaphoresis, and crackles and wheezing on auscultation of the lungs.

Decreased hematocrit resulting from hemodilution, arterial blood gas results indicative of respiratory alkalosis and hypox-emia, and decreased serum sodium and osmolality from retention of fluid may occur with edema. BUN and creatinine levels in-crease, urine specific gravity decreases as the kidneys attempt to excrete excess water, and the urine sodium level drops due to increased aldosterone production.

The goal of treatment is to preserve or restore the circulating intravascular fluid volume. In addition to treating the cause, other treatments may include diuretic therapy, restriction of fluids and sodium, elevation of the extremities, application of elastic com-pression stockings, paracentesis, dialysis, or continuous arterio-venous hemofiltration in cases of renal failure or life-threatening fluid volume overload.