Study Guides for Adult Health, Study notes of Nursing

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Electrolyte Imbalances

Sodium Imbalances

 Sodium (Na+) is the most abundant electrolyte in the ECF; its concentration ranges from 135 to 145 mEq/L (135 to 145 mmol/L), and it is the primary determinant of ECF volume and osmolality.  Sodium has a major role in controlling water distribution throughout the body, because it does not easily cross the plasma membrane and because of its abundance and high concentration in the body.  Sodium is regulated by ADH, thirst, and the renin–angiotensin–aldosterone system.  A loss or gain of sodium is usually accompanied by a loss or gain of water.  Sodium also functions in establishing the electrochemical state necessary for muscle contraction and the transmission of nerve impulses.  The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) may be associated with sodium imbalance. o When there is a decrease in the circulating plasma osmolality, blood volume, or blood pressure, ADH (also called arginine vasopressin [AVP]) is released from the posterior pituitary. o Oversecretion of ADH can cause SIADH. o Patients at risk for SIADH include older adults; those who have had brain surgery or have a brain tumor, pulmonary malignancy, or acquired immune deficiency syndrome (AIDS); those on mechanical ventilation; and those taking selective serotonin reuptake inhibitors (SSRIs).

Hyponatremia – Sodium Deficit

 Hyponatremia refers to a serum sodium level that is less than 135 mEq/L (135 mmol/L).  Hyponatremia can present as an acute or chronic form. o Acute hyponatremia is commonly the result of a fluid overload in a surgical patient.  This is a dilutional hyponatremia because the excess water dilutes the sodium in the bloodstream. o Chronic hyponatremia is seen more frequently in patients outside the hospital setting, has a longer duration, and has less serious neurologic sequelae.  Another type of hyponatremia is exercised-associated hyponatremia, which is more frequently found in women and those of smaller stature.  It can occur during extreme temperatures, because of excessive fluid intake before exercise, or prolonged exercise that results in excess loss of sodium through perspiration.

Pathophysiology

 Hyponatremia primarily occurs due to an imbalance of water rather than sodium. o Checking the urine sodium value can assist in differentiating renal from nonrenal causes of hyponatremia. o Low sodium in the urine occurs as the nephrons of the kidney retain sodium to compensate for nonrenal fluid loss (i.e., vomiting, diarrhea, sweating). o High sodium concentration in the urine is associated with renal salt wasting that occurs in renal dysfunction or diuretic use. o In dilutional hyponatremia, the ECF volume has excess water but there is no edema, and the excess water dilutes the sodium.  A deficiency of aldosterone, as occurs in adrenal insufficiency, also predisposes to sodium deficiency. o Lack of aldosterone causes lack of sodium and water reabsorption into the bloodstream at the nephrons. o In addition, the use of certain medications, such as anticonvulsants (e.g., carbamazepine, oxcarbazepine, levetiracetam), SSRIs (e.g., fluoxetine, sertraline, paroxetine), or desmopressin acetate, have side effects that increase the risk of hyponatremia.

Clinical Manifestations

 Clinical manifestations of hyponatremia depend on the cause, magnitude, and speed with which the deficit occurs, which includes: o Poor skin turgor o Dry mucosa o Headache

o Decreased saliva production o Orthostatic fall in blood pressure o Nausea o Vomiting o Abdominal cramping can occur  Neurologic changes, including altered mental status, status epilepticus, and coma, are related to the cellular swelling and cerebral edema associated with hyponatremia. o As the extracellular sodium level decreases, the cellular fluid becomes relatively more concentrated and pulls water into the cells. o In general, patients with an acute decrease in serum sodium levels have more cerebral edema and higher mortality rates than do those with more slowly developing hyponatremia. o Acute decreases in sodium, developing in less than 48 hours, may be associated with cerebral edema. o Cerebral edema can lead to compression of brain stem structures and brain herniation. o Chronic decreases in sodium, developing over 48 hours or more, can occur in status epilepticus and other neurologic conditions.  Clinical features of hyponatremia associated with sodium loss and water gain include anorexia, muscle cramps, and a feeling of exhaustion.  The severity of symptoms increases with the degree of hyponatremia and the speed with which it develops.  When the serum sodium level decreases to less than 115 mEq/L (115 mmol/L), signs of increasing intracranial pressure, such as lethargy, confusion, muscle twitching, focal weakness, hemiparesis, papilledema, seizures, and death, may occur.

Assessment & Diagnostic Findings

 Targeted assessment includes: o History and physical examination with a focused neurologic examination o Evaluation of signs and symptoms as well as laboratory test results o Identification of current IV fluids, if applicable o A review of all medications the patient is taking  Regardless of the cause of hyponatremia, the serum sodium level is less than 135 mEq/L; in SIADH, it may be lower than 100 mEq/L (100 mmol/L).  Serum osmolality is usually decreased.  When hyponatremia is due to lack of sodium ingestion, the urinary sodium content is less than 20 mEq/L (20 mmol/L) and the specific gravity is low (1.002 to 1.004). o However, when hyponatremia is due to SIADH, the urinary sodium content is greater than 20 mEq/L, and the urine specific gravity is usually greater than 1.012.  Although the patient with SIADH retains water abnormally there is no peripheral edema; instead, fluid accumulates inside the cells. o This phenomenon sometimes manifests as pitting edema.

Medical Management

 The key to treating hyponatremia is an assessment that focuses on the clinical symptoms of the patient and signs of hyponatremia (including laboratory values). As a general rule, treating the underlying condition will bring the sodium level back to normal.

Sodium Replacement

 The most common treatment for hyponatremia is careful administration of sodium by mouth, nasogastric tube, or a parenteral route. o For patients who can eat and drink, sodium is easily replaced, because sodium is consumed abundantly in a normal diet. o For those who cannot consume sodium, lactated Ringer’s solution or isotonic saline (0.9% sodium chloride) solution may be prescribed.  Serum sodium must not be increased by more than 12 mEq/L in 24 hours to avoid neurologic damage due to demyelination.

o This condition may occur when the serum sodium concentration is overcorrected (exceeding 140 mEq/L) too rapidly or in the presence of hypoxia or anoxia. o It may produce lesions that show symmetric myelin destruction affecting all fiber tracts that can present with altered cognition and decreased alertness, ataxia, paraparesis, dysarthria, horizontal gaze paralysis, pseudobulbar palsy, and coma.  The usual daily sodium requirement in adults is approximately 100 mEq, provided there are not excessive losses.  In SIADH, the administration of hypertonic saline solution alone cannot change the plasma sodium concentration. o Excess sodium would be excreted rapidly in highly concentrated urine. o With the addition of the diuretic furosemide, urine is not concentrated, and isotonic urine is excreted to effect a change in water balance. o In patients with SIADH, in whom water restriction is difficult, lithium can antagonize the osmotic effect of ADH on the nephrons’ collecting ducts.

Water Restriction

 In patients with normal or excess fluid volume, hyponatremia is usually treated effectively by restricting fluid. o However, if neurologic symptoms are severe (e.g., seizures, delirium, coma), or in patients with traumatic brain injury, it may be necessary to administer small volumes of a hypertonic sodium solution with the goal of alleviating cerebral edema. o Incorrect use of these fluids is extremely dangerous, because 1 L of 3% sodium chloride solution contains 513 mEq of sodium and 1 L of 5% sodium chloride solution contains 855 mEq of sodium. o The recommendation for hypertonic saline administration in patients with craniocerebral trauma is 3% saline between 0.10 and 1.0 mL/kg of body weight per hour (Sterns, 2017d).

Pharmacologic Therapy

 AVP receptor antagonists (also called ADH receptor antagonists) are pharmacologic agents that treat hyponatremia by blocking the effect of ADH at the nephron, which in turn allows diuresis to occur and leads to water excretion.  Use of IV conivaptan HCl, an AVP receptor antagonist, is limited to the treatment of hospitalized patients.  It may be a useful therapy for those patients with moderate to severe symptomatic hyponatremia but is contraindicated in patients with seizures, delirium, or coma, which warrants the use of hypertonic saline.  Tolvaptan is an oral medication indicated for clinically significant hypervolemic and euvolemic hyponatremia that must be initiated and monitored in the hospital setting.

Nursing Management

 The nurse needs to identify and monitor patients at risk for hyponatremia.  The nurse monitors I&O as well as daily body weight. o I&O can be used to identify excess water input or lack of sufficient water output.  The nurse needs to get a thorough history to identify if the patient is a performance athlete. o Performance athletes (i.e., marathon runners) may use salt tablets to compensate for loss of sodium with sweating, hoping to decrease sodium loss during prolonged exercise; however, there is no evidence that this practice works, and it is not recommended.  Hyponatremia is a frequently overlooked cause of confusion in older patients, who are at increased risk because of decreased renal function and subsequent inability to excrete excess fluids. o Administration of prescribed and OTC medications that cause sodium loss or water retention is often the predisposing factor. o A diminished sense of thirst or decreased ability to access food or fluids may also contribute to the problem.

Detecting & Controlling Hyponatremia

 For patients at risk, the nurse closely monitors fluid I&O as well as daily body weight.  It is also necessary to monitor laboratory values (i.e., sodium) and be alert for GI manifestations such as anorexia, nausea, vomiting, and abdominal cramping.  The nurse must be alert for central nervous system changes, such as lethargy, confusion, muscle twitching, and seizures.

o Neurologic signs are associated with very low sodium levels that have fallen rapidly because of fluid overloading.  Serum sodium is monitored very closely in patients who are at risk for hyponatremia; when indicated, urine sodium and specific gravity are also monitored.  For a patient with abnormal losses of sodium who can consume a general diet, the nurse encourages foods and fluids with high sodium content to control hyponatremia. o For example, broth made with one beef cube contains approximately 900 mg of sodium; 8 oz of tomato juice contains approximately 700 mg of sodium.  The nurse also needs to be familiar with the sodium content of parenteral fluids.  If the primary cause of hyponatremia is water retention, it is safer to restrict fluid intake than to administer sodium.  In normovolemia or hypervolemia, administration of sodium predisposes a patient to fluid volume overload.  In severe hyponatremia, the aim of therapy is to elevate the serum sodium level only enough to alleviate neurologic signs and symptoms.  It is generally recommended that the serum sodium concentration be increased to no greater than 125 mEq/L ( mmol/L) with a hypertonic saline solution.  For the patient taking lithium, the nurse observes for lithium toxicity, particularly when sodium is lost. o In such instances, supplemental salt and fluid are given. o Because diuretics promote sodium loss, the patient taking lithium is instructed not to use diuretics without close medical supervision. o For all patients on lithium therapy, normal salt, and oral fluid intake (approximately 6- to 15-g sodium and 2.5- to 3.0-L fluid/day) should be encouraged and a sodium restricted diet should be avoided.  Excess water supplements are avoided in patients receiving isotonic or hypotonic enteral feedings, particularly if abnormal sodium loss occurs or water is being abnormally retained (as in SIADH).  Actual fluid needs are determined by evaluating fluid I&O, urine specific gravity, and serum sodium levels. Hypernatremia – Sodium Excess  Hypernatremia is a serum sodium level higher than 145 mEq/L (145 mmol/L).  It can be caused by a gain of sodium in excess of water or by a loss of water in excess of sodium.  It can occur in patients with normal fluid volume or in those with FVD or FVE. o With water loss, the patient loses more water than sodium; as a result, the serum sodium concentration increases, and the increased concentration pulls fluid out of the cell.  This is both an extracellular and an intracellular FVD. o In sodium excess, the patient ingests or retains more sodium than water.

Pathophysiology

 A common cause of hypernatremia is fluid deprivation in patients who do not respond to thirst. o Most often affected are patients who are very old, very young, or cognitively impaired.  Administration of hypertonic enteral feedings without adequate water supplements leads to hypernatremia, as does watery diarrhea and greatly increased insensible water loss through the lungs or skin (e.g., hyperventilation, burns).  In addition, diabetes insipidus, which is a lack of ADH due to posterior pituitary dysfunction, can lead to lack of adequate reabsorption of water into the bloodstream at the level of the nephron. o This leads to inadequate water volume in the bloodstream which leads to hypernatremia if the patient does not respond to thirst, or if fluids are excessively restricted.  Less common causes of hypernatremia are heatstroke, nonfatal drowning in seawater (which contains a sodium concentration of approximately 500 mEq/L), and malfunction of hemodialysis or peritoneal dialysis systems.  IV administration of hypertonic saline or excessive use of sodium bicarbonate also causes hypernatremia.  Exertional dysnatremia can occur in performance athletes.

Clinical Manifestations

 The clinical manifestations of hypernatremia are due to increased plasma osmolality caused by an increase in plasma sodium concentration.  Water moves out of the cell into the ECF, resulting in cellular dehydration.  Dehydration (resulting in hypernatremia) is often overlooked as the cause of mental status and behavioral changes in older patients.  Body temperature may increase mildly, but it returns to normal after the hypernatremia is corrected.

 A primary characteristic of hypernatremia is thirst. o Thirst is a strong defender of normal serum sodium levels in healthy people. o Because of thirst, hypernatremia does not occur unless the person is unconscious or cannot access water. o However, those who are ill and older adults may have an impaired thirst mechanism.

Assessment & Diagnostic Findings

 In hypernatremia, the serum sodium level exceeds 145 mEq/L (145 mmol/L) and the serum osmolality exceeds 300 mOsm/kg (300 mmol/L).  The urine specific gravity and urine osmolality are increased as the kidneys attempt to conserve water (provided the water loss is from a route other than the kidneys).  Patients with diabetes insipidus do not reabsorb water into the bloodstream at the nephron. o These patients consequently develop excess urine output, dehydration, and hypernatremia. o Without ADH, these patients excrete very dilute urine with a urine osmolality less than 250 mOsm/kg.

Medical Management

 Treatment of hypernatremia consists of a gradual lowering of the serum sodium level by the infusion of a hypotonic solution (e.g., 0.45% sodium chloride) or an isotonic nonsaline solution (e.g., dextrose 5% in water [D5W]). o D5W can be used when water needs to be replaced without sodium. o However, hypotonic sodium chloride solution (0.45% NaCl) is thought to be safer than D5W because it allows a gradual reduction in the serum sodium level.  Gradual reduction in serum sodium decreases the risk of cerebral edema.  Hypotonic sodium chloride solution (0.45% NaCl) is the IV solution of choice in severe hyperglycemia with hypernatremia.  A rapid reduction in the serum sodium level that occurs with D5W temporarily decreases the plasma osmolality below that of the fluid in the brain tissue, causing dangerous cerebral edema.  Alternatively in hypernatremia, diuretics can be prescribed to treat the excess sodium.  There is no consensus about the exact rate at which serum sodium levels should be reduced. o As a general rule, the serum sodium level is reduced at a rate no faster than 0.5 to 1 mEq/L/h to allow sufficient time for readjustment through diffusion across fluid compartments.  Desmopressin acetate, a synthetic ADH, may be prescribed to treat diabetes insipidus if it is the cause of hypernatremia.

Nursing Management

 Fluid losses and gains are carefully monitored in patients who are at risk for hypernatremia.  The nurse should assess for abnormal losses of water or low water intake and for large gains of sodium, as might occur with ingestion of OTC medications that have a high sodium content (e.g., Alka-Seltzer).  In addition, the nurse obtains a medication history, because some prescription medications have a high sodium content.  The nurse also notes the patient’s thirst or elevated body temperature and evaluates it in relation to other clinical signs and symptoms.  The patient is monitored closely for changes in behavior, such as restlessness, disorientation, and lethargy.

Preventing Hypernatremia

 The nurse attempts to prevent hypernatremia by providing oral fluids at regular intervals, particularly in patients who are unable to perceive or respond to thirst.  If fluid intake remains inadequate or the patient is unconscious, the nurse consults with the primary provider to plan an alternative route for intake, either by enteral feedings or by the parenteral route.  If enteral feedings are used, sufficient water should be given to keep the serum sodium and BUN within normal limits. o As a rule, the higher the osmolality of the enteral feeding, the greater is the need for water supplementation. o Some herbal medications can also increase serum sodium levels.  For patients with diabetes insipidus, adequate water intake must be ensured.  If the patient is alert and has an intact thirst mechanism, merely providing access to water may be sufficient.  If the patient has a decreased level of consciousness or other disability interfering with adequate fluid intake, parenteral fluid replacement may be prescribed.

o This therapy can be anticipated in patients with neurologic disorders, particularly in the early postoperative period.

Correcting Hypernatremia

 When parenteral fluids are necessary for managing hypernatremia, the nurse monitors the patient’s response to the infusion of fluids by reviewing serial serum sodium levels and by observing for changes in neurologic status, such as confusion, disorientation, and possible decreased level of consciousness.  With a gradual decrease in the serum sodium level, neurologic status should improve. o However, too rapid reduction in the serum sodium level renders the plasma temporarily hypoosmotic compared to the intracellular fluid within the brain cells. o This can cause fluid in the plasma to shift into the brain cells which can produce the dangerous state of cerebral edema. Potassium Imbalances  Potassium (K+) is the major intracellular electrolyte; in fact, 98% of the body’s potassium is inside the cells.  The remaining 2% is in the ECF and is important to neuromuscular and cardiac function.  Potassium influences both skeletal and cardiac muscle activity. o For example, alterations in K+ concentration can change myocardial irritability and rhythm.  Under the influence of the sodium–potassium pump, potassium is constantly being pumped into the cells.  The normal serum potassium concentration ranges from 3.5 to 5 mEq/L (3.5 to 5 mmol/L), and even minor variations are significant.  Potassium imbalances are commonly associated with various diseases, injuries, medications (e.g., NSAIDs and ACE inhibitors), and acid–base imbalances.  The two types of potassium imbalances are potassium deficit and potassium excess.  To maintain potassium balance, the renal system must function, because 80% of the potassium excreted daily leaves the body by way of the kidneys; the other 20% is lost through the bowel and in sweat. o The kidneys regulate potassium balance by adjusting the amount of potassium that is excreted in the urine. o As serum potassium levels increase, so does the potassium level in the renal tubular cell.

o A concentration gradient occurs, favoring the movement of potassium into the renal tubule and excretion of potassium in the urine. o Aldosterone also increases the excretion of potassium by the kidney. o Because the kidneys do not conserve potassium as well as they conserve sodium, potassium may still be lost in urine in the presence of a potassium deficit.

Hypokalemia – Sodium Deficit

 Hypokalemia (serum potassium level below 3.5 mEq/L [3.5 mmol/L]) usually indicates a deficit in total potassium stores.  However, it may occur in patients with normal potassium stores: When alkalosis (high blood pH) is present, a temporary shift of serum potassium into the cells occurs.

Pathophysiology

 Potassium-losing diuretics, such as the thiazides and loop diuretics, can induce hypokalemia. o Other medications that can lead to hypokalemia include corticosteroids, sodium penicillin, and amphotericin B.  GI loss of potassium is another common cause of potassium depletion. o Vomiting and gastric suction frequently lead to hypokalemia, because potassium is lost when gastric fluid is lost and because potassium is lost through the kidneys in response to metabolic alkalosis. o Because relatively large amounts of potassium are contained in intestinal fluids, potassium deficit occurs frequently with diarrhea, which may contain as much potassium as 30 mEq/L. o Potassium deficit also occurs from prolonged intestinal suctioning, recent ileostomy, and villous adenoma (a tumor of the intestinal tract characterized by excretion of potassium-rich mucus).  Alterations in acid–base balance have a significant effect on potassium distribution due to shifts of hydrogen and potassium ions between the cells and the ECF. o Respiratory or metabolic alkalosis promotes the transcellular shift of potassium and can have a variable and unpredictable effect on serum potassium.  For example, hydrogen ions move out of the cells into the bloodstream in alkalotic states to help correct the high pH, and potassium ions move into the cells to maintain an electrically neutral state.  Aldosterone from the adrenal gland acts on the nephron to increase sodium and water reabsorption into the bloodstream. o It simultaneously secretes potassium into the renal tubules which in turn is excreted in the urine. o In hyperaldosteronism, potassium is constantly secreted into the nephron tubule fluid which leads to loss of potassium into the urine. o Hyperaldosteronism causes renal potassium wasting and can lead to severe potassium depletion. o Primary hyperaldosteronism is seen in patients with adrenal adenomas (tumors). o Secondary hyperaldosteronism occurs in patients with cirrhosis, nephrotic syndrome, heart failure, or malignant hypertension.  Insulin promotes the entry of potassium into cells from the bloodstream; therefore, patients with persistent insulin hypersecretion may experience hypokalemia. o Patients receiving high carbohydrate parenteral nutrition will have increased secretion of insulin. o This will cause the shift of potassium into the cells from the bloodstream, causing hypokalemia. o In diabetic ketoacidosis (DKA), potassium moves out of the cell since H+ ions are high; during this acute phase it seems as though the patient has hyperkalemia. o With insulin treatment of DKA, potassium moves back into the cells, causing hypokalemia.  Patients who are not able to eat a normal diet for a prolonged period are at risk for hypokalemia. o This may occur in debilitated older adults and in patients with alcoholism or anorexia nervosa. o In addition to poor intake, people with bulimia frequently experience increased potassium loss through self- induced vomiting and overuse of laxatives, diuretics, and enemas. o These patients may also be deficient in magnesium. o Magnesium depletion also causes renal potassium loss and must be corrected first; otherwise, urine loss of potassium will continue.

Clinical Manifestations

 Potassium deficiency can result in widespread derangements in physiologic function.

 Severe hypokalemia can cause death through cardiac or respiratory arrest.  Clinical signs develop when the potassium level decreases to less than 3 mEq/L (3 mmol/L).  If prolonged, hypokalemia can lead to an inability of the kidneys to concentrate urine, causing dilute urine (resulting in polyuria, nocturia) and excessive thirst.  Potassium depletion suppresses the release of insulin and results in glucose intolerance.

Assessment & Diagnostic Findings

 In hypokalemia, the serum potassium concentration is less than the lower limit of normal, which is 3.5 mEq/L.  Electrocardiographic (ECG) changes can include flat T waves or inverted T waves or both, suggesting ischemia, and depressed ST segments. o An elevated U wave is specific to hypokalemia.  Metabolic alkalosis is commonly associated with hypokalemia.  The source of the potassium loss is usually evident from a careful history. o However, if the cause of the loss is unclear, a 24-hour urinary potassium excretion test can be performed to distinguish between renal and extrarenal loss. o Urinary potassium excretion exceeding 20 mEq/day with hypokalemia suggests that renal potassium loss is the cause.

Medical Management

 If hypokalemia cannot be prevented by conventional measures such as increased intake in the daily diet or by oral potassium supplements for deficiencies, then it is treated cautiously with IV replacement therapy.  Potassium loss must be corrected daily; administration of 40 to 60 mEq/day of potassium is adequate in the adult if there are no abnormal losses of potassium.  For patients who are at risk for hypokalemia, a diet containing sufficient potassium should be provided. o Dietary intake of potassium in the average adult is 50 to 100 mEq/day. o Foods high in potassium include most fruits and vegetables, legumes, whole grains, milk, and meat.  When dietary intake is inadequate for any reason, oral or IV potassium supplements may be prescribed. o Many salt substitutes contain 50 to 60 mEq of potassium per teaspoon and may be sufficient to prevent hypokalemia. o If oral administration of potassium is not feasible, the IV route is indicated.  The IV route is mandatory for patients with severe hypokalemia (e.g., serum level of 2 mEq/L).  Although potassium chloride (KCl) is usually used to correct potassium deficits, potassium acetate or potassium phosphate may be prescribed.

Nursing Management

 Because hypokalemia can be life-threatening, the nurse needs to monitor for its early presence in patients at risk.  Fatigue, anorexia, muscle weakness, decreased bowel motility, paresthesias, and arrhythmias are signals that warrant assessing the serum potassium concentration.  When available, the ECG may provide useful information. o For example, patients receiving digitalis who are at risk for potassium deficiency should be monitored closely for signs of digitalis toxicity, because hypokalemia potentiates the action of digitalis.

Preventing Hypokalemia

 The nurse helps prevent hypokalemia by encouraging patients at risk to eat foods rich in potassium (when the diet allows).  Consumption of foods high in potassium should be encouraged; examples include bananas, melon, citrus fruits, fresh and frozen vegetables (avoid canned vegetables), lean meats, milk, and whole grains.  If the hypokalemia is caused by abuse of laxatives or diuretics, patient education may help alleviate the problem.  Part of the health history and assessment should be directed at identifying problems that are amenable to prevention through education.  Careful monitoring of fluid I&O is necessary, because 40 mEq of potassium is lost for every liter of urine output.  The ECG is monitored for changes, and arterial blood gas (ABG) values are checked for elevated bicarbonate and pH levels.

Correcting Hypokalemia

 The oral route is ideal to treat mild to moderate hypokalemia because oral potassium supplements are well absorbed.  Care should be exercised when administering potassium, particularly in older adults, who have lower lean body mass and total-body potassium levels and therefore lower potassium requirements.  In addition, because of the physiologic loss of renal function with advancing years, potassium may be retained more readily in older than in younger people.

Administering Intravenous Potassium

 Potassium should be given only after adequate urine output has been established. o A decrease in urine volume to less than 20 mL/h for 2 consecutive hours is an indication to stop the potassium infusion and notify the primary provider. o Potassium is primarily excreted by the kidneys; when oliguria occurs, potassium administration can cause the serum potassium concentration to rise to dangerous levels.  Administration of IV potassium is done with extreme caution using an infusion pump with the patient monitored by continuous ECG. o Caution must be used when selecting a premixed solution of IV fluid containing KCl, as the concentrations range from 10 to 40 mEq/100 mL. o Renal function should be monitored through BUN and serum creatinine levels and urine output if the patient is receiving potassium replacement. o During replacement therapy, the patient should be monitored for signs of worsening hypokalemia as well as hyperkalemia. Hyperkalemia – Potassium Excess  Hyperkalemia (serum potassium level greater than 5 mEq/L [5 mmol/L]) seldom occurs in patients with normal renal function.  In older adults, there is an increased risk of hyperkalemia due to decreases in renin and aldosterone as well as an increased number of comorbid cardiac conditions.  Like hypokalemia, hyperkalemia is often caused by iatrogenic (treatment-induced) causes.  Although hyperkalemia is less common than hypokalemia, it is usually more dangerous because cardiac arrest is more frequently associated with high serum potassium levels.

Pathophysiology

 Major causes of hyperkalemia are decreased renal excretion of potassium, rapid administration of potassium, and movement of potassium from the ICF compartment to the ECF compartment.  Hyperkalemia is commonly seen in patients with untreated kidney injury, particularly those in whom potassium levels increase as a result of infection or excessive intake of potassium in food or medications.  Patients with hypoaldosteronism or Addison disease are at risk for hyperkalemia because of a lack of aldosterone. o Lack of aldosterone activity at the nephron causes inadequate sodium and water reabsorption into the bloodstream and inadequate excretion of potassium in the urine. o Therefore, deficient adrenal hormones lead to sodium loss and potassium retention.  Medications have been identified as a probable contributing factor in more than 60% of hyperkalemic episodes. o Medications commonly implicated are KCl, heparin, ACE inhibitors, NSAIDs, beta-blockers, cyclosporine, tacrolimus, and potassium-sparing diuretics. o Potassium regulation is compromised in acute and chronic kidney disease, with a glomerular filtration rate less than 10% to 20% of normal.  Improper use of potassium supplements predisposes all patients to hyperkalemia, especially if salt substitutes are used. o Not all patients receiving potassium-losing diuretics require potassium supplements, and patients receiving potassium-conserving diuretics should not receive supplements.  In acidosis, (low blood pH), potassium moves out of the cells and into the ECF. o This occurs as hydrogen ions enter the cells to buffer the pH of the ECF.  An elevated ECF potassium level should be anticipated when extensive tissue trauma has occurred, as in burns, crushing injuries, or severe infections. o Similarly, it can occur with lysis of malignant cells after chemotherapy (i.e., tumor lysis syndrome).

o Any disorder that causes high amounts of cellular lysis or deterioration can cause hyperkalemia.  Pseudohyperkalemia (a false hyperkalemia) has several causes, including the improper collection or transport of a blood sample, a traumatic venipuncture, and use of a tight tourniquet around an exercising extremity while drawing a blood sample, producing hemolysis of the sample before analysis. o Other causes include marked leukocytosis (white blood cell count exceeding 200,000/mm3) and thrombocytosis (platelet count exceeding 1 million/mm3); drawing blood above a site where potassium is infusing; and familial pseudohyperkalemia, in which potassium leaks out of the RBCs while the blood is awaiting analysis. o Lack of awareness of these causes of pseudohyperkalemia can lead to aggressive treatment of a nonexistent hyperkalemia, resulting in serious lowering of serum potassium levels. o Therefore, measurements of grossly elevated levels of potassium in the absence of clinical manifestations (e.g., normal ECG) should be verified by retesting.

Clinical Manifestations

 The most important consequence of hyperkalemia is its effect on the myocardium. o Cardiac effects of elevated serum potassium are usually not significant when the level is less than 7 mEq/L ( mmol/L); however, they are almost always present when the level is 8 mEq/L (8 mmol/L) or greater. o As the plasma potassium level rises, disturbances in cardiac conduction occur. o The earliest changes, often occurring at a serum potassium level greater than 6 mEq/L (6 mmol/L), are peaked, narrow T waves; ST-segment depression; and a shortened QT interval. o If the serum potassium level continues to increase, the PR interval becomes prolonged and is followed by disappearance of the P waves.  Finally, there is decomposition and widening of the QRS complex.  Ventricular arrhythmias and cardiac arrest may occur.

Assessment & Diagnostic Findings

 Serum potassium levels and ECG changes are crucial to the diagnosis of hyperkalemia.  Analysis may reveal either a metabolic or a respiratory acidosis. o Correcting the acidosis helps correct the hyperkalemia.

Medical Management

 In disorders involving potassium level changes, an ECG should be obtained immediately. o Shortened repolarization and peaked T waves are seen initially in hyperkalemia. o To verify results, a repeat serum potassium level should be obtained from a vein that is not concomitantly infusing an IV solution containing potassium.  In nonacute situations, restriction of dietary potassium and potassium-containing medications may correct the imbalance. o For example, eliminating the use of potassium-containing salt substitutes in a patient who is taking a potassium-conserving diuretic may be all that is needed to deal with mild hyperkalemia.  Administration, either orally or by retention enema, of cation exchange resins (e.g., sodium polystyrene sulfonate) may be necessary. o The use of cation exchange resins requires normal bowel function.  For instance, cation exchange resins cannot be used if the patient has a paralytic ileus (i.e., absence of peristalsis in the intestine), because intestinal perforation can occur. o Sodium polystyrene sulfonate binds with potassium and then is eliminated in the feces. o Other cations in the GI tract can also be depleted which can cause hypomagnesemia and hypocalcemia. o Sodium polystyrene sulfonate may also cause sodium retention and fluid overload and should be used with caution in patients with heart failure.  Patiromer sorbitex calcium is another oral agent that is a potassium-removing resin used to treat hyperkalemia. o It exchanges calcium for potassium in the lower intestine, thereby increasing fecal excretion of potassium. o Side effects include GI intolerance, hypomagnesemia, and edema.

Emergency Pharmacologic Therapy

 If serum potassium levels are dangerously elevated, it may be necessary to administer IV calcium gluconate. o Within minutes after administration, calcium antagonizes the action of hyperkalemia on the heart but does not reduce the serum potassium concentration. o Calcium chloride and calcium gluconate are not interchangeable; calcium gluconate contains 4.5 mEq of calcium, and calcium chloride contains 13.6 mEq of calcium. o Therefore, caution is required when using calcium preparations to reduce potassium levels.  Monitoring the blood pressure is essential to detect hypotension, which may result from the rapid IV administration of calcium gluconate. o The ECG should be continuously monitored during administration; the appearance of bradycardia is an indication to stop the infusion. o The myocardial protective effects of calcium last about 30 minutes. o Extra caution is required if the patient has received an accelerated dose of a digitalis-based cardiac glycoside to reach a desired serum digitalis level rapidly as parenteral administration of calcium sensitizes the heart to digitalis and may precipitate digitalis toxicity.  IV administration of sodium bicarbonate may be necessary in severe metabolic acidosis to alkalinize the plasma, shift potassium into the cells, and furnish sodium to antagonize the cardiac effects of potassium. o Effects of this therapy begin within 30 to 60 minutes and may persist for hours; however, they are temporary. o Circulatory overload and hypernatremia can occur when large amounts of hypertonic sodium bicarbonate are given. o Bicarbonate therapy should be guided by the bicarbonate concentration or calculated base deficit obtained from blood gas analysis or laboratory measurement.  IV administration of regular insulin and a hypertonic dextrose solution causes a temporary shift of potassium into the cells. o Glucose and insulin therapy have an onset of action within 30 minutes and lasts for several hours. o Loop diuretics, such as furosemide, increase excretion of water by inhibiting sodium, potassium, and chloride reabsorption in the ascending loop of Henle and distal renal tubule.  Beta-2 agonists, such as albuterol, are highly effective in decreasing potassium; however, their use is not without risk as they can cause tachycardia and chest discomfort. o Beta-2 agonists, administered intravenously or via nebulizer, move potassium into the cells and may be used in the absence of ischemic cardiac disease. o Their use is a stopgap measure that only temporarily protects the patient from hyperkalemia.  If the hyperkalemic condition is not transient, removal of potassium from the body can also be done through peritoneal dialysis, hemodialysis, or other forms of renal replacement therapy.

Nursing Management

 Patients at risk for potassium excess (e.g., those with kidney disease) need to be identified and closely monitored for signs of hyperkalemia.  The nurse monitors I&O and observes for signs of muscle weakness and arrhythmias.  When measuring vital signs, an apical pulse should be taken.  The presence of paresthesias and GI symptoms such as nausea and intestinal cramping should be noted.  Serum potassium levels, as well as BUN, serum creatinine, serum glucose, and ABG values, should be monitored for patients at risk for developing hyperkalemia.

Preventing Hyperkalemia

 Measures should be taken to prevent hyperkalemia in patients at risk, when possible, by encouraging the patient to adhere to the prescribed potassium restriction.  Potassium-rich foods to be avoided include many fruits and vegetables, legumes, whole-grain breads, lean meat, milk, eggs, coffee, tea, and cocoa.  Conversely, foods with minimal potassium content include butter, margarine, cranberry juice or sauce, ginger ale, gumdrops or jellybeans, hard candy, root beer, sugar, and honey.  Labels of cola beverages must be checked carefully because some are high in potassium, and some are not.

Correcting Hyperkalemia

 It is possible to exceed the tolerance for potassium if given rapidly by the IV route. o Therefore, careful monitoring is necessary when administering potassium solutions.

o Particular attention is paid to the solution’s concentration and rate of administration. IV administration should only be via an infusion pump.  The nurse must caution patients to use salt substitutes sparingly if they are taking other supplementary forms of potassium or potassium-conserving diuretics. o In addition, potassium-conserving diuretics, potassium supplements, and salt substitutes should not be given to patients with kidney injury. Calcium Imbalances  More than 99% of the body’s calcium (Ca++) is located in the skeletal system; it is a major component of bones and teeth.  About 1% of skeletal calcium is rapidly exchangeable with blood calcium, and the rest is more stable and only slowly exchanged.  The small amount of calcium located outside the bone circulates in the serum, partly bound to protein and partly ionized.  Calcium plays a major role in transmitting nerve impulses and helps regulate muscle contraction and relaxation, including cardiac muscle.  Calcium is instrumental in activating enzymes that stimulate many essential chemical reactions in the body, and it also plays a role in blood coagulation.  Because many factors affect calcium regulation, both hypocalcemia and hypercalcemia are relatively common disturbances.  The normal adult total serum calcium level is 8.8 to 10.4 mg/dL (2.2 to 2.6 mmol/L).  Calcium exists in plasma in three forms: ionized, bound, and complex.  Approximately 50% of the serum calcium exists in a physiologically active ionized form that is important for neuromuscular activity and blood coagulation; this is the only physiologically and clinically significant form.  The normal ionized serum calcium level is 4.5 to 5.1 mg/dL (1.1 to 1.3 mmol/L).  Less than half of the plasma calcium is bound to serum proteins, primarily albumin. o The remainder is combined with nonprotein anions: phosphate, citrate, and carbonate.  Calcium is absorbed from foods in the presence of normal gastric acidity and vitamin D.  It is excreted primarily in the feces, with the remainder excreted in the urine.  The serum calcium level is controlled by PTH and calcitonin.  As ionized serum calcium decreases in the bloodstream, the parathyroid glands secrete PTH. o This, in turn, increases calcium absorption from the GI tract, increases calcium reabsorption from the renal tubule, and releases calcium from the bone. o The resultant increase in calcium ion concentration in the bloodstream then suppresses PTH secretion.  When calcium increases excessively, the thyroid gland secretes calcitonin, which inhibits calcium reabsorption from bone and decreases the serum calcium concentration.

Hypocalcemia – Calcium Deficit  Hypocalcemia (serum calcium value lower than 8.8 mg/dL [2.20 mmol/L]) occurs in a variety of clinical situations.  A patient may have a total-body calcium deficit (as in osteoporosis) but a normal serum calcium level.  Older adults and those with disability have an increased risk of hypocalcemia because immobility, particularly lack of weight-bearing activity, increases bone resorption.

Pathophysiology

 The parathyroid glands are instrumental in regulating blood and body calcium levels. o Several factors can cause hypocalcemia, including primary hypoparathyroidism and surgical hypoparathyroidism. o Surgical hypoparathyroidism is more common as a result of unintentional trauma or devascularization of the parathyroid glands. o Not only is hypocalcemia associated with thyroid and parathyroid surgery, but it can also occur after radical neck dissection and is most likely in the first 24 to 48 hours after surgery. o Transient hypocalcemia can occur with massive administration of citrated blood (i.e., massive hemorrhage and shock), because citrate can combine with ionized calcium and temporarily remove it from the circulation.  Inflammation of the pancreas causes the breakdown of proteins and lipids. o It is thought that calcium ions combine with the fatty acids released by lipolysis, forming soap-like compounds. o As a result of this process, hypocalcemia occurs and is common in pancreatitis. o Hypocalcemia may also be related to excessive secretion of glucagon from the inflamed pancreas, which results in increased secretion of calcitonin from the thyroid gland.  Hypocalcemia is common in patients with acute kidney injury because these patients frequently have elevated serum phosphate levels. o Hyperphosphatemia usually causes a reciprocal drop in the serum calcium level. o Other causes of hypocalcemia include inadequate vitamin D consumption, magnesium deficiency, medullary thyroid carcinoma, low serum albumin levels, alkalosis, and alcohol abuse. o Medications predisposing to hypocalcemia include aluminum-containing antacids, aminoglycosides, caffeine, cisplatin, corticosteroids, mithramycin, phosphates, isoniazid, loop diuretics, and proton pump inhibitors.

Clinical Manifestations

 Tetany, the most characteristic manifestation of hypocalcemia and hypomagnesemia, refers to the entire symptom complex induced by increased neural excitability.  Clinical signs and symptoms are caused by spontaneous discharges of both sensory and motor fibers in peripheral nerves.  Chvostek sign consists of twitching of muscles innervated by the facial nerve in response to tapping of the muscle just below the zygomatic arch.  Trousseau sign can be elicited by inflating a blood pressure cuff on the upper arm to about 20 mm Hg above systolic pressure; within 2 to 5 minutes, carpal spasm will occur as ischemia of the ulnar nerve develops.  Hypocalcemia can cause seizures because low calcium levels increase irritability of the central and peripheral nervous systems.  Other changes associated with hypocalcemia include mental changes such as depression, impaired memory, confusion, delirium, and hallucinations.  A prolonged QT interval is seen on the ECG due to prolongation of the ST segment, and torsades de pointes, a type of ventricular tachycardia, may occur.  Respiratory effects with decreasing calcium include dyspnea and laryngospasm.  Signs and symptoms of chronic hypocalcemia include hyperactive bowel sounds, dry and brittle hair and nails, and abnormal clotting.  Osteoporosis is associated with prolonged low intake of calcium and represents a total-body calcium deficit, even though serum calcium levels are usually normal. o This disorder occurs in millions of Americans and is most common in postmenopausal women. o It is characterized by loss of bone mass, which causes bones to become porous and brittle and therefore susceptible to fracture.

Assessment & Diagnostic Findings

 When evaluating serum calcium levels, the serum albumin level and the arterial pH must also be considered. o Because abnormalities in serum albumin levels may affect interpretation of the serum calcium level, it may be necessary to calculate the corrected serum calcium if the serum albumin level is abnormal. o For every decrease in serum albumin of 1 g/dL below 4 g/dL, the total serum calcium level is underestimated by approximately 0.8 mg/dL.  Clinicians often discount a low serum calcium level in the presence of a similarly low serum albumin level. o The ionized calcium level is usually normal in patients with reduced total serum calcium levels and concomitant hypoalbuminemia. o When the arterial pH increases (alkalosis), more calcium becomes bound to protein. o As a result, the ionized portion decreases.  Symptoms of hypocalcemia may occur with alkalosis. o Acidosis has the opposite effect—that is, less calcium is bound to protein and therefore more exists in the ionized form. o However, relatively small changes in serum calcium levels occur in these acid–base abnormalities.  Ideally, the ionized level of calcium should be measured in the laboratory. o However, in many laboratories, only the total calcium level is reported; therefore, the concentration of the ionized fraction must be estimated by simultaneous measurement of the serum albumin level. o Magnesium and phosphorus levels need to be assessed to identify possible causes of decreased calcium.

Medical Management

 Acute symptomatic hypocalcemia is life-threatening and requires prompt treatment with IV administration of a calcium salt. o Parenteral calcium salts include calcium gluconate and calcium chloride. o Although calcium chloride produces a significantly higher ionized calcium level than calcium gluconate does, it is not used as often because it is more irritating and can cause sloughing of tissue if it infiltrates.  IV administration of calcium is particularly dangerous in patients receiving digitalis-derived medications, because calcium ions exert an effect similar to that of digitalis and can cause digitalis toxicity, with adverse cardiac effects. o The IV site that delivers calcium must be observed often for any evidence of infiltration because of the risk of extravasation and resultant cellulitis or necrosis. o A 0.9% sodium chloride solution should not be used with calcium because it increases renal calcium loss. o Solutions containing phosphates or bicarbonate should not be used with calcium because they cause precipitation when calcium is added. o The nurse must clarify with the primary provider and pharmacist which calcium salt to administer, because calcium gluconate yields 4.5 mEq of calcium and calcium chloride provides 13.6 mEq of calcium. o Calcium replacement can cause orthostatic hypotension; therefore, the patient should remain in bed during IV infusion, and blood pressure is monitored.

Nutritional Therapy

 Vitamin D therapy may be instituted to increase calcium absorption from the GI tract; otherwise, the amount of calcium absorbed may not satisfy the body’s calcium requirement. o In addition, aluminum hydroxide, calcium acetate, or calcium carbonate antacids may be prescribed to decrease elevated phosphorus levels before treating hypocalcemia in the patient with chronic kidney disease.  Increasing the dietary intake of calcium to at least 1000 to 1500 mg/day in the adult is recommended.  Calcium supplements must be given in divided doses of no higher than 500 mg to promote calcium absorption.  Calcium-containing foods include milk products; green, leafy vegetables; canned salmon; canned sardines; and fresh oysters.  Hypomagnesemia can also cause tetany; if the tetany responds to IV calcium, then a low magnesium level is considered as a possible cause in chronic kidney dysfunction.

Nursing Management

 It is important to assess for hypocalcemia in at-risk patients.  Seizure precautions are initiated if hypocalcemia is severe.

 The status of the airway is closely monitored because laryngospasm can occur.  Safety precautions are taken, as indicated, if confusion is present.  The nurse must educate the patient with hypocalcemia about foods that are rich in calcium. o The nurse must also advise the patient to consider calcium supplements if sufficient calcium is not consumed in the diet. o Such supplements should be taken in divided doses with meals.  Alcohol and caffeine in high doses inhibit calcium absorption, and moderate cigarette smoking increases urinary calcium excretion.  The patient is also cautioned to avoid the overuse of laxatives and antacids that contain phosphorus, because their use decreases calcium absorption. Hypercalcemia – Calcium Excess  Hypercalcemia (serum calcium value greater than 10.4 mg/dL [2.6 mmol/L]) can affect many organ systems.  Symptoms depend on the degree of hypercalcemia and the rate of rise of calcium in the bloodstream.  Mild hypercalcemia usually causes no apparent symptoms if the rise in calcium level is chronic over a long period of time.  Moderate hypercalcemia can also be well tolerated.  Marked symptoms occur when rise in calcium level is acute.

Pathophysiology

 The most common causes of hypercalcemia are malignancies and hyperparathyroidism. o Malignant tumors can produce hypercalcemia by various mechanisms.  The most common malignancies that are associated with hypercalcemia are breast, lung, renal, and multiple myeloma. o In hyperparathyroidism, excessive PTH secretion causes increased release of calcium from the bones and increased intestinal and renal absorption of calcium.  Calcifications of soft tissue occur when the calcium–phosphorus product (serum calcium × serum phosphorus) exceeds 70 mg/dL.  Calcium levels are inversely related to phosphorus levels.  Bone calcium is lost during immobilization, and sometimes this causes elevation of total (and especially ionized) calcium in the bloodstream. o However, symptomatic hypercalcemia from immobilization is rare; when it does occur, it is limited to people with high calcium turnover rates (e.g., adolescents during a growth spurt). o Most cases of hypercalcemia secondary to immobility occur after severe or multiple fractures or spinal cord injury.  Thiazide diuretics can cause a slight elevation in serum calcium levels because they potentiate the action of PTH on the kidneys, reducing urinary calcium excretion.  Vitamin A and D intoxication, as well as chronic lithium use and theophylline toxicity, can cause calcium excess.  Hypercalcemia reduces neuromuscular excitability because it suppresses activity at the myoneural junction. o Decreased tone in smooth and striated muscle may cause symptoms such as muscle weakness, incoordination, anorexia, and constipation. o Lethal arrhythmias (e.g., ventricular fibrillation) can occur when the serum calcium level is about 18 mg/dL (4.5 mmol/L). o Calcium enhances the inotropic effect of digitalis; therefore, hypercalcemia aggravates digitalis toxicity.

Clinical Manifestations

 The symptoms of hypercalcemia are proportional to the degree of elevation of the serum calcium level. o The more severe symptoms tend to appear when the serum calcium level climbs rapidly and may be as high as 16 mg/dL (4 mmol/L) or higher. o However, some patients become profoundly disturbed with serum calcium levels of only 12 mg/dL ( mmol/L). o These symptoms resolve as serum calcium levels return to normal after treatment.  Hypercalcemic crisis refers to an acute rise in the serum calcium level. o Severe thirst and polyuria are often present.

o Other findings may include muscle weakness, intractable nausea, abdominal cramps, severe constipation, diarrhea, peptic ulcer symptoms, and bone pain. o Lethargy, confusion, and coma may also occur. o This condition is dangerous and may result in cardiac arrest. o Emergency treatment with calcitonin is indicated.

Assessment & Diagnostic Findings

 In hypercalcemia, the serum calcium level is greater than 10.4 mg/dL (2.6 mmol/L).  Cardiovascular changes may include a variety of arrhythmias (e.g., heart blocks) and shortening of the QT interval and ST segment. o The PR interval is sometimes prolonged.  The double-antibody PTH test may be used to differentiate between primary hyperparathyroidism and malignancy as a cause of hypercalcemia: PTH levels are increased in primary or secondary hyperparathyroidism and suppressed in malignancy.  X-rays may reveal bone changes if the patient has hypercalcemia secondary to a malignancy, bone cavitations, or urinary calculi.  Urine calcium can be normal or elevated in hyperparathyroidism and hypercalcemia caused by malignancy.

Medical Management

 Therapeutic aims include decreasing the serum calcium level and reversing the process causing the hypercalcemia.  Treating the underlying cause (e.g., chemotherapy for a malignancy, partial parathyroidectomy for hyperparathyroidism) is essential.

Pharmacologic Therapy

 To treat hypercalcemia, measures include administering fluids to dilute serum calcium and promote its excretion by the kidneys, mobilizing the patient, and restricting dietary calcium intake. o IV administration of 0.9% sodium chloride solution temporarily dilutes the serum calcium level and increases urinary calcium excretion by inhibiting tubular reabsorption of calcium. o Administering IV phosphate can cause a reciprocal drop in serum calcium. o Furosemide is often used in conjunction with administration of a saline solution; in addition to causing diuresis, furosemide increases calcium excretion. o Although often overlooked, fluids and medications that contain calcium and dietary sources of calcium should be halted.  Calcitonin can be used to lower the serum calcium level and is particularly useful for patients with heart disease or acute kidney injury who cannot tolerate large sodium loads. o Calcitonin reduces bone resorption, increases the deposition of calcium and phosphorus in the bones, and increases urinary excretion of calcium and phosphorus. o Although several forms are available, calcitonin derived from salmon is commonly used. o Skin testing for allergy to salmon calcitonin may be necessary before the hormone is given. o Systemic allergic reactions are possible because this hormone is a protein; resistance to the medication may develop later because of antibody formation. o Calcitonin is administered by intramuscular injection or intranasal spray rather than subcutaneously, because patients with hypercalcemia have poor perfusion of subcutaneous tissue.  For patients with cancer, treatment is directed at controlling the condition by surgery, chemotherapy, or radiation therapy. o Corticosteroids may be used to decrease bone turnover and tubular reabsorption for patients with sarcoidosis, myelomas, lymphomas, and leukemias; patients with solid tumors are less responsive. o Some bisphosphonates (e.g., pamidronate disodium, ibandronate sodium) inhibit osteoclast activity. IV forms of bisphosphonates can cause fever, transient leukopenia, eye inflammation, nephrotic syndrome, and jaw osteonecrosis.  Mithramycin, a cytotoxic antibiotic, inhibits bone resorption and thus lowers the serum calcium level. o This agent must be used cautiously because it has significant side effects, including thrombocytopenia, nephrotoxicity, rebound hypercalcemia when discontinued, and hepatotoxicity.

o Inorganic phosphate salts can be given orally or by nasogastric tube (in the form of Phospho-Soda or Neutra- Phos), rectally (as retention enemas), or IV. o IV phosphate therapy is used with extreme caution in the treatment of hypercalcemia, because it can cause severe calcification in various tissues, hypotension, tetany, and acute kidney injury.

Nursing Management

 Interventions such as increasing patient mobility and encouraging fluids can help prevent hypercalcemia, or at least minimize its severity.  Hospitalized patients at risk should be encouraged to ambulate as soon as possible.  Those who are outpatients and receive home care are educated about the importance of frequent ambulation.  When encouraging oral fluids, the nurse considers the patient’s likes and dislikes. o Fluids containing sodium should be given unless contraindicated, because sodium assists with calcium excretion. o Patients are encouraged to drink 2.8 to 3.8 L (3 to 4 quarts) of fluid daily. o Adequate fiber in the diet is encouraged to offset the tendency for constipation.  Safety precautions are implemented, as necessary, when altered mental status is present. o The patient and family are informed that these mental changes are reversible with treatment.  Increased calcium increases the effects of digitalis; therefore, the patient on digitalis should be frequently assessed for signs and symptoms of digitalis toxicity.  Because ECG changes (premature ventricular contractions, paroxysmal atrial tachycardia, and heart block) can occur, the cardiac rate and rhythm are monitored for any abnormalities. Magnesium Imbalances  Magnesium (Mg++) is an abundant intracellular cation.  It acts as an activator for many intracellular enzyme systems and plays a role in both carbohydrate and protein metabolism.  The normal serum magnesium level is 1.8 to 2.6 mg/dL (0.74 to 1.07 mmol/L).  Approximately one third of serum magnesium is bound to protein; the remaining two thirds exist as free cations—the active component (Mg++).  Magnesium balance is important in neuromuscular function.  Because magnesium acts directly on the myoneural junction, variations in the serum level affect neuromuscular irritability and contractility. o For example, an excess of magnesium diminishes the excitability of the muscle cells, whereas a deficit increases neuromuscular irritability and contractility.

 Magnesium produces its sedative effect at the neuromuscular junction, probably by inhibiting the release of the neurotransmitter acetylcholine.  It also increases the stimulus threshold in nerve fibers.  Magnesium imbalances are magnesium deficit and magnesium excess.  Magnesium also affects the cardiovascular system, acting peripherally to produce vasodilation and decreased peripheral resistance.  Most magnesium in the body is stored within bone, whereas magnesium ions in the blood are bound to protein, such as albumin, or free as Mg++ ions. Hypomagnesemia – Magnesium Deficit  Hypomagnesemia refers to a below-normal serum magnesium concentration and is frequently associated with hypokalemia and hypocalcemia.  Magnesium is similar to calcium in two aspects: o (1) it is the ionized fraction of magnesium that is primarily involved in neuromuscular activity and other physiologic processes. o (2) magnesium levels should be evaluated in combination with albumin levels.  Because about 30% of magnesium is protein bound, principally to albumin, a decreased serum albumin level can reduce the measured total magnesium concentration; however, it does not reduce the ionized plasma magnesium concentration.  Magnesium is essential for the function of the Na+/K+ pump, and low Mg++ levels have effects on intracellular influxes of K+ and myocardial ion fluxes.

Pathophysiology

 An important route of magnesium loss is the GI tract; such loss can occur with nasogastric suction, diarrhea, or fistulas. o Because fluid from the lower GI tract has a higher concentration of magnesium (10 to 14 mEq/L) than fluid from the upper tract (1 to 2 mEq/L), losses from diarrhea and intestinal fistulas are more likely to induce magnesium deficit than are those from gastric suction. o Although magnesium losses are relatively small in nasogastric suction, hypomagnesemia occurs if losses are prolonged, and magnesium is not replaced through IV infusion. o Because the distal small bowel is the major site of magnesium absorption, any disruption in small bowel function (e.g., intestinal resection or inflammatory bowel disease) can lead to hypomagnesemia. o Hypomagnesemia is a common yet often overlooked imbalance in acutely and critically ill patients.  Studies suggest that up to 65% of patients in intensive care are magnesium deficient. o Hypomagnesemia may occur with withdrawal from alcohol and administration of tube feedings or parenteral nutrition.  Chronic alcohol abuse is a major cause of symptomatic hypomagnesemia in the United States. o The serum magnesium level should be measured at least every 2 or 3 days in patients undergoing withdrawal from alcohol. o The level may be normal on admission but may decrease as a result of metabolic changes, such as the intracellular shift of magnesium associated with IV glucose administration.  During nutritional replacement, the major cellular electrolytes move from the serum to intracellular compartments of newly synthesized cells. o Therefore, if the enteral or parenteral feeding formula is deficient in magnesium content, serious hypomagnesemia can occur. o Because of this, serum magnesium levels should be measured at regular intervals in patients who are receiving parenteral or enteral feedings, especially those who have undergone a period of starvation.  Other causes of hypomagnesemia include the administration of aminoglycosides, cyclosporine, cisplatin, diuretics, digitalis, proton pump inhibitors, and amphotericin, as well as the rapid administration of citrated blood, especially to patients with renal or hepatic disease.  Magnesium deficiency often occurs in DKA, secondary to increased renal excretion during osmotic diuresis and shifting of magnesium into the cells with insulin therapy.  A magnesium IV solution can be used to counteract seizures due to preeclampsia or eclampsia, the cardiac arrhythmia torsades de pointes, asthma, and hypertension.

Clinical Manifestations

 Some clinical manifestations of hypomagnesemia are due directly to the low serum magnesium level; others are due to secondary changes in potassium and calcium metabolism.  Symptoms do not usually occur until the serum magnesium level has dropped to less than 1.8 mEq/L (0.75 mmol/L).  Chvostek and Trousseau signs occur, in part, because of accompanying hypocalcemia.  Hypomagnesemia may be accompanied by marked alterations in psychological status. o Apathy, depressed mood, apprehension, and extreme agitation have been noted, as well as ataxia, dizziness, insomnia, and confusion. o At times, delirium, auditory or visual hallucinations, and frank psychoses may occur.  Magnesium deficiency can disturb the ECG by prolonging the QRS, depressing the ST segment, and predisposing to cardiac arrhythmias, such as premature ventricular contractions, supraventricular tachycardia, torsades de pointes, and ventricular fibrillation.  Increased susceptibility to digitalis toxicity is associated with low serum magnesium levels.  Patients receiving digoxin are also likely to be receiving diuretic therapy, predisposing them to renal loss of magnesium.  Concurrent hypokalemia and hypocalcemia must be addressed in addition to hypomagnesemia. o These electrolyte disturbances are difficult to correct until magnesium has been replenished. o Additionally, hypocalcemia can be worsened by isolated treatment of hypomagnesemia with IV magnesium sulfate because sulfate binds ionized calcium.

Assessment & Diagnostic Findings

 On laboratory analysis, the serum magnesium level is less than 1.8 mg/dL (0.74 mmol/L).  Urine magnesium may help identify the cause of magnesium depletion, and levels are measured after a loading dose of magnesium sulfate is given.  Additional diagnostic techniques (nuclear magnetic resonance spectroscopy and the ion-selective electrode) are sensitive and direct means of measuring ionized serum magnesium levels.

Medical Management

 Mild magnesium deficiency can be corrected by diet alone.  Principal dietary sources of magnesium include green leafy vegetables, beans, lentils, white potatoes, wheat bran, dry roasted almonds, and peanut butter.  If necessary, magnesium salts can be given orally in an oxide or gluconate form to replace continuous losses but can produce diarrhea.  Patients receiving parenteral nutrition require magnesium in the IV solution to prevent hypomagnesemia.  Vital signs must be assessed frequently during magnesium administration to detect changes in cardiac rate or rhythm, hypotension, and respiratory distress.  Monitoring urine output is essential before, during, and after magnesium administration as this is how Mg++ is excreted; the primary provider is notified if urine volume decreases to less than 100 mL over 4 hours.  Calcium gluconate must be readily available to treat hypocalcemic tetany or hypermagnesemia.

Nursing Management

 The nurse should be aware of patients at risk for hypomagnesemia and observe them for its signs and symptoms.  Patients receiving digitalis are monitored closely, because a deficit of magnesium can predispose them to digitalis toxicity.  If hypomagnesemia is severe, seizure precautions are implemented.  Other safety precautions are instituted, as indicated, if confusion is observed.  Patients should be screened for dysphagia (difficulty in swallowing), as this may occur in those with magnesium depletion.  The patient is educated about sources of magnesium-rich foods, including green vegetables, nuts, legumes, bananas, and oranges. Hypermagnesemia – Magnesium Excess  Hypermagnesemia (serum magnesium level higher than 2.6 mg/dL [1.07 mmol/L]) is a rare electrolyte abnormality, because the kidneys efficiently excrete magnesium.

 A serum magnesium level can appear falsely elevated if blood specimens are allowed to hemolyze or are drawn from an extremity with a tourniquet that was applied too tightly.

Pathophysiology

 The most common cause of hypermagnesemia is kidney injury. o In fact, most patients with advanced kidney injury have at least a slight elevation in serum magnesium levels. o This condition is aggravated when such patients receive magnesium to control seizures.  Hypermagnesemia can occur in patients with untreated DKA when catabolism causes the release of cellular magnesium that cannot be excreted because of profound fluid volume depletion and resulting oliguria.  A surplus of magnesium can also result from excessive magnesium given to treat hypertension of pregnancy or to treat hypomagnesemia.  Increased serum magnesium levels can also occur in adrenocortical insufficiency, Addison disease, or hypothermia.  Excessive use of magnesium-based antacids or laxatives and medications that decrease GI motility, including opioids and anticholinergics, can also increase serum magnesium levels.  Decreased elimination of magnesium or its increased absorption due to intestinal hypomotility from any cause can contribute to hypermagnesemia.  Lithium intoxication can also cause an increase in serum magnesium levels.  Extensive soft tissue injury or necrosis as with trauma, shock, sepsis, cardiac arrest, or severe burns can also result in hypermagnesemia.

Clinical Manifestations

 Acute elevation of the serum magnesium level depresses the central nervous system as well as the peripheral neuromuscular junction.  The respiratory center is depressed when serum magnesium levels exceed 10 mEq/L (5 mmol/L).  Coma, atrioventricular heart block, and cardiac arrest can occur when the serum magnesium level is greatly elevated and not treated.  High levels of magnesium also result in platelet clumping and delayed thrombin formation.

Assessment & Diagnostic Findings

 In hypermagnesemia, the serum magnesium level is greater than 2.6 mg/dL (1.07 mmol/L).  Increased potassium and calcium are present concurrently.  As creatinine clearance decreases to less than 3.0 mL/min, the serum magnesium levels increase.  ECG findings may include a prolonged PR interval, tall T waves, a widened QRS, and a prolonged QT interval, as well as an atrioventricular block.

Medical Management

 Hypermagnesemia can be prevented by avoiding the administration of magnesium to patients with kidney injury and by carefully monitoring seriously ill patients who are receiving magnesium salts.  In patients with severe hypermagnesemia, all parenteral and oral magnesium salts are discontinued.  In emergencies, such as respiratory depression or defective cardiac conduction, ventilatory support and IV elemental calcium as a magnesium antagonist are indicated.  In addition, hemodialysis with a magnesium-free dialysate can reduce the serum magnesium to a safe level within hours.  Administration of loop diuretics (e.g., furosemide) and sodium chloride or lactated Ringer’s IV solution enhances magnesium excretion in patients with adequate renal function.  IV calcium antagonizes the cardiovascular and neuromuscular effects of magnesium.

Nursing Management

 If hypermagnesemia is suspected, the nurse should monitor the vital signs, noting hypotension and shallow respirations.  The nurse should be aware that arrhythmias, bradycardia, and heart block can occur.  The nurse also observes for decreased deep tendon reflexes (DTRs), muscle weakness, and changes in the level of consciousness.

 Medications that contain magnesium are not given to patients with compromised renal function, and patients with kidney injury are cautioned to check with their primary providers before taking OTC supplements.  Administration of fluids and diuretics are often used in treatment and monitoring of I&O is important.  Hemodialysis may be necessary in severe hypermagnesemia, particularly if cardiovascular or neurologic manifestations are present. o Hemodialysis is also necessary in patients with severe hypermagnesemia and kidney injury. Phosphorous Imbalances  Phosphorus (HPO4−) is a critical constituent of all body tissues and is plentiful in the average diet of people living in developed countries.  Intake of phosphorus usually exceeds body requirements, and the kidney excretes the excess.  Phosphorus is essential to the function of muscle and RBCs; the formation of adenosine triphosphate (ATP) and of 2,3- diphosphoglycerate, which facilitates the release of oxygen from hemoglobin; and the maintenance of acid–base balance, as well as the nervous system and the intermediary metabolism of carbohydrate, protein, and fat.  It is a major component of the cell structure, phospholipids, nucleotides, and nucleic acids (DNA and RNA).  It provides structural support to bones and teeth.  Phosphorus is the primary anion of the ICF and requires active transport mechanisms to maintain its presence inside the cells.  Most intracellular phosphorus is bound to proteins and lipids.  About 85% of phosphorus is located in bones and teeth, 14% in soft tissue, and less than 1% in the ECF.  The normal serum phosphorus level is 2.7 to 4.5 mg/dL (0.87 to 1.45 mmol/L) in adults.  Phosphorus homeostasis is maintained through absorption and secretion in the GI tract, filtration and absorption in the kidneys, and shifts into and out of bone.  PTH and vitamin D assist in phosphate homeostasis by varying phosphate reabsorption in the proximal tubule of the kidney.  PTH allows the shift of phosphate from bone to plasma.  Phosphorus deficit and phosphorus excess are less common electrolyte imbalances. Hypophosphatemia – Phosphorus Deficit  Hypophosphatemia is indicated by a value below 2.7 mg/dL (0.87 mmol/L).  Although it often indicates phosphorus deficiency, hypophosphatemia may occur under a variety of circumstances in which total-body phosphorus stores are normal.  Phosphorus deficiency can also occur as an abnormally low content of phosphorus in lean tissues without evidence of low phosphate in the bloodstream.

 Hypophosphatemia can be due to lack of sufficient intake, excess excretion (renal phosphate wasting), shift of phosphorus from extracellular to intracellular spaces, or by decreased intestinal absorption of phosphorus.

Pathophysiology

 Hypophosphatemia rarely occurs due to inadequate intake, as there are many dietary sources of phosphate (e.g., meats, dairy products, beans). o However, phosphate can become depleted in GI malabsorption disorders such as chronic diarrhea, Crohn’s disease, or celiac disease.  Hypophosphatemia can also occur in anorexia, bulimia, and alcoholism.  Vitamin D deficit can cause low phosphate levels in the bloodstream. o Vitamin D regulates intestinal absorption of calcium and phosphate ion; therefore, a deficiency of vitamin D can cause both decreased calcium and phosphorus levels. o These deficiencies can lead to osteomalacia (softened and brittle bones) in the adult.  Hypophosphatemia can occur if there is high intake of antacids—particularly those containing calcium, magnesium, or aluminum. o Excess phosphorus binding by antacids may decrease the phosphorus available from the diet to an amount lower than required to maintain serum phosphorus balance. o The degree of hypophosphatemia depends on the amount of phosphorus in the diet compared to the dose of antacid.  Hypophosphatemia can also occur during the administration of calories to patients who have had severe protein–calorie malnutrition. o This syndrome can be induced in any person with severe malnutrition (e.g., patients with anorexia nervosa or alcoholism, older patients who are debilitated and unable to eat). o Feeding a patient who is nutritionally deprived stimulates a large insulin release that can cause shift of phosphate from the extracellular to the intracellular compartment. o Also, marked hypophosphatemia can develop in patients who are malnourished who receive parenteral nutrition that does not contain sufficient phosphorus.  Other causes of hypophosphatemia include heatstroke, prolonged intense hyperventilation, alcohol withdrawal, DKA, respiratory alkalosis, hepatic encephalopathy, and major thermal burns.  Hyperparathyroidism can also cause increased urinary losses of phosphorus leading to hypophosphatemia.  Loss of phosphorus through the kidneys also occurs with acute volume expansion, osmotic diuresis, the use of carbonic anhydrase inhibitors (acetazolamide), and some malignancies.  Respiratory alkalosis can cause a decrease in phosphorus in the bloodstream because of an intracellular shift of phosphorus. o Respiratory alkalosis, commonly caused by extreme hyperventilation, can reduce serum phosphate concentrations to very low levels and is a common cause of marked hypophosphatemia in patients who are hospitalized.  Some genetic disorders, such as Fanconi syndrome and X-linked hypophosphatemic rickets, cause renal phosphate wasting.  Acquired oncogenic osteomalacia, a paraneoplastic syndrome that occurs with some types of cancer, can also cause low phosphate levels.  Hypophosphatemia is also a frequent complication of renal transplantation.

Clinical Manifestations

 Most of the signs and symptoms of phosphorus deficiency result from a deficiency of ATP, 2,3-diphosphoglycerate, or both.  ATP deficiency impairs cellular energy resources; diphosphoglycerate deficiency impairs oxygen delivery to tissues, resulting in generalized weakness and neurologic manifestations.  Muscle damage may develop as the ATP level in the muscle tissue declines.  Clinical manifestations are muscle weakness, which may be subtle or profound and may affect any muscle group; muscle pain; and at times acute rhabdomyolysis (breakdown of skeletal muscle).  Weakness of the diaphragm and intercostal muscles may greatly impair ventilation.  Bone pain, altered mental status, seizures, focal neurologic signs, and heart failure can occur with severe hypophosphatemia.

Assessment & Diagnostic Findings

 On laboratory analysis, the serum phosphorus level is less than 2.7 mg/dL (0.87 mmol/L).  When reviewing laboratory results, the nurse should keep in mind that glucose or insulin administration causes a decrease in the serum phosphorus level.  Acute hypophosphatemia can occur during the treatment of DKA due to high doses of insulin.  Elevated PTH levels that occur as a result of hyperparathyroidism can lower blood levels of phosphate. o A 24-hour urine collection for phosphorus can be done if renal-phosphate wasting is suspected.  Fanconi syndrome causes loss of glucose, amino acids, uric acid, and phosphate in the urine.  X-rays and bone density studies may show skeletal changes of reduced bone mineralization caused by osteomalacia or rickets.  A technetium (Tc99m) sestamibi scan of the neck can be done to check for hyperparathyroidism.  CT scan, MRI, or indium-111 octreotide scan may show oncogenic osteomalacia (decreased bone density due to cancer).

Medical Management

 Prevention of hypophosphatemia is the goal. o In patients at risk for hypophosphatemia, serum phosphate levels should be closely monitored, and correction initiated before deficits become severe. o Adequate amounts of phosphorus should be added to parenteral solutions, and attention should be paid to the phosphorus levels in enteral feeding solutions.  Oral phosphate supplements are usually adequate for mild hypophosphatemia. o Sources of phosphorus include dairy foods, meats, and beans. o Oral supplements may be sufficient to treat renal-wasting disorders, malabsorption, or oncogenic osteomalacia until an exact etiology is found. o Vitamin D may also be necessary to enhance absorption of phosphorus and calcium.  Aggressive IV phosphorus correction is usually limited to the patient whose serum phosphorus levels decrease to less than 1 mg/dL (0.3 mmol/L). o Possible effects of IV administration of phosphorus include tetany from hypocalcemia and calcifications in tissues (blood vessels, heart, lung, kidney, eyes) from hyperphosphatemia.  Recently a monoclonal antibody-type drug, burosumab, has been approved for patients with renal phosphate wasting disorders and hypophosphatemic rickets. o This drug has been found to normalize phosphate levels, improve bone mineralization, and heal fractures in rickets.  If hyperparathyroidism is caused by parathyroid tumor, surgery may be necessary. o A parathyroid tumor, termed an adenoma, can cause hyperparathyroidism with resulting demineralization of bone (osteomalacia). o Patients with hyperparathyroidism can also be given calcimimetic medications, such as cinacalcet, which activate the calcium receptor in the gland and decrease PTH secretion.  Patients with oncogenic osteomalacia should be treated for the cancer causing this syndrome. o If malabsorption is the cause of hypophosphatemia, treatment of the GI disorder is necessary. o Because patients with osteomalacia are at high risk for fracture, fall precautions should be observed.  If hypophosphatemia is caused by an eating disorder, the patient should obtain behavioral counseling and nutritional therapy.

Nursing Management

 Patients who are malnourished and receiving parenteral nutrition are at risk when calories are introduced too aggressively, preventive measures involve gradually introducing the solution to avoid rapid shifts of phosphorus into the cells.  Vitamin D and calcium levels should also be monitored as phosphate levels are influenced by these levels. o Vitamin D supplementation may be needed to enhance calcium and phosphate absorption.  In patients requiring correction of phosphorus losses, the nurse frequently monitors serum phosphorus levels and documents and reports early signs of hypophosphatemia (apprehension, confusion, change in level of consciousness).  If the patient experiences mild hypophosphatemia, foods such as milk and milk products, organ meats, beans, nuts, fish, poultry, and whole grains should be encouraged.  With moderate hypophosphatemia, supplements such as Neutra-Phos capsules, K-Phos, and Fleet Phospho-Soda may be prescribed.

 For patients with severe hypophosphatemia, IV preparations of phosphorus are available as sodium or potassium phosphate. o The rate of phosphorus administration should not exceed 3 mmol/h, and the site should be carefully monitored because tissue sloughing, and necrosis can occur with infiltration. o Serum calcium and phosphate blood levels should be monitored every 6 hours with IV therapy. Hyperphosphatemia – Phosphorus Excess  Hyperphosphatemia is a serum phosphorus level that exceeds 4.5 mg/dL (1.45 mmol/L).  Abnormally high levels of phosphate in the bloodstream can arise from excessive intake of phosphorus, decreased excretion of phosphorus, or a disorder that shifts intracellular phosphate into the extracellular space.

Pathophysiology

 Various conditions can lead to hyperphosphatemia; however, the most common is kidney injury, which diminishes urinary phosphate excretion.  When renal insufficiency progresses to 40% to 50% of renal function, hyperphosphatemia can occur.  Other causes include increased intake or a shift of phosphate from the intracellular to extracellular space.  Conditions such as excessive vitamin D intake, administration of total parenteral nutrition, chemotherapy for neoplastic disease, hypoparathyroidism, pseudohypoparathyroidism, metabolic or respiratory acidosis, DKA, acute hemolysis, high phosphate intake, profound muscle necrosis, and increased phosphorus absorption may also lead to this phosphorus imbalance.  Hypoparathyroidism causes hyperphosphatemia by failure of the kidneys to inhibit renal reabsorption of phosphate. o The kidneys reabsorb excessive phosphate into the bloodstream.  Pseudohypoparathyroidism is a disorder caused by end-organ resistance to PTH.  Excessive use of phosphate-containing laxatives or enemas can also lead to hyperphosphatemia.  False elevation of phosphate in the bloodstream can occur with elevated protein or bilirubin levels, dyslipidemia, or hemolysis.  The primary complication of increased phosphorus is metastatic calcification in the organs, soft tissues, joints, and arteries.  Arterial calcification is a risk factor for myocardial infarction, stroke, and peripheral arterial disease.

Clinical Manifestations

 Most symptoms result from decreased calcium levels and soft tissue calcifications.  The most important short-term consequence is tetany (severe muscle cramping). o Because of the reciprocal relationship between phosphorus and calcium, a high serum phosphorus level tends to cause a low serum calcium concentration. o Hypocalcemia causes neuromuscular irritability and muscle spasms.  The major long-term consequence is soft tissue calcification, which occurs mainly in patients with a reduced glomerular filtration rate. o High serum levels of inorganic phosphorus promote precipitation of calcium phosphate in nonosseous sites, which can decrease urine output, impair vision, and produce palpitations. o Skin and soft tissue deposits of calcium can cause pruritus.

Assessment & Diagnostic Findings

 On laboratory analysis, the serum phosphorus level exceeds 4.5 mg/dL (1.5 mmol/L).  The serum calcium level is useful also for diagnosing the primary disorder and assessing the effects of treatments.  X-rays may show skeletal changes with abnormal bone development.  PTH levels are decreased in hypoparathyroidism. BUN and creatinine levels are used to assess renal function.

Medical Management

 Phosphate intake should be reduced, and phosphate binders can be given with meals to reduce hyperphosphatemia.  When possible, treatment is directed at the underlying disorder. o For example, hyperphosphatemia may be related to volume depletion or respiratory or metabolic acidosis.

o Correction of these disorders may normalize the blood level of phosphate.  Calcium carbonate or calcium citrate are phosphate binders that can be used to lower blood phosphate levels. o However, careful monitoring of calcium is essential as hypercalcemia can result. o Phosphate binding resins that do not contain calcium include sevelamer and lanthanum. o Sucroferric oxyhydroxide can also be used particularly in patients who require iron supplementation.  Forced diuresis with a loop diuretic or saline diuresis can be used in patients with normal renal function.  Hemodialysis can also lower phosphorus. Nursing Management  If a low phosphorus diet is prescribed, the patient is instructed to avoid phosphorus-rich foods, such as hard cheeses, cream, nuts, meats, whole-grain cereals, dried fruits, dried vegetables, kidneys, sardines, and dairy foods.  When appropriate, the nurse instructs the patient to avoid phosphate-containing laxatives and enemas.  When administering phosphate binders, calcium levels should be monitored as well.  During diuresis the nurse monitors urine output.  The nurse also educates the patient about recognizing the signs of hypocalcemia, such as muscle cramping.