Nutrilyte (sodium/potassium/magnes/calcium/chloride/acetate/gluconate)

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There are no contraindication interactions for this drug.

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

Intravenous Calcium Products/Digitalis Glycosides

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

MECHANISM OF ACTION: The mechanism of action of digitalis glycosides involves its ability to cause an increase in excitation-contraction coupling mediated through the effects of calcium. Excitable tissues in the heart experience inhibition of sodium/potassium ATPase (the membrane "sodium pump") by digitalis glycosides and so attain relatively higher intracellular sodium and lower potassium concentrations. Higher intracellular sodium concentrations facilitate exchange of extracellular calcium ions and the inward and internal flux of calcium results in modified transmembrane potentials and stronger contractions of cardiac muscle. Elevated extracellular concentrations of calcium after parenteral calcium salts further facilitate these inward calcium fluxes.

CLINICAL EFFECTS: Rapid administration of calcium via the intravenous route may result in digitalis toxicity, including arrhythmias.(1)

PREDISPOSING FACTORS: Low body weight, advanced age, impaired renal function, hypokalemia, hypercalcemia, and/or hypomagnesemia may increase the risk of digoxin toxicity.

PATIENT MANAGEMENT: In patients maintain on a digitalis glycosides, administer intravenous calcium slowly and with caution. If cardiac toxicity develops, supportive measures without additional antiarrhythmics may be sufficient.

DISCUSSION: Effects of digitalis glycosides on the heart are increased by elevated extracellular concentrations of ionic calcium. Intravenous administration of calcium salts during digitalis therapy may result in altered cardiac electrophysiologic activity such as tachycardia or arrhythmias. Oral calcium carbonate has not been shown to affect the bioavailability of oral digitalis.

Intravenous Calcium Products/Intravenous Ceftriaxone

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

MECHANISM OF ACTION: Intravenous ceftriaxone and intravenous calcium may form an insoluble precipitate if administered too closely together.

CLINICAL EFFECTS: Intravenous administration of calcium-containing products with intravenous ceftriaxone may have serious risks in all patients, especially in the neonate population. NEONATES: Intravenous administration of calcium-containing products within 48(1-2) to 120(3) hours of intravenous administration of ceftriaxone may result in damage to the lungs and/or kidneys in neonates. Fatalities in neonates have been reported.(1-7) OLDER CHILDREN and ADULTS: Sequential administration requires proper line flushing. Use within 48 hours may result in the formation of kidney stones in older children(5) and the formation of "sludge" in the gallbladder.(2) Simultaneous administration in patients older than 28 days may result in the formation of an insoluble ceftriaxone-calcium precipitate.(1-7)

PREDISPOSING FACTORS: Neonates, both preterm and term, may be a greatest risk of death from this interaction.(1-4) Young age may predispose patients to formation of ceftriaxone-calcium precipitates in the kidney.(5) High doses of ceftriaxone may also increase the risk of precipitates.(6)

PATIENT MANAGEMENT: The US manufacturer of ceftriaxone, Health Canada, and the US Food and Drug Administration (FDA) state that the concomitant use of ceftriaxone and intravenous calcium-containing products is contraindicated in neonates less than or equal to 28 days of age. Ceftriaxone should not be used in neonates less than or equal to 28 days of age if they are receiving or are expected to receive calcium-containing intravenous products.(2,3,7) The US manufacturer of ceftriaxone, Health Canada, and the US FDA state that in patients older than 28 days of age, ceftriaxone and calcium-containing products may be administered sequentially, provided the infusion lines are thoroughly flushed between infusions with a compatible fluid.(2,3,7) The US manufacturer of ceftriaxone, Health Canada, and the US FDA state that ceftriaxone must not be administered simultaneously with intravenous calcium-containing solutions via a Y-site in any age group.(2,3,7)

DISCUSSION: Isolated reports of neonatal (both term and preterm infants) deaths have been associated with ceftriaxone-calcium precipitates in the lungs and kidneys. A total of 7 cases have been reported to the FDA, resulting in 5 deaths. All 5 deaths were in neonates of 3 weeks or less in age. Six of the 7 patients received calcium gluconate, 1 received calcium via hyperalimentation.(6) In some cases, ceftriaxone and the calcium product were administered by different routes,(1) lines,(2) and/or at different times.(1,2) Reports of a ceftriaxone-calcium salt precipitate in the gall-bladder have also been reported.(2) In in vitro studies in adult and neonatal plasma, ceftriaxone recovery was examined with ceftriaxone concentrations up to 1 mM (in excess of concentrations seen with 2 g ceftriaxone infused over 30 minutes) and calcium concentrations up to 12 mM (48 mg/dL). Ceftriaxone recovery was reduced with calcium concentrations of 6 mM (24 mg/dL) in adult plasma and 4 mM (16 mg/dL) in neonatal plasma. This may indicate ceftriaxone-calcium precipitation formation.(2,7) There have been no reports associated with concurrent use of oral calcium products and the US manufacturer of ceftriaxone states that there is no risk with oral calcium products or use of intramuscular ceftriaxone.(4)

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)

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/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.

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• Digitalis toxicity
• Familial hyperkalemic periodic paralysis
• Hypercalcemia
• Hyperchloremia
• Hyperkalemia

• Chronic kidney disease stage 4 (severe) GFR 15-29 ml/min
• Chronic kidney disease stage 5 (failure) GFr<15 ml/min
• Complete atrioventricular block
• Hypercalcinuria
• Hyporeninemic hypoaldosteronism
• Kidney disease with reduction in glomerular filtration rate (GFr)
• Myotonia congenita - autosomal dominant form
• Severe burns

• Chronic kidney disease stage 3B (moderate) GFR 30-44 ml/min
• Kidney disease with reduction in glomerular filtration rate (GFr)
• Sarcoidosis

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Less Frequent

• Cardiac arrhythmia
• Dyspnea
• Hyperkalemia
• Hypoesthesia

Rare or Very Rare

• Anaphylaxis
• Angioedema
• Bradycardia
• Cardiac arrest
• Complete atrioventricular block
• Dermal necrosis
• Encephalopathy
• Extravasation injury
• Hyperchloremic acidosis
• Hypertension
• Hyponatremia
• Phlebitis after infusion
• Tachycardia
• Thrombophlebitis
• Tingling sensation of hands or feet
• Ventricular fibrillation

More Frequent

• Hypervolemia

Rare or Very Rare

• Abdominal pain with cramps
• Acute abdominal pain
• Chest pain
• Chills
• Diarrhea
• Fever
• Injection site sequelae
• Nausea
• Pruritus of skin
• Skin rash
• Skin ulcer
• Vomiting

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