Depending on a patient's condition, even a small imbalance in fluid and electrolytes can be serious.1 In this and subsequent articles, I'll review common electrolyte imbalances and how to intervene. This article focuses on hyponatremia; the next article will focus on hypernatremia.

The role of sodium

Sodium is absorbed into the body through the intestines and is excreted from the body by the renal system.2 Sodium is primarily an extracellular fluid (ECF) cation (see Reviewing fluid balance); normal ECF sodium levels range from 135 to 145 mEq/L. Sodium found in the intracellular fluid (ICF) is present at a much lower level, about 10 mEq/L.3

Because it doesn't cross cellular membranes easily, sodium's major role is to control fluid distribution within the body.4 Sodium also transmits electrical impulses contributing to contractions in the cardiac, skeletal, and smooth muscle systems; contributes to protein synthesis and acid-base balance; and regulates ECF osmolality.1,3

Osmolality and osmolarity are indicators of fluid balance in the body. Osmolality refers to the total measure of solutes in fluid, and osmolarity refers to the number of solutes per unit volume of fluid.5 When thinking about the effect sodium has on osmolality, remember the key point that water chases sodium. Serum osmolality and fluid distribution change when serum sodium levels change (see Osmolality and fluid status).1 The higher the osmolality, the drier the patient will be. Although serum osmolality levels can tell you much about the patient's fluid status, they don't tell you the cause of the imbalance.

Recognizing hyponatremia

Hyponatremia, defined as a serum sodium level below 135 mEq/L, may manifest as a true sodium loss or as a fluid excess that dilutes the serum sodium concentration.4 Two patients may have the same sodium level but completely opposite presentations.

Consider a patient with any of the following: vomiting, diarrhea, adrenal insufficiency, diaphoresis, excessive use of thiazide diuretics, hormonal changes related to hypothyroidism, gastric suctioning, or malnutrition. All are common causes of true hyponatremia, the loss of sodium and fluid.2,4,6 The patient may have dry skin, dry mucous membranes, abdominal cramps, weight loss, and oliguria.6 An increased thirst, decreased BP, and increased heart rate may also be noted in response to the lowered fluid volume.

Monitor patients experiencing these signs and symptoms closely because of the increased risk of hypovolemic shock.3 Consider medications, notably diuretics, as possible contributing factors. Also consider the patient's age: Poor skin turgor may be a manifestation of true hyponatremia, but also is a common physical assessment finding in older adults because of the loss of skin elasticity associated with normal aging. The normal aging process may also affect thirst perception; therefore, an older adult may have inadequate fluid intake placing them at increased risk for fluid volume deficit.7

Interventions

Treatment for hyponatremia will depend on the type of hyponatremia, as well as the patient's diagnosis, clinical manifestations, and serum sodium level.5 When sodium and water are lost, as occurs with true hyponatremia, both must be replaced. The tonicity of the fluid needs to be considered when selecting the most appropriate I.V. solution to correct a sodium imbalance.

Increasing the patient's volume with I.V. boluses of 0.9% sodium chloride solution is a good choice when hypotension is the primary concern, or for patients who've had a low sodium level for more than 2 days with few or no signs and symptoms.5 An isotonic solution, 0.9% sodium chloride solution replaces sodium and volume without causing fluid shifts between the ECF and ICF compartments.

Patients with acute drops in sodium below 120 mEq/L require more aggressive therapy.5 For these patients, and those who have moderate signs and symptoms of hyponatremia, replacing sodium becomes a crucial factor. A hypertonic I.V. solution such as 3% sodium chloride solution may be used to draw fluid into the vascular compartment from the ICF. This treatment provides fluid volume and much needed sodium, and can help prevent cerebral edema from hyponatremia.5

Although replenishing sodium is critical to prevent severe neurologic complications, use caution not to administer replacement too quickly. Too-rapid administration may lead to cellular shrinkage, causing osmotic demyelination syndrome. This severe neurologic syndrome is related to damage of the axonal myelin sheaths in the brainstem, and may lead to brain injury, respiratory paralysis, and death.2,3,5

The infusion rate depends on the patient's weight, the desired rate of sodium increase, and the severity of the patient's signs and symptoms.5 Closely monitor the patient's neurologic and respiratory status, urine output, and serum electrolytes during replacement therapy with hypertonic saline. Also weigh the patient daily when managing conditions that may contribute to fluid imbalances.

Dilutional hyponatremia

More common than true hyponatremia, dilutional hyponatremia is the result of sodium being diluted because of fluid volume increases. Common causes of dilutional hyponatremia include chronic kidney disease, heart failure, syndrome of inappropriate secretion of antidiuretic hormone (SIADH), hyperglycemia, cirrhosis, administration of hypotonic I.V. fluid, and tap-water enemas. Another cause of this condition is psychogenic polydipsia, or increased fluid intake because of excessive thirst, often associated with psychiatric disorders.4,6

Patient assessment findings may include weight gain, fatigue, muscle cramps, edema, and lethargy. When increased fluid volume dilutes sodium to levels less than 120 mEq/L, just as with true hyponatremia, significant neurologic symptoms may occur because of increased intracranial pressure. Weakness, confusion, decreased level of consciousness, and seizures may occur.4,6 Ultimately, cerebral edema may occur if equilibrium isn't restored.

How to intervene

Fluid restriction and diuretic therapy are the treatments for dilutional hyponatremia.7 Assess for and respond immediately to indications of fluid overload: distended neck veins; pulmonary crackles; increased BP and central venous pressure; widened pulse pressure; increased urine output; ascites; weight gain (not otherwise explained); peripheral or pulmonary edema; shortness of breath; and tachycardia.3,4 Cardiac and pulmonary function is a primary focus with patients who are fluid overloaded.

Medications such as angiotensin-converting enzyme (ACE) inhibitors, and beta-blockers also may be prescribed.5 If diuretics aren't effective, tolvaptan, an oral vasopressin receptor antagonist, may be prescribed.2 While the underlying cause of the hyponatremia is sought, closely monitor the patient's serum electrolytes, especially during diuretic therapy. Cardiac monitoring and serial ECGs also should be included in the plan for care.

Hyponatremia is a common problem for patients in hospitals and long-term-care facilities.3 Whether true or dilutional, patient management for hyponatremia must include daily weights and strict intake and output monitoring.1 Because low sodium levels may lead to cellular edema, mental status assessments must be a particular focus.2 Quality assessment skills and an ongoing observation of the patient's fluid and electrolyte status are central to preventing imbalances and averting further decline in the patient's clinical status.

Putting it all together

Consider Mr. A, 59, who's admitted with worsening heart failure secondary to poor renal function. His BP is 196/88, and his heart rate is 112. He has shortness of breath, bilateral pulmonary crackles, and 2+ bilateral lower extremity edema. Although he appears to be somewhat distracted, he tells you that he stopped taking "the pill that constantly sends me to the bathroom." Blood work results show sodium, 130 mEq/L; potassium, 3.8 mEq/L; and blood urea nitrogen (BUN), 32 mg/dL.

The physical assessment findings and blood work results reflect fluid volume overload with sodium dilution, so fluid therapy isn't part of the initial treatment plan. Decreasing fluid volume should have a positive effect on the patient's BP and tachycardia. Fortunately, Mr. A has minimal to no neurologic changes. Strict fluid restriction and medications are initial choices for treatment.5,7

Mr. A is treated with diuretic therapy, an ACE inhibitor, and a beta-blocker.5 Remember that vasopressin receptor antagonists may be used to reduce fluid volume.2 Weigh Mr. A daily, document intake and output, and closely monitor his neurologic, cardiac, renal, and pulmonary status.

Table Osmolality and fluid status

Watching the balance

Signs and symptoms of sodium imbalances may occur acutely or chronically.3 By understanding the causes and effects of imbalances and knowing the appropriate interventions, you can help your patient get appropriate care.

Reviewing fluid balance

In adults, the total body fluid accounts for greater than one-half of the body's weight. About 75% of the water in the body is inside cells (intracellular) and 25% is outside cells (extracellular). Most of the ECF is intravascular, with the remaining fluid found between the vessels and cells (interstitial).1,6 A small percentage of fluid is transcellular, and includes cerebrospinal fluid, synovial fluid, and fluid found in the peritoneum, pericardial, and pleural spaces.1

Fluid balance is maintained by fluid shifting between the ECF and ICF spaces; however, not all fluid is used by the body, presenting another type called third-space fluid.1 Urine and intestinal fluids are examples of normal third-space fluids. Some fluid, however, may become trapped within the interstitial spaces.

When excess fluid is removed from the circulatory system and isn't excreted from the body, edema results. Cardiac output may become compromised, and the patient may have signs and symptoms of hypovolemia such as hypotension and oliguria, along with weight gain.4 Burns, wounds, and liver, renal, and heart failure are examples of conditions from which abnormal third-space fluid shift may occur.4,6

Electrolytes combined with fluid create a solution containing dissolved ions, which may carry a negative (anion) or positive (cation) charge.3 The charged particles can conduct the electric current needed for nerve impulse transmission, heart automaticity, chemical reactions, and other bodily responses. Some electrolytes have a greater concentration in the ECF, while others have a greater concentration in the ICF.3

The body constantly expends energy in attempts to maintain homeostasis, that is, an equal number of positive and negative ions.1 The renal system plays a critical role in regulating fluid and electrolyte balance. In addition, several hormones influence kidney function, causing an increase or decrease in urine output, and a change in the delicate fluid and electrolyte balance.6

REFERENCES

1. Culleiton AL, Simko LC.Keeping electrolytes & fluids in balance. Nursing Critical Care. 2011;6(2):30-35. [Context Link]

2. Crawford A, Harris H.Balancing act: Na+ sodium K+ potassium. Nursing. 2011;41(7):44-50. [Context Link]

3. Vroman R.Electrolyte imbalances. Part 1: sodium balance disorders. EMS World. 2011;40(2):37-38, 40-43. [Context Link]

4. Smeltzer SC, Bare BG, Hinkle JL, Cheever KH.Brunner & Suddarth's Textbook of Medical-Surgical Nursing. 11th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2008:300-354-2001, 1999-2001. [Context Link]

5. Assadi F.Hyponatremia: a problem-solving approach to clinical cases. J Nephrol. 2012;25(4):473-480. [Context Link]

6. Russell SS.Fluid/electrolyte/acid-base imbalances. In: Craven H, ed. Core Curriculum for Medical-Surgical Nursing. 4th ed. Pitman, NJ: Academy of Medical Surgical Nursing; 2009:116-125. [Context Link]

7. Capezuti E, Zwicker D, Mezey M, Fulmer T, eds. Evidence-based Geriatric Nursing Protocols for Best Practice. 3rd ed. New York, NY: Springer Publishing; 2008:431-458. [Context Link]

RESOURCE

Wilson BK.Nursing care of patients with fluid, electrolyte, and acid-base imbalances. In: Williams L, Hopper P, eds. Understanding Medical-Surgical Nursing. 4th ed. Philadelphia, PA: F.A. Davis Co.; 2010:69-87.