Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
60-1 HYPOKALEMIA AND HYPOMAGNESEMIA A Super Bowl Party. . . . . . . . . . . . . . . . . . . . . . . . . . . . . Level III CASE SUMMARY A 45-year-old Caucasian woman with a history of nonischemic cardiomyopathy with ICD placement, pulmonary hypertension, hypertension, hypothyroidism, asthma, diabetes, and other medical problems presents to the emergency department with increased shortness of breath. History, physical examination, and diagnostic tests are indicative of an acute exacerbation of chronic heart failure with volume overload. Laboratory evaluation reveals hypokalemia, hypomagnesemia, hyponatremia, hypocalcemia, and hypoalbuminemia. The patient has multiple possible causes for the electrolyte abnormalities, including diuretic use. Correction of the serum calcium concentration for hypoalbuminemia suggests that no treatment is required for hypocalcemia. The reader is asked to develop a cohesive plan to diurese the patient and treat both the hypokalemia and hypomagnesemia on an inpatient basis. QUESTIONS Problem Identification 1.a. Create a list of the patient’s drug therapy problems. • Hypokalemia, hypomagnesemia, hyponatremia that are not treated; pseudohypocalcemia • Hypervolemia secondary to HF • Hyperglycemia • Medications without an indication: omeprazole, loratadine, meclizine, and folic acid • Untreated pulmonary hypertension 1.b.What information (signs, symptoms, and laboratory values) indicates the presence and severity of the electrolyte abnormalities? Hypokalemia: • The normal range for serum potassium concentration is 3.5– 5.0 mEq/L. Mild hypokalemia is defined as a serum potassium between 3.0 and 3.5 mEq/L; moderate hypokalemia is defined as a serum potassium of 2.5–3.0 mEq/L; and severe hypokalemia is defined as a level <2.5 mEq/L. This patient has moderate hypokalemia (2.8 mEq/L). • The signs and symptoms of hypokalemia are quite variable, depend on the acuteness of the electrolyte loss, and are usually not observed until the serum potassium concentration falls below 3.0 mEq/L. Most symptoms are caused by changes in the cellular resting potential and membrane excitability, which are related to the ratio of intracellular-to-extracellular potassium. Hypokalemia causes a hyperpolarization of the resting membrane potential, resulting in impaired muscle contraction. Many patients with mild hypokalemia have no symptoms, but as hypokalemia progresses, nonspecific symptoms such Hypomagnesemia: • The normal range for serum magnesium is 1.5–2.0 mEq/L. This patient’s level of 1.3 mEq/L signifies a mild magnesium deficit; however, serum magnesium is not an accurate indicator of body magnesium stores because magnesium is a major intracellular cation. • The patient does not exhibit any signs or symptoms of hypomagnesemia such as tremor, twitching, or palpitations. Refer to the textbook chapter on potassium and magnesium homeostasis for a complete discussion of hypomagnesemia. • The patient also appears to have hypocalcemia (see below), which often accompanies hypomagnesemia. Hyponatremia: • The normal range for serum sodium is 135–145 mEq/L. This patient’s level of 130 mEq/L signifies mild hyponatremia. Symptoms of hyponatremia are often not seen until the sodium drops to <125 mEq/L (nausea and malaise). A serum sodium between 115–120 mEq/L often correlates with symptoms of headache, lethargy, confusion, or unsteadiness. Once the serum sodium drops to <115 mEq/L, a patient may develop delirium, seizures, coma, respiratory arrest, or death. This patient does not exhibit any of these symptoms. Hypocalcemia: • The normal range for total calcium is 8.5–10.5 mg/dL. The occurrence of signs and symptoms of hypocalcemia may be directly related to the time course over which the abnormality occurs. Currently, she is not showing any signs of hypocalcemia. See the textbook chapter on calcium and phosphorus homeostasis for a complete discussion of hypocalcemia. With a total serum calcium concentration of 8.3 mg/dL, the patient appears to be hypocalcemic, but a serum albumin is necessary to correctly assess total serum calcium concentrations because of calcium’s affinity for albumin. A normalized or corrected calcium concentration (Cacorr) can be calculated with the following equation: Cacorr = O bserved calcium + 0.8 (normal albumin – observed albumin) Cacorr = 8.3 mg/dL + 0.8 (4.0 – 3.0) = 9.1 mg/dL Because the corrected calcium is within the normal range, this suggests that the patient’s ionized calcium is within normal limits and no calcium replacement is necessary. 1.c. What are the potential causes of the electrolyte disorders in this patient? Hypokalemia: • Diuretic use is the most common pharmacologic cause of hypokalemia. Both thiazide and loop diuretics can cause an increase in the renal excretion of potassium, and the incidence of hypokalemia is related to both dose and treatment Copyright © 2017 by McGraw-Hill Education. All rights reserved. Hypokalemia and Hypomagnesemia Denise R. Sokos, PharmD, BCPS • Hypokalemia can result in a variety of cardiac arrhythmias, ranging from bradycardia to ventricular fibrillation; however, they are very rare. In patients with cardiovascular ischemia or heart failure, even small decreases in serum potassium can result in arrhythmias. An ECG was performed in this patient, and hypokalemia-associated ECG changes (broad T waves and the occurrence of a U wave) were not found. Polyuria and polydipsia may also occur in chronic hypokalemia. The patient is also hypomagnesemic, which often occurs in conjunction with hypokalemia. CHAPTER 60 60 as generalized weakness and fatigue can occur. Patients with a chronic loss of potassium may have few symptoms because intracellular potassium moves extracellularly, thus restoring the intracellular-to-extracellular potassium ratio. 60-2 SECTION 5 duration.1 In addition to increased renal losses of potassium, hypovolemia induced by the diuresis causes the release of aldosterone, which can further increase potassium loss. A potassium-sparing diuretic can be used in combination with a potassium-wasting diuretic to prevent hypokalemia. This particular patient is receiving furosemide, metolazone, spironolactone, and a potassium supplement. The spironolactone and potassium are not sufficient to offset the potassium-wasting effects of the furosemide and metolazone in this case. Renal Disorders • Diarrhea is one of the most common nonpharmacologic causes of hypokalemia. The normal concentrations of potassium and bicarbonate in the stool are very high (approximately 10 and 40 mEq/L, respectively) and increase proportionally with the volume of stool. Diarrhea may cause both decreased absorption and increased secretion of potassium. The loss of bicarbonate and potassium commonly causes a hypokalemic metabolic acidosis. This patient does not complain of diarrhea but may have GI losses due to her magnesium supplementation, which often causes diarrhea. Diuretic-induced hypokalemia usually results in metabolic alkalosis, and the patient does appear to have a metabolic alkalosis based on serum bicarbonate levels; however, arterial blood gases are not available. • Insufficient intake of potassium is rarely a cause of hypokalemia due to the kidney’s ability to efficiently conserve potassium. However, in periods of increased losses, intake may not be sufficient to make up for the amount of potassium loss. The patient is prescribed a potassium supplement, but the dose is inadequate to overcome her losses. • Hypomagnesemia is often a concomitant disorder in patients with hypokalemia, especially those taking diuretics. Diabetic ketoacidosis is another clinical situation in which hypokalemia and hypomagnesemia commonly occur together. Hypomagnesemia may lead to increases in both renal and fecal losses of potassium via decreased intracellular transport of potassium. Hypomagnesemia exacerbates hypokalemia via increasing distal potassium secretion in the nephron.2 Therefore, hypokalemia cannot be corrected until hypomagnesemia is corrected. A serum magnesium concentration should always be checked in patients with persistent hypokalemia, especially those resistant to replacement therapy. Hypomagnesemia: • Both thiazide and loop diuretics inhibit the reabsorption of magnesium, and hypomagnesemia commonly occurs with diuretic use.3 In fact, more than one-third of patients receiving thiazide or loop diuretics have this electrolyte disorder (refer to the textbook chapter on potassium and magnesium homeostasis). Proton-pump inhibitors are also known to cause hypomagnesemia, although the mechanism is unclear. • Diarrhea (especially if chronic) can result in significant magnesium losses, as intestinal fluids contain approximately 14 mEq/L of magnesium. Although this patient is not complaining of diarrhea, she is taking a magnesium supplement, which can cause diarrhea. • Malnutrition commonly results in hypomagnesemia because of decreased magnesium intake and increased renal elimination of magnesium. The patient is hypoalbuminemic, which may be suggestive of malnutrition; however, this patient is obese. Therefore, the hypoalbuminemia is more likely related to heart failure than to malnutrition. Hyponatremia: • There are three classifications of hyponatremia: hypervolemic hyponatremia, euvolemic hyponatremia, and hypovolemic Copyright © 2017 by McGraw-Hill Education. All rights reserved. hyponatremia. In a heart failure patient exhibiting signs and symptoms of fluid overload, the most likely classification is hypervolemic hyponatremia (a.k.a. dilutional hyponatremia). In this case, there is an excess of sodium and fluid, but the excess fluid predominates. Heart failure exacerbations lead to tissue hypoperfusion, which triggers ADH secretion, causing reabsorption of water in the collecting tubules of the kidneys. This culminates in hyponatremia. • Medications (eg, diuretics) can also cause hyponatremia. In this case, the thiazide diuretic is the most likely cause. There are three contributing factors to thiazide-induced hyponatremia: excess free-water intake, reduced free-water clearance, and renal sodium and/or potassium losses. Thiazide diuretics inhibit sodium reabsorption in the distal convoluted tubule leading to an inhibition of urinary dilution capacity. Additionally, due to diuretic action and an increase in ADH, sodium losses may be higher than water losses. • Hypokalemia can also cause hyponatremia because sodium will enter cells to account for the reduction of intracellular potassium to maintain cellular electroneutrality. Hypocalcemia: • Hypoalbuminemia is the most common cause of laboratoryreported hypocalcemia. In this case, a corrected calcium concentration should be calculated or an ionized calcium concentration measured. Hypoalbuminemia is common in chronic heart failure and may be related to an underlying inflammatory process. In this patient, the decrease in albumin concentration may also be a dilutional effect related to volume overload. Heart failure can induce a catabolic state leading to cachexia, but this is not the case in this obese patient. 1.d.What additional information is needed to satisfactorily assess this patient’s electrolyte disorders? • For evaluation of the hypokalemia, urinary sodium, potassium, and osmolality, with concurrent serum values, are usually necessary to investigate the source of losses and the patient’s volume status. If the urinary potassium is <20 mEq/L, then extrarenal losses are more likely. Urinary potassium concentrations of >20 mEq/L generally indicate renal potassium losses. In this patient, urinary potassium concentrations should be elevated because the patient is receiving furosemide and metolazone. Spironolactone decreases urinary potassium levels, thus further complicating the diagnostic utility of the test and making it unnecessary. • Low urinary sodium concentrations indicate a volumedepleted state; however, because of the patient’s current diuretic use, urinary sodium concentrations are expected to be high. The patient’s clinical presentation suggests volume overload (ie, edema in the pulmonary vasculature and lower extremities, shortness of breath). Because of this and the normal pathology associated with heart failure, urinary sodium concentration would not provide valuable assessment information. • Urinary osmolality is normally 900–1400 mOsm/kg. In a hypokalemic state, the osmolality slowly decreases over weeks but generally does not fall below 300 mOsm/kg. Because of this, urine output normally stays below 3 L per day. Maximal osmolality begins to fall when the total body potassium deficit exceeds 200 mEq and reaches a minimum with a deficit of 400 mEq (the reflective serum concentration should be below 3.0 mEq/L). This is in contrast to diabetes insipidus, where the osmolality may be below 150 mOsm/kg. Because of this 60-3 Desired Outcome 2.What are the goals of pharmacotherapy in this patient? Primary outcomes: • Replace potassium and magnesium deficiencies without overcorrecting. • Treat hyperglycemia and prevent hypoglycemia. • Prevent further losses of electrolytes. Secondary outcomes: • Prevent future heart failure exacerbations. • Prevent venous thromboembolism. • Continue to treat hypertension, asthma, hypothyroidism, and anxiety disorder. • Treat pulmonary hypertension. • Discontinue unnecessary medications. • Ensure preventive health measures are up to date or scheduled. Therapeutic Alternatives 3.What feasible pharmacotherapeutic alternatives are available for treatment of hypervolemia, hypokalemia, and hypomagnesemia in this patient? Hypervolemia: • The patient has clinical signs and symptoms of significant volume overload probably due to her recent diet choices. Although she is taking furosemide, metolazone, and spironolactone orally, she is retaining excess fluid. Heart failure patients have a delay in the time of absorption as well as a delay in the overall extent of absorption of oral furosemide causing an unpredictable response. Some patients respond more favorably to torsemide or bumetanide, as they are more bioavailable. Current practice guidelines recommend intravenous loop diuretics as the first choice for the treatment of acute fluid overload.4 • Loop diuretics have a relatively short half-life, and sodium reabsorption in the tubule resumes after the tubule concentration of the diuretic declines. To obtain an adequate diuresis, some patients may require dosing of the diuretic several times per day. Some providers may choose to use a continuous IV infusion. However, there is not a statistically significant difference in symptoms, diuresis, or outcomes between continuous infusion and intermittent doses. Provider preference will dictate whether multiple daily doses or continuous infusions are used. • The addition of intravenous vasodilator therapy should be considered if the response to diuretic therapy is not adequate. The patient’s blood pressure is adequate at the time of presentation and vasodilator therapy could be used if needed. • Note that the treatment of hypervolemia will also treat the hyponatremia in this patient. Hypokalemia: • Because the kidneys are the primary regulators of potassium excretion, a patient’s renal function should be assessed before instituting potassium replacement. In patients with renal insufficiency, potassium replacement should be approached cautiously, because hyperkalemia may develop. The patient’s IBW kg (female) = 45.5 kg + 2.3 (height in inches above 60) IBW = 45.5 kg + 2.3 (5) = 57 kg For drug dosing, use the Cockcroft–Gault equation to calculate the patient’s CLcr: CLcr (female) = CLcr = (140 – age) × IBW(kg) × 0.85 72 × SCr (140 – 45) × 57 kg × 0.85 72 × 1.0 mg/dL CLcr = 64 mL/min Based on this calculation, this patient does not have renal insufficiency. Note that to correctly calculate CLcr, use IBW rather than total body weight (TBW). If the patient’s TBW (87 kg) were used in the above equation, the result of 96 mL/min would be an overestimation of her true renal function. • Potassium chloride, phosphate, and bicarbonate salts are the available formulations of potassium and are equally efficacious. The oral route is preferred unless there are life-threatening symptoms or the patient is unable to tolerate oral intake. Chloride salts are generally used in patients with alkalosis to replenish chloride stores depleted by diuretic use, vomiting, or nasogastric suctioning. Normally, sodium is reabsorbed in the renal tubules with chloride; however, when chloride stores are depleted, hydrogen and/or potassium ions are exchanged for sodium ions. When hypokalemia occurs, hydrogen ions are exchanged for sodium, resulting in a metabolic alkalosis. Chloride and fluid replenishment decrease the exchange of hydrogen ions for sodium ions in the renal tubules, therefore helping to correct the alkalosis. Phosphate salts should be reserved for concomitant hypophosphatemia. Bicarbonate salts are used in metabolic or renal tubular acidosis to replace bicarbonate. • Oral potassium is available in four dosage forms: elixirs, powders, capsules, and tablets. The extended-release tablets are available as wax-matrix or microencapsulated formulations. The microencapsulated formulations are preferred because they disintegrate better in the stomach and cause less GI erosion. The elixir is the least expensive formulation but has very poor patient adherence during chronic therapy because of its unpleasant taste and resulting nausea. Regardless of the preparation used, all products are well absorbed. • Parenteral potassium replacement is the preferred route when the patient is unable to take oral medications, when signs and symptoms of hypokalemia are present, or when hypokalemia is life threatening. In general, 10–20 mEq/hour can be safely administered and repeated based on serum potassium concentrations. In rare instances of severe hypokalemia with life-threatening symptoms, a rate of 40–100 mEq/hour may be used. ECG monitoring is required if potassium is to be administered at a rate of 20 mEq/hour or greater and may be warranted if administration exceeds 10 mEq/hour. The maximum concentration for peripheral administration is 40 mEq/L; higher concentrations may be painful and cause venous irritation. When potassium is administered through a central line, 10–20 mEq/100 mL may be given over 1 hour, with concurrent ECG monitoring. Whenever parenteral therapy is used, frequent laboratory monitoring is necessary.5 High variability exists in dosing recommendations; therapy should be guided by the patient’s condition and laboratory results. Copyright © 2017 by McGraw-Hill Education. All rights reserved. Hypokalemia and Hypomagnesemia • Treat hypervolemia and hyponatremia. current weight is 87 kg, but she is obese, and her ideal body weight (IBW) should be calculated to accurately estimate her creatinine clearance (CLcr): CHAPTER 60 patient’s diuretic use and history of heart failure, the urine osmolality will be difficult to interpret. 60-4 Hypomagnesemia: SECTION 5 • As with potassium, the kidneys are the primary regulators of magnesium homeostasis, and renal function should be assessed before initiating magnesium replacement. In the setting of renal insufficiency, the risk of hypermagnesemia with replacement is much greater. This patient’s CLcr is 64 mL/min, indicating that she does not have impaired renal function. Patients are not considered to have clinically important renal dysfunction until their CLcr is <60 mL/min. Renal Disorders • Oral magnesium gluconate or oxide may be given in most situations and is the treatment of choice for asymptomatic patients. Magnesium gluconate is the preferred agent because magnesium oxide can cause an osmotic diarrhea. • IV magnesium sulfate is warranted when the serum concentration is <1.0 mEq/L or when acute symptoms are present. For life-threatening symptoms, give a 2 g IV bolus over 1 minute followed by an infusion of 0.5 mEq/kg lean body weight (LBW) over 5–6 hours. An additional 0.5 mEq/kg LBW should be administered as a continuous infusion over the next 18 hours. For serum concentrations of <1.0 mEq/L without lifethreatening symptoms, a total of 1.0 mEq/kg LBW should be given over 24 hours. Initially, one-half of the dose (0.5 mEq/kg LBW) should be given as an infusion over 2–6 hours (not to exceed 150 mg/min), with the remainder of the dose given as a continuous infusion. Extended replacement is warranted because even when severe deficiencies are present, approximately 50% of an administered dose is excreted in the urine. Optimal Plan 4.a. Given the therapeutic alternatives outlined above, what is the most appropriate therapy for treatment of hypervolemia, hypokalemia, and hypomagnesemia in this patient? Hypervolemia: • This patient developed edema on an oral dose of furosemide 80 mg BID; practice guidelines recommend initiating an intravenous dose that is equal to or exceeds her oral dose.4 The oral bioavailability of furosemide has large intra- and interpatient variability. In general, the bioavailability is considered to be 50%. That is, 40 mg orally is equivalent to 20 mg intravenously. A reasonable choice is to start with furosemide 80 mg IV BID. Monitoring should include the laboratory parameters of BUN, serum creatinine, and the BUN/SCr ratio and the physical examination findings of pulmonary and lower-extremity edema, supine and standing vital signs, volume intake, urine output, and daily weights. • Spironolactone is not available intravenously and the oral formulation should be continued at its current dose. Consider discontinuing the metolazone, as it may be a contributor to the hyponatremia. While hospitalized, her fluid status can be balanced with intravenous loop diuretic dose titration. Hypokalemia: • The first step in the assessment of this patient’s hypokalemia is to calculate the potassium deficit. In the early phases of hypokalemia, a 1 mEq/L decrease in the serum potassium concentration reflects a 100–200 mEq total body loss. However, once the serum potassium is <2.5 mEq/L, a further 1 mEq/L drop in serum potassium represents total body deficits of 200–400 mEq. This patient’s deficit is approximately 200 mEq. This implies that a single dose will not be sufficient to correct her serum potassium. For mild deficits, 40–80 mEq per day is appropriate. More severe deficits may require 300–400 mEq Copyright © 2017 by McGraw-Hill Education. All rights reserved. per day with frequent monitoring. These are only estimates as potassium replacement is guided by the serum potassium concentration. • Because the patient is receiving a higher dose of IV furosemide, intravenous potassium chloride should be administered to correct her current potassium deficit and to replace the potassium she will lose. A starting dose of 60 mEq IV in divided doses is appropriate. Her oral supplements may be continued. Additional IV doses of KCl will likely be necessary to replenish her stores. During replacement therapy, intracellular potassium must be restored before changes will be reflected in the serum potassium. Laboratory results will determine the dose and frequency of additional KCl doses. • Because this patient is also hypomagnesemic, magnesium replacement is necessary for potassium replacement to be successful. Hypomagnesemia: • The patient is currently taking magnesium oxide 400 mg PO TID for hypomagnesemia. Increase the dose to 800 mg PO BID with close monitoring of serum levels, because she will likely have additional losses with the higher dose of furosemide. The dose may be increased as necessary to maintain normal serum magnesium levels. Intravenous magnesium sulfate may be indicated if the serum level falls below 1.0 mEq/L. In that scenario, give 1 mEq/kg LBW (55 mEq); one-half of the dose as a bolus infusion over 2–6 hours, and the remainder as a continuous infusion on day 1. On days 2–5, give 0.5 mEq/kg LBW per day (30 mEq) as a continuous infusion. To be practical, doses should be rounded to the nearest 5 mEq or 0.5 g of magnesium sulfate. Treatment Summary: • Continue the spironolactone. Increase the magnesium oxide dose to 800 mg PO BID. Intravenous KCl 20 mEq given over 2 hours × 3 with telemetry ECG monitoring (because of KCl at a rate of 10 mEq/hour and the heart failure) is an appropriate initial strategy. Continue the oral KCl 80 mEq BID. Discontinue the oral furosemide and initiate furosemide 80 mg IV BID with the monitoring outlined above. If the diuresis is inadequate, there are two options: (1) if the 80-mg dose does not provide an increase urine output, then a higher dose will be necessary; (2) if the 80 mg dose increases urine output, but there is rebound sodium resorption during time when the diuretic blood levels are low, then additional daily doses would be necessary. Multiple daily doses provide more diuresis and less physiologic disturbance than larger single doses. The diuretic dose should be titrated to alleviate symptoms and reduce extracellular fluid volume excess. 4.b.What therapy changes should be made for the patient’s heart failure and hyperglycemia? • For the treatment of heart failure, she is receiving all of the recommended medications at appropriate doses except for digoxin. The recommended dose is 0.125 mg per day. Clinical practice guidelines recommend decreasing the dose to avoid toxicity; especially in the setting of hypokalemia as the arrhythmogenic potential of digoxin is enhanced in the setting of hypokalemia. Increasing the spironolactone dose to 50 mg daily is not recommended because of the risk of hyperkalemia; adjusting the potassium dose is preferred. This patient’s requirement for supplemental potassium is unusual; in most clinical scenarios when spironolactone is initiated potassium supplementation is discontinued or titrated downward as most 60-5 Outcome Evaluation 5.What clinical and laboratory parameters are necessary to evaluate the therapy for the desired therapeutic outcome and prevention of adverse effects? • While the patient is hospitalized, monitor serum potassium concentrations initially every 4 hours (after every 30–40 mEq has been given). After initial replacement, potassium should be monitored daily until stable. • Monitor magnesium concentration twice daily initially, and then every few days after the electrolytes are stable. • A 12-lead ECG does not need to be monitored for her electrolyte abnormalities alone unless signs and symptoms of hypokalemia or hyperkalemia are present. However, the majority of patients admitted with acute exacerbations of heart failure are continuously monitored via telemetry during their hospitalization. • Monitor HR (inpatient and outpatient) because the digoxin dose is being reduced. In heart failure, the beta-blocker dose is titrated to a HR of 50–60 bpm or the target dose recommended in practice guidelines. Adjustments could be made as necessary in the future. • Monitor renal function daily while hospitalized to assess for the development of azotemia secondary to the diuresis. • Measure fluid intake, urine output, and vital signs (especially for hypotension) every shift. The patient’s weight and lowerextremity edema should be assessed daily. • Monitor other electrolytes daily to assess for the development of hypo- or hyper-electrolyte disorders (or any time signs or symptoms of a disorder are noted). These monitoring guidelines are valid only during hospitalization; outpatient monitoring is less intensive and much more difficult. After this patient is discharged, she should return in approximately 3 days to have her serum magnesium and potassium concentrations measured. She should then return weekly for serum magnesium and potassium concentration measurements until stable. • Monitor the patient for signs of toxicity from the electrolyte replacement therapy: ✓Discontinue potassium therapy if the serum levels are >5.0 mEq/L, if peaked T waves are noticed on ECG, or if there is a sudden onset of muscle weakness. Additionally, the patient should be monitored for pain and phlebitis with IV therapy and GI irritation when switched to oral therapy. ✓Discontinue magnesium therapy if the serum concentrations are >2.0 mEq/L. Additionally, monitor the patient for muscle weakness and cardiac and respiratory abnormalities. ✓Monitor the serum phosphate and chloride concentrations during potassium and magnesium replenishment. If the serum phosphate concentration drops below 2.5 mg/dL, potassium phosphate can be used instead of potassium chloride. Magnesium sulfate is also compatible with potassium phosphate in solution. Patient Education 6.What information should be provided to the patient to enhance adherence, ensure successful therapy, and minimize adverse effects? Potassium chloride (eg, K-Dur tablets): • This medication is a potassium supplement called K-Dur. The dose is 80 mEq (four tablets) three times a day. This dose may go up or down if your blood levels show too much or too little potassium in your body. Continue to take this medicine as prescribed until your doctor tells you to stop. • Potassium is essential for the proper function of the heart, kidneys, muscles, nerves, and digestive system. Normally, people get enough potassium from their diet, but because you take diuretics (water pills), your body loses too much potassium. • Take this medicine right after each meal. Take it with a full glass of water or juice and swallow the tablets whole. If you cannot swallow the tablets whole, break them in half and take each half separately with a glass of water. • If you forget to take a dose, take it as soon as you remember. If it is <4 hours until your next dose, skip the missed dose completely; never take a double dose. • Side effects of potassium tablets are generally very mild; you may notice some abdominal discomfort, nausea, vomiting, or diarrhea. If you develop confusion or a tingling, burning sensation in your arms or legs, notify your doctor because your dose may be too high. Do not adjust the dose on your own. • Store this medicine at room temperature and out of reach of children. Magnesium (eg, Mag-Ox): • This medication is a 400 mg tablet called magnesium oxide or Mag-Ox. Magnesium is essential for the proper functioning of your muscles, heart, and digestive tract. Because you are taking water pills (diuretics), your body loses too much magnesium and it needs to be replaced. • Your doctor prescribed two tablets two times a day, and you should continue this dose until he/she tells you to stop taking the medicine. The dose may increase or decrease if your blood levels show too much or too little magnesium in your body. • Swallow each tablet with a full glass of water. • If you forget to take a dose, take it as soon as you remember and then take any remaining doses at evenly spaced intervals throughout the day. Do not take doses any closer than 4 hours apart; do not take a double dose. If you miss a dose, simply skip the missed dose and go on with your usual regimen. • Magnesium tablets may cause diarrhea in some patients. If you develop diarrhea, notify your physician. • Store this medicine at room temperature and out of the reach of children. Copyright © 2017 by McGraw-Hill Education. All rights reserved. Hypokalemia and Hypomagnesemia • In an attempt to control the patient’s hyperglycemia while hospitalized, her current basal and prandial insulin should be continued. Correction insulin (ie, supplemental insulin that is used in addition to basal and prandial insulin) should be added to her regimen to treat premeal hyperglycemic episodes. Her glycemic goals are premeal blood glucose <140 mg/dL and random blood glucose <180 mg/dL. To prevent hypoglycemia, consider adjusting the insulin regimen if blood glucose levels fall to <100 mg/dL. If IV therapy is administered, the patient should be supine (especially for the bolus) and blood pressure should be monitored. The patient may complain of flushing or sweating during IV magnesium administration. CHAPTER 60 patients will develop hyperkalemia. Also, consider changing her diuretic regimen from furosemide to torsemide because of the increased bioavailability. This might offset the need for metolazone and better balance her fluid status and serum sodium. Refer to the textbook chapter on heart failure for a complete description of the treatment options. 60-6 ■■ FOLLOW-UP QUESTIONS SECTION 5 1.What changes should be made to the patient’s medication regimen at hospital discharge to prevent future electrolyte imbalances? • Increase the potassium chloride dose to 80 mEq PO TID with careful monitoring. • Increase the magnesium oxide to 800 mg PO BID with careful monitoring. Renal Disorders 2.Develop a plan to monitor this patient’s electrolytes after hospital discharge. • The patient should return for follow-up within 3 days to assess her laboratory parameters. If stable, the electrolytes can be monitored weekly for 2–3 weeks and then less frequently once stable. Given this patient’s severity of disease and comorbidities, it is likely that she will require more frequent monitoring and dosage adjustments of her potassium and magnesium supplements. 3.What vaccinations should this patient receive? • The pneumococcal polysaccharide vaccine (PPSV23) is recommended because she is considered high risk for invasive pneumococcal disease (due to diabetes, chronic heart disease, and asthma). • The CDC’s 2015–2016 influenza vaccination recommendations state that all individuals aged 6 months and older receive the vaccine each influenza season regardless of underlying medical conditions. Trivalent and quadrivalent vaccines are available; the CDC does not recommend one vaccine over another. Copyright © 2017 by McGraw-Hill Education. All rights reserved. • Varicella vaccination is appropriate if a reliable history of infection is not obtainable. • Tetanus booster (Td) every 10 years. (Note: Tetanus, diphtheria, pertussis [Tdap] vaccine should replace a single dose of Td in adults <65 years who have not previously received a dose of Tdap. Adults >65 years without an indicator condition may also be immunized.) • Because of her diabetes, the hepatitis B vaccination is indicated. • Any other vaccine as necessary if the patient is unable to provide documentation of childhood immunizations. REFERENCES 1. Cohn JN, Kowey PR, Whelton PK, Prisant M. New guidelines for potassium replacement in clinical practice. A contemporary review by the National Council on Potassium in Clinical Practice. Arch Intern Med 2000;160:2429–2436. 2. Huang CL, Kuo E. Mechanism of hypokalemia in magnesium deficiency. J Am Soc Nephrol 2007;18:2649–2652. 3. Ayuk J, Gittoes NJL. How should hypomagnesaemia be investigated and treated? Clin Endocrinol 2011;75:743–746. 4. Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation 2013;128:e240–e327. 5. Kraft MD, Btaiche IF, Sacks GS, Kudsk KA. Treatment of electrolyte disorders in adult patients in the intensive care unit. Am J Health Syst Pharm 2005;62:1663–1682.