Electrolyte-48 In D5w (electrolyte-48 solution/dextrose 5 % in water)

Dosage of dextrose depends on the age, weight, clinical condition, and fluid, electrolyte, and acid-base balance of the patient. Dextrose may usually be administered IV to healthy individuals at a rate of 0.5 g/kg per hour without producing glycosuria; the maximum infusion rate should generally not exceed 0.8 g/kg per hour.

For the treatment of hypoglycemia resulting from insulin excess or other causes in adults and children, the usual dose is 20-50 mL of 50% dextrose injection administered slowly (e.g., 3 mL/minute) IV; repeated doses and supportive therapy may be required in severe cases. For the treatment of acute symptomatic hypoglycemia in neonates and infants, the usual dose is 2 mL/kg of 10-25% dextrose injection administered slowly IV; higher or repeated doses may be required in severe cases, and subsequent continuous IV infusion of 10-15% dextrose injection may be necessary to maintain sufficient blood glucose concentrations. When patients do not respond to or tolerate dextrose, the use of other drugs (e.g., glucagon, corticosteroids, epinephrine) should be considered.

For the management of hypoglycemia in conscious diabetics, 10-20 g of dextrose may be administered orally as a gel or chewable tablets; the dose may be repeated in 10-20 minutes if necessary. Self monitoring of blood glucose concentration may be useful in determining whether a repeat dose is necessary; some clinicians recommend that if hypoglycemic symptoms are still present and a blood glucose increase of at least 20 mg/dL is not achieved within 20 minutes after oral administration of dextrose, the patient should consider administration of a repeat dose. Each gram of the 40% (w/w) dextrose gel provides 400 mg of dextrose (i.e., 25 g of gel provides 10 g of dextrose).

For further information on chemistry and stability, pharmacology, uses, cautions, and dosage and administration of dextrose, specialized references and the manufacturers'; labeling should be consulted.

Dextrose injections are administered IV. Hypertonic dextrose solutions are preferably administered via an IV catheter placed into a large central vein. If hypertonic (10%) dextrose solutions are administered peripherally, a large arm vein should be used and, if possible, the injection site should be alternated daily. Except in the emergency treatment of severe hypoglycemia, higher concentrations of dextrose injections (e.g., 20% and higher) should be administered via central veins and only after appropriate dilution. When used for the emergency treatment of hypoglycemia, hypertonic dextrose injections may be administered slowly via a peripheral vein.

Concentrated dextrose gels and chewable dextrose tablets are administered orally in the management of acute symptomatic hypoglycemia.

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There is no enhanced messaging for this drug.

There are no contraindication interactions for this drug.

Severe Interaction: Action is required to reduce the risk of severe adverse interaction.

Phosphate Supplements;Urine Ph Modifiers/Phosphate Reducers

SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.

MECHANISM OF ACTION: Lanthanum and sevelamer bind to phosphate.(1-2) Tenapanor is a sodium/hydrogen exchanger 3 (NHE3) inhibitor.(3) All three agents are used to lower phosphate absorption in the body.(1-3)

CLINICAL EFFECTS: Concurrent use of phosphate supplements or urinary pH modifiers high in phosphate with agents that reduce serum phosphorus may decrease the effectiveness of both agents.

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: Patients should normally not receive phosphate supplements or urinary pH modifiers high in phosphate concurrently with agents that reduce serum phosphorus.

DISCUSSION: Lanthanum, sevelamer, and tenapanor are indicated to control phosphorus levels. Consider discontinuing or holding phosphate supplements and urinary pH modifiers high in phosphate in patients receiving these agents.

Potassium Supplements/Eplerenone

SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.

MECHANISM OF ACTION: Eplerenone increases serum potassium levels.(1)

CLINICAL EFFECTS: Concurrent use of eplerenone with a potassium supplement may result in hyperkalemia.(1)

PREDISPOSING FACTORS: Renal impairment.

PATIENT MANAGEMENT: The manufacturer of eplerenone states that the use of eplerenone for the treatment of hypertension in patients receiving potassium supplements is contraindicated.(1)

DISCUSSION: The main risk of eplerenone therapy is hyperkalemia. The risk of hyperkalemia can be reduced by avoiding potassium supplements during eplerenone therapy.(1)

Potassium Supplements/Potassium Binders

SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.

MECHANISM OF ACTION: Patiromer, sodium polystyrene sulfonate and sodium zirconium cyclosilicate bind to potassium.(1-3)

CLINICAL EFFECTS: Concurrent use of potassium supplements and patiromer, sodium polystyrene sulfonate or sodium zirconium cyclosilicate may decrease the effectiveness of both agents.

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: Patients should normally not receive potassium supplements and patiromer, sodium polystyrene sulfonate or sodium zirconium cyclosilicate concurrently.(1-3) Patiromer, sodium polystyrene sulfonate or sodium zirconium cyclosilicate are indicated for management of hyperkalemia. Consider discontinuing or holding potassium supplements in patients who develop hyperkalemia requiring treatment.

DISCUSSION: Patiromer, sodium polystyrene sulfonate and sodium zirconium cyclosilicate are indicated for hyperkalemia. Consider discontinuing or holding potassium supplements in patients receiving sodium polystyrene sulfonate or sodium zirconium cyclosilicate.

Potassium Supplements/Potassium Sparing Diuretics

SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.

MECHANISM OF ACTION: Decreased renal excretion of potassium, resulting from administration of a potassium sparing diuretic.

CLINICAL EFFECTS: May observe hyperkalemia which may be severe or even fatal.

PREDISPOSING FACTORS: Renal function impairment.

PATIENT MANAGEMENT: If both drugs are administered, monitor potassium levels. Adjust the dose of the drugs accordingly. This combination should probably be avoided if possible.

DISCUSSION: The interaction is well documented. Patients with decreased renal function are especially at risk of developing hyperkalemia from this drug combination. A commonly held belief is that a potassium sparing diuretic formulated in combination with a thiazide diuretic, such as Dyazide, will not exhibit this interaction. Although the likelihood of hyperkalemia occurring may be reduced somewhat, a danger still exists.

Potassium Supplements/Trimethoprim

SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.

MECHANISM OF ACTION: Trimethoprim may increase serum potassium levels by reduction in potassium elimination.(1-3) The combination of trimethoprim and potassium supplements can have an additive effect on serum potassium resulting in potentially dangerous levels.

CLINICAL EFFECTS: Concurrent use of trimethoprim and potassium supplements may result in hyperkalemia, which may be severe.

PREDISPOSING FACTORS: Patients who are elderly, have any degree of renal insufficiency or heart failure have an increased risk for hyperkalemia.(1-9) Concomitant use with other drugs associated with hyperkalemia risk (e.g. ACE Inhibitors, angiotensin II receptor antagonists, aldosterone antagonists, NSAIDs) and high doses of trimethoprim further increase the risk for hyperkalemia.(1-8) Interaction risk and severity is greater in patients with multiple risk factors.

PATIENT MANAGEMENT: Assure adequate monitoring for hyperkalemia.(1-9) Patients receiving trimethoprim and a potassium supplement concurrently should have their serum potassium monitored at baseline and during treatment. Potassium supplementation may need to be held during antibiotic therapy, especially when other predisposing factors for hyperkalemia are present. Peak potassium increase due to trimethoprim is delayed and generally occurs after 4 or more days of therapy.(3,5,6) When possible, alternative antibiotic therapy should be considered in patients with one or more risk factors for hyperkalemia, e.g. renal impairment, heart failure, age > 65 years, and/or receiving additional meds associated with hyperkalemia risk (e.g. ACE inhibitors, angiotensin II receptor blockers, aldosterone antagonists, NSAIDs).(6)

DISCUSSION: A nested case-control study evaluated the risk for hyperkalemia in 19,194 patients with newly diagnosed heart failure. Over a mean follow-up of 3.9 years 2,176 cases of hyperkalemia (96.7% with a potassium value of => 5.5 mmol/L) were identified. Study authors found that trimethoprim independently increased the risk for hyperkalemia (OR 2.82; 95% CI 1.88-4.23).(4) A retrospective cohort study evaluated the risk for hospitalization due to hyperkalemia in 393,039 elderly women (age >65 years) treated for a urinary tract infection (UTI) with trimethoprim-sulfamethoxazole (TMP-SMX) or another antibiotic (amoxicillin, ciprofloxacin, norfloxacin, nitrofurantoin). Baseline renal function was similar in all five antibiotic groups. When compared with amoxicillin, TMP-SMX use was associated with a 3.3-fold increased risk for hospitalization due to hyperkalemia. Ciprofloxacin, norfloxacin, and nitrofurantoin were not associated with a risk for hyperkalemia.(9) A prospective study of hospitalized patients evaluated the risk for hyperkalemia in patients who received standard dose TMP-SMX (<= 320 mg trimethoprim, <= 1600 mg sulfamethoxazole daily) versus a control group who received a different antibiotic for at least 5 days. The two groups were similar in age, renal function and use of potassium altering medications. Serum potassium concentration increased in TMP-SMX patients by 1.21 mmol/L (CI 1.09 - 1.32 mmol/L), a change which was statistically significant in patients with a pretreatment serum creatinine = or > 1.2. In control patients, serum potassium decreased during antibiotic therapy (change not quantitated by authors).(5)

Serum Phosphate Level-Altering Drugs/Erdafitinib

SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.

MECHANISM OF ACTION: Medications that alter serum phosphate may interfere with interpretation of phosphate levels that are needed to determine initial erdafitinib dose.(1)

CLINICAL EFFECTS: Serum phosphate levels that are elevated by concomitant medications may result in an inappropriately low dose and decreased effectiveness of erdafitinib. Serum phosphate levels that are decreased by concomitant medications may result in an inappropriately high dose and increased toxicity from erdafitinib.

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: The manufacturer of erdafitinib states that agents that alter serum phosphate levels should be avoided before the initial dose increase period for erdafitinib based on serum phosphate levels (days 14 to 21).(1)

DISCUSSION: Concomitant administration of serum phosphate level-altering agents during the initial dose increase period of erdafitinib based on serum phosphate levels (days 14 to 21) may interfere with serum phospate levels and lead to incorrect dosing of erdafitinib.(1) Agents that may alter serum phosphate levels linked to this monograph include: aluminum carbonate, aluminum hydroxide, calcium acetate, calcium carbonate, calcium citrate, cod liver oil, ferric citrate, lanthanum, magnesium carbonate, magnesium hydroxide, potassium phosphate, sevelamer, sodium phosphate, sucroferric oxyhydroxide, tenapanor, and vitamin D.(1)

Urinary Alkalinizers/Dextroamphetamine Transdermal

SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.

MECHANISM OF ACTION: Urinary alkalinizers decrease the renal elimination of dextroamphetamine.(1)

CLINICAL EFFECTS: Concurrent use of dextroamphetamine and urinary alkalinizers may result in increased dextroamphetamine levels and side effects.

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: Coadministration of dextroamphetamine with urinary alkalinizing agents should be avoided.(1)

DISCUSSION: Concurrent use of alkalinizing agents with dextroamphetamine decreases the renal elimination of dextroamphetamine. Co-administration of these should be avoided because of the potential of increased actions of dextroamphetamine.(1)

Moderate Interaction: Assess the risk to the patient and take action as needed.

Agents That Increase Potassium/Baxdrostat

SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.

MECHANISM OF ACTION: The combination of baxdrostat and agents that increase potassium such as aldosterone receptor antagonists, potassium-sparing diuretics, and potassium supplements can have an additive effect on serum potassium levels.

CLINICAL EFFECTS: Concurrent use of baxdrostat and agents that increase potassium may result in hyperkalemia, which may be severe.

PREDISPOSING FACTORS: More frequent monitoring is recommended for patients at increased risk of hyperkalemia (e.g., patients greater than or equal to 65 years or age, those with diabetes mellitus or chronic kidney disease).(1)

PATIENT MANAGEMENT: The manufacturer of baxdrostat states concurrent use with medications that may increase potassium warrants more frequent monitoring of serum potassium.(1) Assess serum potassium prior to initiation of baxdrostat and monitor periodically during treatment. Correct serum potassium abnormalities prior to initiation of baxdrostat.(1) If hyperkalemia occurs, treat hyperkalemia and consider interrupting or discontinuing baxdrostat. Consider more frequent monitoring of serum potassium in patients who restart baxdrostat after experiencing hyperkalemia. Permanently discontinue baxdrostat if clinically significant hyperkalemia recurs.(1)

DISCUSSION: Baxdrostat may increase potassium. Concurrent use with aldosterone receptor antagonists, potassium-sparing diuretics, and potassium supplements may have additive effects on serum potassium levels, resulting in hyperkalemia. The risk of hyperkalemia can be reduced by monitoring serum potassium more frequently when baxdrostat is administered concomitantly with these agents.

Magnesium Salts, Injectable/Nondepolarizing Muscle Relaxants

SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.

MECHANISM OF ACTION: Magnesium may reduce postjunctional membrane neuromuscular blocking action of nondepolarizing muscle relaxants. Parenterally administered magnesium may potentiate the effects of the nondepolarizing muscle relaxants.

CLINICAL EFFECTS: Increased neuromuscular blockade with profound sedation, respiratory depression, coma, and/or death.

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: Monitor respiratory function when parenteral magnesium and nondepolarizing muscle relaxants are administered concurrently. Adjust the dose of the neuromuscular blocking agent accordingly. If concurrent use is necessary, monitor patients for unusual dizziness or lightheadedness, extreme sleepiness, slowed or difficult breathing, or unresponsiveness.

DISCUSSION: The effects of nondepolarizing muscle relaxants have been reported to be increased in laboratory animals and in humans by concomitant administration of magnesium sulfate. Respiratory depression has been reported.

Potassium Supplements/Aliskiren

SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.

MECHANISM OF ACTION: Aliskiren may decrease the renal excretion of potassium.

CLINICAL EFFECTS: Concurrent use of potassium supplements with aliskiren may result in hyperkalemia.

PREDISPOSING FACTORS: Impaired renal function; diabetes mellitus.

PATIENT MANAGEMENT: Monitor serum potassium and adjust the dosage accordingly in patients receiving concurrent therapy with potassium supplements and aliskiren.

DISCUSSION: Several studies have indicated that serum potassium levels increase when ACE inhibitors and ARB therapy is initiated and decrease when the drug is lowered. Increased potassium levels have also been seen with aliskiren. Based on this data, serum potassium levels should be monitored in patients receiving potassium supplements with aliskiren.

Potassium Supplements/Angiotensin Ii Receptor Blocker (ARB)

SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.

MECHANISM OF ACTION: Angiotensin II receptor blockers (ARBs) may decrease the renal excretion of potassium.

CLINICAL EFFECTS: Concurrent use of potassium supplements with ARBs may result in hyperkalemia.

PREDISPOSING FACTORS: Impaired renal function; diabetes mellitus.

PATIENT MANAGEMENT: Monitor serum potassium and adjust the dosage accordingly in patients receiving concurrent therapy with potassium supplements and ARBs.

DISCUSSION: Several studies have indicated that serum potassium levels increase when ARB therapy is initiated and decrease when the drug is lowered. Based on this data, serum potassium levels should be monitored in patients receiving potassium supplements with ARBs.

Potassium Supplements/Drospirenone

SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.

MECHANISM OF ACTION: Drospirenone has antimineralocorticoid activity and may cause hyperkalemia. Potassium supplements also increase potassium levels.(1)

CLINICAL EFFECTS: Concurrent use of drospirenone and potassium supplements may result in hyperkalemia.(1)

PREDISPOSING FACTORS: Renal insufficiency, hepatic dysfunction, adrenal insufficiency, and use of potassium-sparing diuretics, ACE inhibitors, angiotensin II receptor antagonists, heparin, and NSAIDs may increase potassium levels.(1)

PATIENT MANAGEMENT: Patients receiving drospirenone with a potassium supplement should have their serum potassium level checked during the first treatment cycle.(1)

DISCUSSION: Drospirenone has antimineralocorticoid activity comparable to 25 mg of spironolactone and may result in hyperkalemia. Concurrent use of potassium-supplements also increase potassium levels.(1)

Potassium Supplements/Selected Ace Inhibitors

SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.

MECHANISM OF ACTION: ACE inhibitors may decrease the renal excretion of potassium. MECHANISM OF ACTION: ACE inhibitors may decrease the renal excretion of potassium.

CLINICAL EFFECTS: Concurrent use of potassium supplements with ACE inhibitors may result in hyperkalemia. CLINICAL EFFECTS: Concurrent use of potassium supplements with ACE inhibitors may result in hyperkalemia.

PREDISPOSING FACTORS: Impaired renal function; diabetes mellitus. PREDISPOSING FACTORS: Impaired renal function; diabetes mellitus.

PATIENT MANAGEMENT: Monitor serum potassium and adjust the dosage accordingly in patients receiving concurrent therapy with potassium supplements and ACE inhibitors. PATIENT MANAGEMENT: Monitor serum potassium and adjust the dosage accordingly in patients receiving concurrent therapy with potassium supplements and ACE inhibitors.

DISCUSSION: Several studies have indicated that serum potassium levels increase when ACE inhibitors is initiated and decrease when the drug is lowered. Based on this data, serum potassium levels should be monitored in patients receiving potassium supplements with ACE inhibitors. Selected ACE inhibitors linked to this monograph include: alacepril, cilazapril, delapril, imidapril, perindopril, spirapril, temocapril, and zofenopril. DISCUSSION: Several studies have indicated that serum potassium levels increase when ACE inhibitors is initiated and decrease when the drug is lowered. Based on this data, serum potassium levels should be monitored in patients receiving potassium supplements with ACE inhibitors. Selected ACE inhibitors linked to this monograph include: benazepril, captopril, enalapril, fosinopril, lisinopril, moexipril, quinapril, ramipril, and trandolapril.

Urinary Alkalinizers/Quinidine

SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.

MECHANISM OF ACTION: Quinidine elimination is impaired by urinary alkalinization.

CLINICAL EFFECTS: Potentiation of quinidine effects may be observed.

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: Monitoring quinidine levels and cardiac function may be indicated. The quinidine dose may need to be adjusted when a urinary alkalinizer is started or stopped.

DISCUSSION: Additional documentation is necessary to confirm this potential interaction.

Urinary Alkalinizers/Sympathomimetics

SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.

MECHANISM OF ACTION: Unionized sympathomimetic amines will be reabsorbed into systemic circulation from the distal tubules of the kidneys.

CLINICAL EFFECTS: Enhanced sympathomimetic activity and increased risk of sympathomimetic toxicity.

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: Watch patient for enhanced sympathomimetic side effects when urinary alkalinizers are concomitantly used. A lower dose of certain sympathomimetics may be required.

DISCUSSION: Signs and symptoms of sympathomimetic toxicity include euphoria, confusion, delirium, hallucinations and nervousness.

There is no enhanced messaging for this drug.

There are no contraindication contraindications for this drug.

There are no severe contraindications for this drug.

There are no moderate contraindications for this drug.

There is no enhanced messaging for this drug.

There are no severe adverse reactions for this drug.

There are no less severe adverse reactions for this drug.

No enhanced messaging available.

No enhanced messaging available.

No enhanced messaging available.

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