Principles in the Selection of Intravenous Solutions Replacement : Sodium and Water Balance

Abstract

Inappropriate intravenous fluid therapy results in increased patient morbidity and mortality. By far the most common fluid and electrolyte problems that confront both chronically and critically ill patients are disturbances in sodium and water balance. Thus, it is important for the infusion therapy nurse to understand the basic pathophysiology of sodium imbalances as well as therapeutic approaches for their correction. Adding to this need is the recognition that, in hospital settings, disorders of sodium and water balance are often iatrogenic.

Inappropriate intravenous fluid therapy, such as giving too much or too little fluid, or an incorrect fluid, results in increased patient morbidity and mortality.1 By far the most common fluid and electrolyte problems that confront both chronically and critically ill patients are disturbances in sodium and water balance. Thus, it is important for the infusion therapy nurse to understand the basic pathophysiology of sodium imbalances as well as therapeutic approaches for their correction. Adding to this need is the recognition that, in hospital settings, disorders of sodium and water balance are often iatrogenic.2 It is interesting to note that dysnatremias, hypo- and hypernatremia, may have a prevalence approaching 20% to 30% in intensive care units.3-5

SODIUM AND WATER REGULATION

Sodium is the major electrolyte in the extracellular fluid (ECF) compartment, and its level represents its relative concentration in relation to water.6 Because of this relationship, dysnatremias can be the result of losses or gains of sodium, or losses or gains of water. A detailed history in conjunction with a physical examination and battery of laboratory tests may be needed to distinguish the cause of the sodium imbalance because it is sometimes difficult to discern the precise cause and desired treatment for the imbalance.7

The body typically controls the concentration of sodium in the ECF within a rather narrow range, defined as 135 to 145 mEq/L in most laboratories, via the actions of aldosterone, arginine vasopressin, angiotensin II, and atrial natriuretic peptide.6 Aldosterone stimulates sodium reabsorption in the distal nephron and the distal colon.8 The kidneys regulate serum sodium concentrations by greatly varying the amount of sodium excreted in the urine. The kidneys are capable of concentrating urine up to 400 mmol/d or as little as 1 mmol/d, depending on sodium intake.9 Arginine vasopressin, also called antidiuretic hormone (ADH), is synthesized in the hypothalamus and stored in the posterior pituitary gland. When the plasma osmolality rises in a healthy individual, ADH output is increased and results in increased thirst and water conservation by the kidney. Conversely, a reduced plasma osmolality, perhaps caused by a large intake of water, causes a reduced output of ADH and a resultant water diuresis.

Unfortunately, a variety of disease conditions and medications can disrupt sodium balance, producing either hyponatremia (serum Na < 135 mEq/L) or hypernatremia (serum Na > 145 mEq/L). Although dysnatremia can result in a series of problems, the most serious are neurological problems. For example, hyponatremia predisposes the patient to cerebral edema, and hypernatremia predisposes the patient to cerebral dehydration.10 Cerebral swelling is the result of water being pulled into the brain cells because of the relatively dilute ECF; in contrast, the relatively concentrated ECF associated with hypernatremia pulls water out of the brain cells.11

HYPONATREMIA

As indicated above, hyponatremia can result from a loss of sodium, as in vomiting or diarrhea, or from a gain of water, as in the excessive administration of a sodium-free intravenous fluid; it can also be caused by an inappropriate secretion of antidiuretic hormone (SIADH).11-13 Hospitalized patients are more likely to develop hyponatremia because of dilutional causes; in contrast, hyponatremia in outpatients is more often due to sodium loss via diuretic use coupled with a low-salt diet.14 Hyponatremia can be present in the following: (1) patients with dilutional hyponatremia caused by abnormal retention of water as in SIADH, (2) patients with fluid overload as in congestive heart failure or cirrhosis of the liver, or (3) patients with fluid volume deficit as in diarrhea and vomiting.11 Hyponatremia can be acute or chronic, and it may be symptomatic or asymptomatic.15 As a result, hyponatremia often presents a diagnostic challenge to clinicians.16

Causes of Hyponatremia

Among the disease conditions associated with hyponatremia are the following 11:

* SIADH: syndrome of inappropriate antidiuretic hormone, as in ectopic production of an ADH-like substance from malignant cells

* Cerebral salt wasting, a condition sometimes present in patients with disorders of the central nervous system, especially after a neurosurgical procedure

* Adrenal insufficiency, which results in a deficiency of aldosterone

* Gastrointestinal fluid losses, resulting in a direct loss of sodium

* Congestive heart failure; in this condition, both the total body sodium and water content are elevated. However, the plasma is disproportionately expanded with water, resulting in a below-normal sodium concentration in plasma

* Cirrhosis of the liver-similar situation as described in congestive heart failure

* Salt-wasting nephropathy, a condition in which sodium cannot be conserved by the kidneys of patients with advanced chronic renal disease

* Primary polydipsia, which is associated with psychiatric illness

It is recognized that hyponatremia is the most common electrolyte imbalance in hospitalized patients.17 And one of the most common causes of hyponatremia in adults and children is the administration of hypotonic fluids.13,18 Postoperative patients are at especially high risk for hyponatremia because they have a multitude of stimuli for ADH production; the most powerful among these stimuli is dehydration.18 When dehydration occurs, an increase in the osmotic pressure of the blood is detected by osmoreceptors near the supraoptic nucleus, thus triggering the release of ADH from the neurohypophysis. As indicated earlier, ADH causes the kidneys to retain water, resulting in dilutional hyponatremia.

Among the drugs that can lower the serum sodium concentration are these 19:

* Diuretics (such as thiazides)

* Antidepressants (such as selective serotonin reuptake inhibitors and tricyclics)

* Antipsychotic drugs (such as phenothiazines)

* Antiepileptic drugs (such as carbamazepine)

* Anticancer agents (such as vincristine, cisplatin, and cyclophosphamide)

* Oxytocin

Clinical Signs of Hyponatremia

The symptoms of hyponatremia correlate with the severity and the rate of decline in serum sodium level.2 Early signs of hyponatremia, such as nausea, irritability, apprehension, confusion, or abdominal cramping, may be difficult to differentiate from other conditions. The most serious manifestations of hyponatremia are neurological in nature. If severe hyponatremia develops over a period of a few hours, the patient may experience seizures, coma, and perhaps even permanent cerebral damage.8 In contrast, patients with chronic hyponatremia may have relatively few symptoms because the brain has had time to adapt to the condition and protect itself from edema.

Management of Hyponatremia

Hyponatremia can be treated by fluid restriction or sodium replacement, or a combination of both. Treatment varies according to the cause of the condition, how severe it is, and how long it has been present. A relatively simple and mild form of hyponatremia due to sodium loss may be treated with an isotonic sodium solution such as 0.9% sodium chloride, which contains 154 mEq of sodium per liter, or with lactated Ringer's solution, which contains 130 mEq of sodium per liter. If the hyponatremia is due to water overload, the first treatment is water restriction; if the serum sodium level is dangerously low and neurological signs are present, it may be necessary to replace sodium cautiously with a solution of hypertonic saline, such as a 3% sodium chloride solution that contains 513 mEq of sodium per liter, or a 5% sodium chloride solution that contains 855 mEq of sodium per liter.11

Treatment of hyponatremia is not without potential complications; therefore, it is crucial to pay careful attention to the rate of correction of the serum sodium concentration.6 Most important, the serum sodium concentration should not be increased too rapidly. The rate of correction is influenced by the length of time that hyponatremia has been present. For example, acute hyponatremia is sometimes defined as having been present less than 48 hours; in this setting, prompt, but cautious, correction of the serum sodium concentration is needed to reduce the risk for cerebral swelling. Conversely, when hyponatremia has been chronically present, its rate of correction can be undertaken more slowly. Although there is no clear consensus regarding the optimal treatment of symptomatic hyponatremia, authorities agree that the rate of correction should be of a sufficient rate and magnitude to reverse the manifestations of hypotonicity but not so fast and large as to pose a risk for osmotic demyelination, also referred to as central pontine myelinolysis.10,17 This condition is associated with destruction of the myelin sheath that covers nerve cells in the brain stem; it is associated with a rapid change in the serum sodium level. The rapid correction of hyponatremia or hypernatremia is frequently associated with increased morbidity and mortality.10 Evidence is limited regarding dosage-response relationships for using hypertonic saline to treat hyponatremia.20

When a patient has hyponatremia associated with euvolemia (normal volume) or hypervolemia, the health care provider may elect to prescribe a number of diuretics, such as a furosemide, a loop diuretic, or a newer class of diuretics known as aquaretics. Aquaretics are vasopressin antagonists that cause water diuresis.6 An example of such a drug is conivaptan, which has been found to be beneficial in treating patients with chronic heart failure.21

HYPERNATREMIA

Hypernatremia is a hyperosmolar state and can result from a relative loss of water or gain of sodium. In healthy individuals, thirst is a major mechanism to protect against the development of hypernatremia. Because elderly persons often do not experience normal thirst, they are at greater risk for hypernatremia than are younger adults. Hypernatremia has been associated with a high mortality rate due to the delay and inadequate treatment of this dysnatremic state.22,23

Causes of Hypernatremia

Most etiologies of hypernatremia are related to impaired water access in conjunction with excessive free-water losses.4,24 Most patients with hypernatremia are also fluid volume depleted. Among the medications that may cause hypernatremia are lithium, demeclocycline, mannitol, and osmotic cathartic agents. Of course, the excessive administration of sodium salts such as sodium chloride and sodium bicarbonate can lead to hypernatremia.

Clinical Signs of Hypernatremia

Much like hyponatremia, the symptoms of hypernatremia are largely neurological in nature and are due to cerebral changes. An increased serum sodium concentration causes an osmotic gradient between the ECF and the intracellular fluid in cerebral cells, causing movement of water out of the cells into the ECF, causing cellular shrinkage. These cerebral changes can result in a series of symptoms, including lethargy, weakness, irritability, seizures, and coma.11,25

Management of Hypernatremia

Management of hypernatremia associated with fluid volume deficit usually requires the administration of isotonic saline to restore the patient's blood volume prior to the correction of the water deficit.4 The amount of free water needed to correct hypernatremia is variable; for this reason, a formula that incorporates the patient's serum sodium level and total body water percentage may be employed.4 It is very important to avoid producing a rapid change in the serum sodium concentration.26 For this reason, it is necessary to measure the serum sodium concentrations frequently during treatment for hypernatremia, particularly when it is severe.

GENERAL PRINCIPLES FOR USE OF INTRAVENOUS FLUIDS

General Principles for Sodium and Water Replacement

* The main objectives of fluid therapy are to (1) provide usual maintenance fluids, (2) replace abnormal fluid losses, and (3) correct existing electrolyte imbalances.11

* For an adult with normal renal function, a typical intravenous fluid prescription may range between 2000 and 3000 mL/d.11

* Accurate intake and output records of fluid gains and losses are needed to facilitate administration of the correct volume and types of fluids.

* Laboratory reports should be carefully monitored to detect fluid and electrolyte abnormalities; any abnormal findings should be promptly reported to the prescribing clinician to ensure that the imbalances are recognized and treated.

Maintenance Fluid Replacement

* The typical adult requires 1 to 2 mEq of sodium per kilogram of body weight per day.14 For example, for maintenance purposes, the daily sodium requirements for a 70-kg adult could be met with 70 to 140 mEq of sodium. A liter of 0.45% sodium chloride provides 77 mEq of sodium, and a liter of 0.9% sodium chloride provides 154 mEq of sodium.11

* Overuse of hypotonic parenteral fluids during the postoperative period greatly increases a patient's risk for developing hyponatremia. Most dangerous is a sodium-free fluid such as 5% dextrose in water; even a dilute sodium-containing fluid, however, can cause dilutional hyponatremia when used in large volumes during the postoperative period because surgical patients have elevated ADH levels due to pain and nausea.11,13,18