FLUID AND ELECTROLYTE IMBALANCES
Fluid and electrolyte balance is essential for homeostasis and assures adequate cellular perfusion and function, and is the key to maintaining electrolyte balance as well. Sodium (Na+), potassium (K+), calcium (Ca2+), and magnesium (Mg2+) play key roles in maintaining cell membrane stability, muscle contractions, cardiac and neuronal conduction, and bone health. This balance may be altered by numerous processes including numerous medications, diseases, alterations in the pH, and nutrition. A thorough history including medication review, physical examination, and analysis of laboratory data is often needed to identify an imbalance, assess for complications, and formulate a plan of care. Nurses should be able to recognize the diagnostics needed to properly identify an imbalance, the associated clinical manifestations, and initial management of these derangements.
Water makes up 50% to 60% of our total body weight, although this varies by age, sex, and muscle and fat composition (Hall, 2016; Harring, Deal, & Kuo, 2014; Kamel & Halperin, 2017). Water is contained in various compartments and can be shifted around if needed by the body. The intracellular space accounts for two thirds of our total body water. The remainder is extracellular and includes intravascular (plasma) and interstitial spaces. Water balance is regulated by the hypothalamic–neurohypophyseal–renal axis; during acute illness this axis is often altered leading to imbalances in many hospitalized patients (Knepper, Kwon, & Nielsen, 2015). By releasing vasopressin or antidiuretic hormone (ADH), altering the thirst response, and altering renal water excretion, this axis works to maintain a serum osmolality of 280 to 295 mmol/kg; as with any lab the accepted values vary. Osmolality is a measure of the concentration of solutes in a solution (Hall, 2016; Harring et al., 2014; Kamel & Halperin, 2017). The higher the osmolality, the higher the concentration of solutes. Osmolality must be balanced between intracellular and extracellular compartments to maintain equilibrium and cell membrane integrity (Kamel & Halperin, 2017; Sterns, 2015). Sodium is the primary extracellular solute and directly influences osmolality, as well as how fluids shift among the body’s compartments. Fluid movement is also influenced by plasma proteins, glucose, and other electrolytes.
Sodium is the most abundant extracellular cation, with an accepted normal range of 135 to 145 mEq/L. Hyponatremia is considered the most common electrolyte imbalance encountered in the hospitalized patient (Cho, 2017). It is estimated that 15% of admitted adults have hyponatremia with an overall mortality rate of 3% to 29% (Harring et al., 2014). The degree of hyponatremia is 68often assessed based on the serum and urine Na+ concentrations and osmolality. Isotonic hyponatremia (osmolality 280–295 mmol/kg) is characterized by a normal serum osmolality and may result from elevated serum lipids or proteins. Hypertonic hyponatremia (osmolality greater than 295 mmol/kg) may be caused by hyperglycemia or osmotic diuretics (Cho, 2017; Craig, 2015; Harring et al., 2014; Kamel & Halperin, 2017).
The most common fluid and electrolyte imbalance is hypotonic hyponatremia (osmolality less than 280 mmol/kg). Children are at particular risk of developing hyponatraemia encephalopathy (Lamont & Crean, 2014). Hypotonic patients can further be categorized as hypovolemic, euvolemic, and hypervolemic. Hypovolemia occurs when there is a loss of both water and Na+ from the body, for example, excessive gastrointestinal (GI) or genitourinary (GU) losses. The Na+ loss usually exceeds the water loss, and these patients often appear dehydrated. Euvolemia occurs when excess free water is gained most often related to ADH release or function, and there is no excess of serum Na+. This may include hypothyroidism, cortisol insufficiency, syndrome of inappropriate antidiuretic hormone (SIADH), exogenous free water intake, and use of certain drugs including thiazide diuretics and 3,4-methylenedioxymethamphetamine (MDMA, ecstasy). As the free water is gained, the serum Na+ is lowered, but there is usually no loss of Na+. However, the patient does not appear dehydrated or volume overloaded. Hypervolemia occurs when there is an increased retention of both body water and Na+ often because of renal disease, heart failure, or cirrhosis. Water is retained more than Na+, leading to a decrease in the serum Na+. These patients usually appear volume overloaded (Cho, 2017; Craig, 2015; Harring et al., 2014; Kamel & Halperin, 2017; Sterns, 2015).
Hypernatremia is most often associated with a decrease in free water intake which leads to cellular dehydration and an increased osmolality. This can be seen in patients with a decreased thirst reflex and those without easy access to water, for example, limited mobility, extremes of age, and comatose states. It is also associated with diabetes insipidus (DI); because of the lack of ADH, the kidneys cannot adequately regulate water balance. Excess loss of water worsens hypernatremia, but unless the thirst reflex is altered or there is limited access to water, insufficient free water intake is the primary cause of hypernatremia (Cho, 2017; Craig, 2015; Harring et al., 2014; Kamel & Halperin, 2017).
Potassium is the most abundant intracellular cation with an accepted serum range of 3.5 to 5.0 mEq/L. Potassium plays a key role in maintaining the resting membrane potential of cardiac and muscle cells. Hypokalemia may be related to increased loss from the GI or GU tract, cellular shifts from alkalosis and beta-2 stimulation, or inadequate dietary intake. Hypomagnesemia can also lead to hypokalemia. Hyperkalemia may result from medications that increase K+ levels, inadequate excretion as seen in renal failure, cellular shifts seen with acidosis and significant tissue trauma, or maybe a measurement error because of cell hemolysis from the lab draw, often referred to as pseudohyperkalemia (Combs & Buckley, 2015; Gooch, 2015; Hall, 2016; Kamel & Halperin, 2017; Medford-Davis & Rafique, 2014).
69Calcium plays an essential role in the neuromuscular function and bone health. A normal Ca2+ level is often considered to be 8.5 to 10.5 mg/dL or an ionized level of 4.6 to 5.3 mg/dL. About half of the serum Ca2+ is bound to proteins; the remainder is free or ionized. Almost all (99%) of the body’s Ca2+ is stored in the bones. Hypocalcemia most often results from inadequate intake or gastrointestinal (GI) absorption, a chronic kidney disease that results in vitamin D deficiency, hypoparathyroidism, or from massive blood transfusions. In the setting of hypoalbuminemia, hypocalcemia may be noted and is often considered a pseudohypocalcemia. Evaluating the ionized Ca2+ level can help determine if a true imbalance exists. Hypercalcemia most often develops from hyperparathyroidism or, in cases of higher levels, malignancy is a prime cause. It is estimated that 20% to 30% of cancer patients experience hypercalcemia (Chang, Radin, & McCurdy, 2014; Cho, 2017; Gooch, 2015; Hall, 2016; Love & Buckley, 2015).
Magnesium is the second most common intracellular cation and plays a similar role as Ca2+ in regards to the nervous system. When outside the normal range of 1.8 to 2.5 mg/dL it may influence K+ and Ca2+ levels. Hypomagnesemia is more common and often results from altered dietary intake or absorption or increased urinary excretion. Hypermagnesemia is rare and often associated with renal failure but could be related to medications that increase magnesium levels (Chang et al., 2014; Cho, 2017; Love & Buckley, 2015).
It is common for acutely ill patients to have one or more imbalances. The nurse should be observant for risk factors and signs or symptoms of these imbalances. Both Na+ imbalances may present similarly, and lab data is needed to properly identify and manage the patient. The patient may have altered mental status, weakness, headache, or seizures. Management is guided by the lab values, clinical findings, and rapidity in which symptoms started. Hypovolemia should be corrected as the patient condition allows. In the stable hyponatremic patient, free water restrictions may be all that is required to stabilize the patient. In the unstable seizing patient, a bolus of hypertonic (3%) saline may be required. In most patients, increasing the serum Na+ by 4 mEq/L is all that is needed to reduce cerebral edema and resolve the seizures. In patients with SIADH or hypervolemic hyponatremia, a vasopressin antagonist may be administered to block ADH receptors in the kidneys and limit the reabsorption of water (Cho, 2017; Craig, 2015; Gooch, 2015).
NURSING INTERVENTIONS, MANAGEMENT, AND IMPLICATIONS
Fluid administration to the pediatric patient is an integral part of the medical management of hospitalized children (Lamont & Crean, 2014). Intravenous (IV) fluids are frequently administered to hospitalized children to provide sufficient water, electrolytes, and glucose to maintain homeostasis during recovery from illness (Lamont & Crean, 2014). Variations in age, size, underlying physiology, 70and disease processes should be considered and in general younger children require more fluid per kilogram than older children owing to a higher metabolic rate, higher body surface area to volume ratio, and a reduction in renal concentrating ability (Lamont & Crean, 2014). Total body water percentages vary with age, most likely seen as a higher percentage of body water in the very young compared to the older pediatric patient (Lamont & Crean, 2014).
Hypernatremia may be managed with isotonic IV fluids initially to restore perfusion. Loop diuretics may be used in volume-overloaded patients to increase the excretion of water and Na+. In the setting of DI, desmopressin (DDAVP) may be given. An important caveat to the management of Na+ imbalances is that the level should not be rapidly changed. If the serum Na+ is increased too quickly, osmotic demyelination or central pontine myelinolysis may occur. If the serum Na+ is reduced too rapidly, cerebral edema often develops. A guideline to prevent complications is to correct the level by no more than 1 to 2 mEq/L/hr and no more than 10 mEq/d (Cho, 2017; Craig, 2015; Gooch, 2015; Sterns, 2015). The more chronic the condition, the slower the correction.
Any patient suspected of having a K+ imbalance should have his or her EKG quickly assessed. Patients may experience muscle cramps or weakness, which could progress to respiratory failure. Flattened or inverted T waves, the appearance of U waves, and ST depression are often seen with hypokalemia. Hypokalemic management is also based on the severity and may require oral or IV K+ replacement. In the setting of hypomagnesemia, the Mg2+ imbalance will have to be corrected first (Cho, 2017; Combs & Buckley, 2015; Gooch, 2015; Medford-Davis & Rafique, 2014).
Of the electrolyte imbalances, hyperkalemia is the most lethal. If there is a concern for hyperkalemia, the ECG should quickly be assessed for the presence of peaked T waves, a prolonged PR interval, or a widened QRS. If these ECG changes are present, IV Ca2+ should be administered to stabilize the resting membrane potential of the cardiac cells and prevent life-threatening arrhythmias. Treatment should not be delayed while awaiting lab values. Hyperkalemia is managed two ways. First, high dose albuterol, insulin with glucose, or sodium bicarbonate may be given to shift the K+ back in the cells temporarily. Subsequently, the excessive K+ should be eliminated. This is most effectively accomplished through hemodialysis, but loop diuretics or cation exchange resins may also be used with caution (Cho, 2017; Combs & Buckley, 2015; Gooch, 2015; Medford-Davis & Rafique, 2014).
Hypocalcemia cause neuromuscular excitability including muscle spasms, paresthesias, hyperactive deep tendon reflexes (DTRs), and eventually seizures. The ECG should also be assessed for a prolonged QT interval and bradycardia. Symptomatic patients may be managed with oral or IV Ca2+ replacement. Patients with hypercalcemia may have lethargy, muscle weakness, hypoactive DTRs, and at higher levels a shortened QT and widened QRS may be noted on the ECG. Patients may develop atrioventricular blocks which can progress to cardiac arrest in levels more than 15 mg/dL. Initially, IV fluids should be given to restore renal perfusion. Depending on the severity of the patient, hemodialysis 71may be used to remove the excess Ca2+. In less severe cases, the patient may be given a loop diuretic, a bisphosphonate, a glucocorticoid, or calcitonin (Chang et al., 2014; Cho, 2017; Gooch, 2015; Love & Buckley, 2015).
Lastly, patients with low serum Mg2+ levels present similarly to those with hypokalemia and hypocalcemia and have weakness and muscle cramps. This can progress to neuromuscular and cardiac irritability. Treatment is focused on replacement with oral or IV Mg2+ depending on the patient’s condition. Hypermagnesemia is similar to hypercalcemia, and patients experience blunted neuromuscular effects including lethargy, paralysis, decreased DTRs, and eventually hypotension, cardiac and respiratory compromise. Calcium may be administered to antagonize the Mg2+ and reverse neuromuscular weakness. If needed, dialysis is effective at removing the excess electrolyte in severe cases (Chang et al., 2014; Cho, 2017; Love & Buckley, 2015).
The fluid prescription for each pediatric patient should be individualized according to the clinical situation. Many hospitalized children are at risk of developing hyponatremia while receiving IV fluids, which may necessitate fluid restriction (Lamont & Crean, 2014). The nurse should include frequent monitoring and observation of the child to ensure the fluid orders are still appropriate. Often a urea and electrolyte profile should be checked at least every 24 hours in pediatric patients receiving IV fluids and more frequently if there are known electrolyte abnormalities (Lamont & Crean, 2014). Asymptomatic electrolyte abnormalities are common and will be detectable only by blood sampling; only fluids with a sodium content above 131 mmol/L should be used for an IV fluid bolus (Lamont & Crean, 2014).
Fluid and electrolyte balance is critical to maintaining all body functions. Sodium and water have an important relationship and imbalances are common in pediatric patients with acute problems. Patients with Na+ imbalances often present with neurological changes and the imbalance cannot be aggressively corrected. Potassium is crucial for cardiac and muscle function; it can be life threatening and often requires rapid identification and correction to prevent complications. Calcium and Mg2+ both play an important role in neuromuscular function and can affect cardiac function as well. Nurses should evaluate for these imbalances in the acutely ill pediatric patient, recalling the patient may have more than one. Labs are often helpful, but history and physical examination findings are also important to identify the imbalance and manage the derangement.
Chang, W.-T. W., Radin, B., & McCurdy, M. T. (2014). Calcium, magnesium, and phosphate abnormalities in the emergency department. Emergency Medicine Clinics of North America, 32(2), 349–366. doi:10.1016/j.emc.2013.12.006