Electrolyte Imbalance: A Matter of Equilibrium

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The human body seeks homeostasis, a state of equilibrium in its internal environment. Homeostasis is controlled and regulated by the body’s physiological processes — with a complicated interplay among water, acid-base balance, and electrolytes. The latter, found in body fluids — sweat, urine, gastric juice, pancreatic juice, and saliva — must be present in the appropriate quantities if metabolism and other important functions are to proceed normally. Nurses witness this great balancing act every day.

What happens when a patient experiences a disturbance in body fluid homeostasis? He or she might have a chronic or acute disease that causes a body fluid disturbance, with subsequent electrolyte imbalances. “In many cases, secondary symptoms of illness, such as diarrhea or vomiting, or treatments such as nasogastric suctioning or medication administration, rather than the primary disease itself, can cause fluid and electrolyte imbalances,” says Diane Cheer, RN, APN-C, advanced practice nurse for the surgical ICU at Hackensack University Medical Center, Hackensack, NJ.

Look at the Volume

Crucial electrolytes include sodium, potassium, calcium, magnesium, chloride, bicarbonate, and phosphate. Some of the most common and easily treated electrolyte imbalances are the result of fluid volume deficit or excesses, says Cheer. Intravascular fluid volume deficit (hypovolemia) occurs as a result of inadequate fluid intake or an increased output caused by vomiting, diarrhea, dehydration, and fluid shifts, such as those seen in burn patients.

Fluid volume excess refers to those situations in which there is increased retention of water and electrolytes in equal proportions. Causes can include excessive fluid intake, excessive sodium intake, and impaired ability to excrete fluid, leading to abnormal fluid retention.

Sodium a Key Component

Hyponatremia (sodium deficiency) is the most common electrolyte disorder, seen in 1% to 4% of hospitalized patients.¹

“Sodium levels are very closely related to fluid balance,” says Barbara Schweiger, RN, BSN, CCRN, clinical educator for critical care at the Hackensack facility. “Decreased sodium levels promote water excretion, while increased sodium levels cause fluid retention.” Sodium deficiency can result from a variety of factors, some of which include —

• Fluid loss from the body, such as that lost from vomiting or diarrhea
• Diuretic therapy
• Nasogastric suctioning
• Adrenal insufficiency
• Syndrome of inappropriate antidiuretic hormone excretion
• Acute or chronic renal failure
• Congestive heart failure

Clinically, the patient with low sodium levels may have anorexia, nausea, vomiting, muscle cramps, lethargy, an altered level of consciousness, and, with severe sodium deficiency, convulsions.

Hypernatremia (sodium excess) can be caused by excessive water loss (such as that caused by diabetes insipidus), inadequate water intake (particularly in the debilitated elders or infants), or seawater ingestion. It may also occur as a result of hyperalimentation. Symptoms include thirst, tented skin turgor, elevated body temperature, tachycardia, central nervous system dysfunction, and peripheral and pulmonary edema. Although the disorder is seen in less than 1% of hospitalized patients, it is a serious electrolyte disorder with a reported mortality of 40% to 60%.²

Potassium — Too Much or Too Little?

Potassium helps muscle and nerve cells to function properly. Nerve cells have to transmit the messages that instruct the muscle to contract properly. “Because the heart is a vital muscular organ,” says Cheer, “potassium plays an important role in cardiac functioning.”

Hypokalemia (decreased serum potassium level) can result from an inadequate dietary potassium intake; GI disorders, such as diarrhea, vomiting, or fistulas; metabolic alkalosis; hyperaldosteronism; or use of medications like carbenicillin, amphotericin B, corticosteroids, or diuretics. Symptoms include fatigue, anorexia, nausea/vomiting, muscle weakness, cardiac dysrhythmia, and decreased bowel motility.

Hyperkalemia (potassium excess) can result from renal failure, acidosis, severe tissue trauma (e.g., burns), hypoaldosteronism, and use of ACE inhibitors. “It’s rare to see high potassium levels unless there is kidney involvement, since dietary potassium intake is generally matched by the body’s ability to excrete,” says Schweiger. Clinical manifestations include cardiac dysrhythmias, muscle weakness/paresthesias, irritability/anxiety, and abdominal cramps with diarrhea.

Consider Calcium

“Only 1% of total calcium circulates in the blood, and of that 1%, about half is bound to plasma protein,” says Schweiger. “When calcium levels are being assessed, clinicians need to differentiate between total calcium and ionized [true] calcium.” Calcium, she adds, is an important electrolyte that’s needed for proper endocrine function, acid/base balance, neuromuscular excitability, and cardiac contractility.

Hypocalcemia (calcium deficiency) can result from hypoparathyroidism, pancreatitis, inadequate vitamin D intake or synthesis, renal failure, septic shock, or the use of certain drugs (cisplatin, penamidine). “Women and geriatric patients may have poor calcium absorption,” says Schweiger. Symptoms of severe calcium hypocalcemia include tetany (i.e., tingling in fingers and circumoral area, muscle spasms), positive Trousseau sign (induced carpopedal spasm), positive Chvostek sign (twitching of muscles supplied by facial nerve), hyperactive deep tendon reflexes, and neuromuscular irritability or seizures.

Hypercalcemia (calcium excess) can be caused by increases in gastrointestinal absorption, vitamin D intoxication, movement of calcium from bones to serum caused by prolonged immobilization or malignancies, renal failure, thiazide diuretics, lithium carbonate use, hyperparathyroidism, endocrine neoplasms, and Paget’s disease of the bone. Symptoms include anorexia, nausea, vomiting, constipation, muscle weakness, an altered level of consciousness, cardiac dysrhythmias, polyuria/polydipsia, and hypoactive deep tendon reflexes.

More on Magnesium

Magnesium, found primarily in bone and intracellular fluid, is absorbed by the small intestine and excreted in urine and feces. Magnesium levels, says Cheer, are regulated by the gastrointestinal and urinary systems.

The etiology of hypomagnesemia (magnesium deficiency) includes poor nutrition, alcoholism, malabsorption syndrome, and gastrointestinal and renal losses without replacement. Symptoms include weakness, seizure, neuromuscular irritability, insomnia, and mood changes. Patients with low serum magnesium levels are at increased risk for potentially lethal cardiac dysrhythmias.

Hypermagnesemia (magnesium excess) can result from renal failure; overuse of antacids, enemas, or laxatives containing magnesium; and severe dehydration as seen in diabetic ketoacidosis. Symptoms include weakness, difficulty swallowing, lethargy, nausea/vomiting, hypotension, and diminished or absent deep tendon reflexes.
Buffer with Phosphorus

Phosphorus, an important buffer in terms of acid-base balance, plays an important role in cell membrane integrity, says Cheer. It’s needed for muscle functioning, nerve conduction, red blood cell functioning, and normal metabolism of carbohydrates, fats, and protein. Adequate vitamin D is necessary for the body to properly regulate phosphorus, and calcium and phosphorus interact in a reciprocal relationship. In children, low levels of phosphate can suppress normal growth. Hypophosphatemia can result from a variety of factors, including diuretic use, diabetic ketoacidosis, hyperparathyroidism, renal tubule defects, Fanconi’s syndrome, anabolic steroid use, burns, chronic alcohol usage, and malabsorption syndromes.

Hyperphosphatemia can result from renal failure, hypoparathyroidism, tumor lysis syndrome, and rhabdomyolysis or crush injury, but is “rarely clinically significant,” says Cheer.

Count on Chloride

High levels of chloride, a major extracellular anion, which are important in acid/base balance, can result from head trauma, bicarbonate loss, or dehydration, while low levels can be caused by renal failure, gastric suctioning, or prolonged vomiting.

Assessment and Action

When working with patients who have electrolyte imbalances, a crisis situation may develop — it may become a matter of life and death. Consider the patient with neurogenic diabetes insipidus, caused by a deficiency of vasopressin, an antidiuretic hormone (ADH). When the secretion of ADH is impaired, too much water is excreted, resulting in dilute urine and hemoconcentration. Normally, the patient with neurogenic diabetes insipidus experiences excessive urination and extreme thirst. But if the disease is left untreated, the patient experiences severe and life-threatening conditions that include hypovolemia, circulatory collapse, hyperosmolality, and seizures.

Diagnosis and treatment are imperative in this critical situation. The nurse must assess the patient’s urine osmolality, urine specific gravity, serum osmolality, and serum sodium. Aggressive treatment to prevent dehydration and restore electrolyte balance is the first priority.

When the RN assesses patients for fluid, electrolyte, and acid-base imbalances, he or she must take a nursing history, perform a physical assessment, look at clinical measurements, review lab test results, and monitor the patient’s cardiac and respiratory status. The nurse should observe the patient’s skin and mucous membranes, level of consciousness, and neurological and neuromuscular status.

RNs who care for patients with electrolyte imbalances must —

• Measure intake and urinary output
• Monitor vital signs
• Restrict or force fluids depending on the nature of the imbalance
• Restore homeostasis through parenteral or oral administration of fluids and/or electrolyte solutions
• Keep the patient safe (e.g., institute seizure precautions)

Education is a crucial part of nursing care. Patient and family education involves teaching about possible risk factors for electrolyte imbalance — for example, diarrhea, persistent vomiting, and profuse perspiration.

Education also involves encouraging the patient to avoid foods high in salt, sugar, and caffeine and stressing the importance of limiting alcohol intake while drinking an adequate amount of fluids before, during, and after strenuous exercise.

It’s also important to teach patients about the side effects of their medications and ways to prevent electrolyte imbalance (e.g., eating potassium-rich foods when on diuretics). Patients also need to learn about the signs and symptoms of electrolyte or fluid imbalances (i.e., sudden weight gain or loss, increased urination, shortness of breath, and ankle swelling) and the importance of reporting signs and symptoms immediately

Dysfunction of a patient’s regulatory mechanisms can lead to an electrolyte imbalance, which can have serious and even potentially fatal consequences. It’s a real balancing act — and RNs must have the knowledge to accurately assess the patient and quickly take action.

Barbra Williams Cosentino, RN, CSW, is a contributing writer for Nursing Spectrum.

References

1. Barkley TW, Myers CM. Practice Guidelines for Acute Care Nurse Practitioners. Philadelphia, PA: WB Saunders; 2001.

2. Water And Sodium Metabolism. Merck Manual. Available at: www.merck.com/mrkshared/mmanual/section2/ chapter12/12b.jsp. Accessed April 13, 2004.

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