Pediatric patients may require magnesium replacement to treat life-threatening emergencies such as torsades de pointe or asthma exacerbations, as well as for the general replacement of magnesium in patients with hypomagnesemia. Clinicians must be aware of recommendations for magnesium administration as the route, dose, timing of administration, and formulation of magnesium can differ for each indication. It is imperative for clinicians to ensure that magnesium is appropriately administered to effectively treat the presenting indication and avoid adverse effects.
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OBJECTIVES
- 1.State the physiology and associated symptoms of magnesium derangements.
- 2.Describe the role of magnesium in the treatment of children with Torsades de Pointe and asthma.
- 3.Describe the pharmacologic treatment of hypomagnesemia.
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INTRODUCTION
Magnesium is the second most abundant intracellular cation in the body and the fourth most abundant cation. Sixty percent of total body magnesium is stored in bone, 20% is located in skeletal muscle, and the remaining 20% is distributed in various organ tissues, including the kidney, liver, and heart (
Grober, Schmidt and Kisters, 2015
). Approximately 0.3% of magnesium is found in the serum (Grober, Schmidt and Kisters, 2015
). Therefore, the determination of the serum magnesium concentration remains the best readily available test for magnesium deficiency, although it provides only an estimate of total body magnesium stores.Magnesium homeostasis is primarily regulated through passive absorption in the gastrointestinal (GI) tract and through excretion and reabsorption by the kidneys (
Grober, Schmidt and Kisters, 2015
). When serum magnesium levels decline, the kidneys reabsorb more magnesium to maintain serum levels, whereas high serum levels will result in an increase in magnesium excretion (Grober, Schmidt and Kisters, 2015
). Magnesium is a cofactor in many enzymatic reactions, including many adenosine triphosphate (ATP)-generating reactions. Through its role in ATP generation, magnesium plays key roles in muscle contraction and relaxation, cell membrane stabilization, heart rhythm, and vascular tone (Hansen & Bruserud, 2018
; - Hansen B.A.
- Bruserud O.
Hypomagnesemia in critically ill patients.
Journal ofIntensive Care. 2018; 621https://doi.org/10.1186/s40560-018-0291-y
Jahnen-Dechent and Ketteler, 2012
). In addition, magnesium has been found to be a regulator of immune function (Hansen & Bruserud, 2018
). Hypomagnesemia may result from a lack of absorption and intake through GI losses, malnutrition, or malabsorption. Certain drug therapies, such as loop and thiazide diuretics, aminoglycosides, cisplatin, pentamidine, and cyclosporine, may also lead to a loss of magnesium through renal wasting (- Hansen B.A.
- Bruserud O.
Hypomagnesemia in critically ill patients.
Journal ofIntensive Care. 2018; 621https://doi.org/10.1186/s40560-018-0291-y
Siddappa, Dandinavar, Ratageri and Wari, 2019
). Hypomagnesemia may potentiate further electrolyte derangements, such as hypokalemia and hypocalcemia, and disturbances to the cardiac conduction system leading to dysrhythmias. Patients with severe hypomagnesemia may experience neuromuscular hyperexcitability (Grober, Schmidt and Kisters, 2015
). Furthermore, hypomagnesemia in critically ill pediatric patients has been associated with an increased mortality rate and increased length of pediatric intensive care unit stay (Siddappa, Dandinavar, Ratageri and Wari, 2019
). This review article provides an overview of key disease states in pediatric patients in which magnesium is part of the treatment. The treatment of hypomagnesemia and hypermagnesemia will be described, with a review of dosing and timing of magnesium administration.TORSADES DE POINTE
Torsades de pointe is a ventricular tachycardia characterized by the QRS complexes twisting around the isoelectric baseline. Torsades de pointe results from a prolonged repolarization phase and early afterdepolarizations (
Cohagan & Brandis, 2020
; Thomas and Behr, 2016
). The prolonged repolarization phase typically results from either medications or congenital conditions inhibiting the potassium channel of myocardial cells (Banai and Tzivoni, 1993
; Cohagan & Brandis, 2020
). Bradycardia and electrolyte imbalances, particularly potassium and magnesium, can also increase the risk of developing torsades de pointe. Although torsades de pointe may be self-limiting, it can lead to further arrhythmias such as ventricular tachycardia or ventricular fibrillation (Banai and Tzivoni, 1993
).According to case reports, torsades de pointe is typically seen with pediatric patients taking medications that cause QT prolongation with additional risk factors (e.g., structural heart disease, left ventricular dysfunction, starvation, hypokalemia, and renal or hepatic failure;
Esch and Kantoch, 2008
). Congenital factors, such as acquired long QT syndrome, a syndrome that functionally inhibits the influx of potassium into the cardiac membrane, may also put a pediatric patient at risk for torsades de pointe (Hanash and Crosson, 2010
). Magnesium is used in the management of torsades de pointe to stabilize the cardiac membrane through facilitating potassium influx, as magnesium is a cofactor for the sodium-potassium-ATPase (Cohagan & Brandis, 2020
; Thomas and Behr, 2016
). Magnesium may function to suppress early afterdepolarizations through blockage of the calcium channel in myocardial cells (Kaye and O'Sullivan, 2002
).The dosing of magnesium for the treatment of torsades has been more commonly evaluated in adult patients (
Banai and Tzivoni, 1993
; Perticone, Adinolfi and Bonaduce, 1986
) with small studies and case reports evaluating magnesium sulfate treatment in pediatric patients. In a study of six pediatric patients (average age 64 months, range 0–109 months) presenting with torsades de pointe, torsades de pointe stopped with a magnesium sulfate bolus of 6.1 ± 4.2 mg/kg (range, 2.3–12 mg/kg; Hoshino et al., 2004
). One patient required an additional bolus to receive 30 mg/kg to completely abolish the rhythm (Hoshino et al., 2004
). In this study, the patients also were given a magnesium infusion ranging from 0.3 to 1.0 mg/kg/hr after the bolus for a minimum of 48 hr (Hoshino et al., 2004
). The American Heart Association Pediatric Advanced Life Support guideline recommends magnesium sulfate 50 mg/kg/dose (maximum 2 g/dose) infused over 10 min in pediatric patients with torsades de pointe (de Caen et al., 2015
).ASTHMA
Recent literature has postulated the use of intravenous (IV) magnesium to treat acute asthma exacerbations, and the 2019 Global Initiative for Asthma guideline recommends the administration of IV magnesium sulfate in patients with severe asthma exacerbations with an inadequate response to intensive initial treatment (
Global Initiative for Asthma, 2019
). Magnesium is proposed to be beneficial in patients with asthma exacerbations through the blockage of calcium channels resulting in bronchial smooth muscle relaxation (Wong, Lee, Tuener and Rehder, 2014
). Magnesium may also play a role as an antiinflammatory agent through attenuating neutrophil activity (Cairns and Kraft, 1996
). A Cochrane review assessed the outcomes of pediatric patients receiving IV magnesium sulfate in the emergency department (ED) and found a 68% reduction in the hospital admission rate in patients given magnesium sulfate (odds ratio = 0.32, 95% confidence interval = [0.14, 0.74]), this result; however, had statistically significant heterogeneity (I2 = 63%, p = .07) and only included three studies with 115 patients (Griffiths and Kew, 2016
).A wide range of dosing strategies for IV magnesium to treat asthma exacerbations have been used in clinical trials. A retrospective review that assessed prescribing patterns of IV magnesium for acute asthma exacerbations in pediatric patients at four hospitals found the median magnesium sulfate dose was 40 mg/kg over an average of 20 min; with doses ranging from 20 to 50 mg/kg over 20–180 min
Kokotajlo et al., 2014
). A randomized double-blinded, placebo-controlled trial by Ciarallo, Sauer and Shannon, 1996
assessed 31 pediatric patients (aged 6–18 years) being treated for an acute asthma exacerbation with either magnesium sulfate or a saline solution (Ciarallo, Sauer and Shannon, 1996
). Patients treated with IV magnesium sulfate were found to have greater improvement in short-term pulmonary function tests than the placebo group. Magnesium sulfate was dosed at 25 mg/kg (maximum 2 g) over 20 min (Ciarallo, Sauer and Shannon, 1996
). A follow-up study assessed a higher magnesium sulfate dose with randomization of 30 pediatric patients with a moderate to severe asthma exacerbation to receive either magnesium sulfate 40 mg/kg (maximum 2 g) or placebo (Ciarallo, Brousseau and Reinert, 2000
). This higher-dose strategy resulted in similar improvements in pulmonary function tests and quicker improvement than the previously used lower-dosing strategy (Ciarallo, Brousseau and Reinert, 2000
).Gürkan et al., 1999
randomized 20 children experiencing a moderate to severe asthma exacerbation to either placebo or magnesium sulfate 40 mg/kg (maximum 2 g) over 20 min, and patients in the IV magnesium group had significantly improved peak expiratory flow rates. A higher dosing strategy of magnesium sulfate 100 mg/kg over 35 min was assessed in a randomized, double-blind, placebo-controlled study (Devi et al., 1997
). This study assessed 47 children presenting to an ED with acute severe asthma and found magnesium sulfate (in addition to aminophylline) to improve peak expiratory flow rates. The higher dose of magnesium sulfate 100 mg/kg over 35 min only had minimal adverse effects, providing some evidence to support a higher dosing strategy for magnesium sulfate in the treatment of acute asthma exacerbations (Devi et al., 1997
).Magnesium administration as a high-dose continuous infusion has also been studied. As higher magnesium serum concentrations result in increasing renal clearance, this strategy is thought to maintain maximum serum levels of magnesium over an extended period (
Irazuzta and Chiriboga, 2017
). This strategy had positive results in a study of 38 patients randomized to either magnesium sulfate 50 mg/kg over 1 hr (bolus group) or magnesium sulfate 50-mg/kg/hr over 4 hr (continuous infusion group). The study found significantly more patients in the continuous infusion group to be discharged home at 24 hr (Irazuzta, Paredes, Pavlicich and Domínguez, 2016
).More recently, interest has grown in the use of inhaled nebulized magnesium sulfate in the setting of acute severe asthma. (
Su, Li and Gai, 2018
) performed a meta-analysis of clinical trials using either IV magnesium sulfate or nebulized magnesium sulfate. Ten randomized and quasi-randomized trials (six IV and four nebulized) were included (Su, Li and Gai, 2018
). They concluded thatIV magnesium sulfate is an effective treatment in children, with the pulmonary function significantly improved and hospitalizations and further treatments decreased. But nebulized magnesium sulfate showed no significant effect on respiratory function or hospital admission and further treatments were needed (
Su, Li and Gai, 2018
).A recent Cochrane review published in 2017 reviewed 25 clinical trials (
Knightly et al., 2017
). Nine trials involved adults, four included adult and pediatric patients, and eight studies enrolled pediatric patients, and they concluded that well-designed clinical trials using nebulized magnesium have failed to demonstrate clinically important benefits; however, it is not associated with an increase in adverse events (Knightly et al., 2017
).The
National Heart, Lung, & Blood Institute, 2007
asthma guidelines recommend a magnesium sulfate dose of 25–75 mg/kg/dose (maximum 2 g/dose) infused over 20 min for patients with moderate to severe asthma. The 2019 Global Initiative for Asthma asthma guidelines recommends 40–50 mg/kg/dose (maximum 2 g/dose) infused over 20 min in children age 2 years or greater with severe asthma exacerbations. Recent inhaled magnesium sulfate studies have failed to demonstrate benefit compared with administration of IV magnesium sulfate. A Cochrane review demonstrated a 68% reduction in hospital admission in pediatric patients administered magnesium sulfate for acute severe asthma; improvements in ED management of severe asthma could have a significant economic impact in the treatment of pediatric asthma (National Heart, Lung and Blood Institute (2007), National Asthma Education and Prevention Program. Expert Panel Report 3: Guidelines for the Diagnosis and Management of Asthma. https://www.nhlbi.nih.gov/sites/default/files/media/docs/EPR-3_Asthma_Full_Report_2007.pdf. Accessed June 29, 2021.
Griffiths and Kew, 2016
). Well-designed ED asthma management pathways, including the use of magnesium sulfate for severe patients, may facilitate early discharge, reduce hospitalization rates, and is cost-effective.HYPOMAGNESEMIA TREATMENT
Hypomagnesemia typically occurs because of either GI or renal magnesium loss. Gastrointestinal losses may be the result of diarrhea, malabsorption, or steatorrhea. Renal magnesium loss can result from medications, including cisplatin, loop diuretics, thiazide diuretics, aminoglycosides, amphotericin B, calcineurin inhibitors, cyclosporine, or pentamidine (
Kaplinsky and Alon, 2013
; Martin, González and Slatopolsky, 2009
). Congenital cases of hypomagnesemia have been reported because of a mutation in the TRPM6 gene, resulting in decreased intestinal magnesium absorption. Gitelman and Bartter syndromes have been associated with renal magnesium wasting (Martin, González and Slatopolsky, 2009
). Pediatric patients with malignancies are prone to hypomagnesemia as hypomagnesemia may result from several oncological medications and result from GI losses and poor nutrition, both of which are commonly experienced in these patients.Symptoms of hypomagnesemia are summarized in Table 1. Clinicians should be aware of concomitant electrolyte disturbances associated with hypomagnesemia. The most common disturbance is hypokalemia occurring in 40%–60% of cases (
Grober, Schmidt and Kisters, 2015
). Hypokalemia is caused in part by the underlying cause of hypomagnesemia, such as diuretic therapy and diarrhea. However, there is evidence that the hypomagnesemia itself may cause increased potassium secretion in the loop of Henle and the cortical collecting tubule.TABLE 1Symptoms of hypomagnesemia
| Symptom category | Symptoms |
|---|---|
| Neuromuscular irritability | Hyperactive deep tendon reflexes Muscle cramps Muscle fibrillation Trousseau and Chvostek signs Dysarthria and dysphagia from esophageal dysmotility |
| CNS hyperexcitability | Irritability and combativeness Disorientation Psychosis Ataxia Nystagmus Vertigo Seizures (levels < 1 mEq/L) |
| Cardiac arrhythmias | Paroxysmal atrial and ventricular arrhythmias Torsades de pointes |
| Neonates | Apnea Weakness Seizures Jitteriness |
| Electrolyte disorders | Hypocalcemia Hypokalemia |
Note. CNS, central nervous system.
Hypokalemia is thought to occur because the sodium-potassium-ATPase pump is dependent on adequate circulating magnesium to function properly. Potassium secretion into the loop of Henle and cortical collecting tubule is mediated by ATP-inhibitable potassium channels. The reduction in cellular magnesium leads to a decline in ATP activity and a concomitant increase in potassium channels. This leads to enhanced urinary potassium losses. Hypokalemia in this setting is relatively refractory to potassium supplementation. Serum magnesium must be replaced before administering potassium replacement for potassium replacement to be successful. Hypocalcemia associated with severe hypomagnesemia (< 1 mg/100 mL) is thought to occur because the calcium cannot be properly mobilized from the bone without the action of parathyroid hormone, which is dependent on circulating magnesium.
Serum magnesium levels less than 1.5 mg/100 mL are considered low and may warrant replacement, particularly if the patient is symptomatic. Magnesium can be replaced orally unless the patient has severely low magnesium levels (Mg < 1.0 mg/100 mL), malabsorption is suspected as the cause of the hypomagnesemia, or the patient has symptoms of hypomagnesemia, in which case the IV route of replacement is preferred. Magnesium oxide is typically used for oral replacement at a dose of 10–20 mg/kg/dose of elemental magnesium (maximum 2 g) up to four times per day. However, magnesium oxide is only commercially available as a 140 mg capsule and 400 mg tablet. Therefore, in pediatric patients, other salt forms may be used to provide the same 10–20 mg/kg/dose of elemental magnesium (Table 2). Magnesium hydroxide is commonly used to treat infants and small children requiring oral magnesium replacement, as it is a liquid that is both sold over the counter and inexpensive. Caution should be used in administering oral magnesium in patients with diarrhea as oral magnesium may worsen diarrhea and not be optimally absorbed. For IV replacement, magnesium sulfate is typically used and can be given as 25–50 mg/kg/dose (maximum 2 g/dose) of magnesium sulfate every 4–6 hr (every 8 hr in neonates) as needed to replete serum magnesium levels (
Kaplinsky and Alon, 2013
). As renal impairment can lead to magnesium accumulation, these dosing recommendations should be decreased by 50% in patients with renal insufficiency. In patients experiencing life-threatening symptoms from dangerously low magnesium levels (i.e., seizures), a more aggressive replacement is warranted. In these cases, magnesium sulfate should be given magnesium sulfate 50 mg/kg (maximum 2 grams/dose) IV push over 1−5 min. Then, assuming the patient has total body depletion of magnesium, they should receive magnesium sulfate 125 mg/kg/day over 24 hr, then 75 mg/kg/day for 3–5 days. Rapid administration of magnesium sulfate is not very helpful in restoring total body deficits. The acute increase in the serum magnesium concentration after a rapid administration exceeds the renal threshold, and rapid renal excretion of magnesium occurs. Therefore, if the patient is not symptomatic, slower administration of magnesium may improve uptake in the body. Suggested rates for optimal magnesium retention are 25 mg/kg (maximum 1 g) per hr (Kraft, Btaiche, Sacks and Kudsk, 2005
). The maximum concentration of magnesium sulfate to be given in a peripheral IV is 60 mg/mL, and the maximum amount of magnesium sulfate to be given via a central line is 200 mg/mL. Serum magnesium levels should be monitored daily in patients receiving IV replacement.TABLE 2
| Elemental magnesium per 1 g of salt | Commercially available formulations | |||
|---|---|---|---|---|
| Magnesium salt | mmol | mg | mEq | Amounts of elemental magnesium |
| Magnesium oxide | 24.8 | 603.25 | 49.64 | 140 mg capsule = 84 mg or 7 mEq 200 mg tablet = 120.5 mg = 9.9 mEq 400 mg tablet = 241 mg or 19.8 mEq Miscellaneous: 420 and 500 mg tablets |
| Magnesium gluconate | 2.22 | 54 | 4.44 | 200 mg/mL = 10.8 mg/mL or 0.96 mEq/ml Tablet: 500 mg (27 mg el) |
| Magnesium/aluminum hydroxide (Maalox Plus or Mylanta II) | 17 | 412.5 | 34 | 80 mg/mL = 33 mg/ml or 2.75 mEq/mL |
| Magnesium hydroxide (milk of magnesia) | 17 | 412.5 | 34 | 80 mg/ml = 33 mg/mL or 2.75 mEq/mL |
| Magnesium sulfate (parenteral) | 4.06 | 98.7 | 8.12 | IV solution (50%): 2, 10, 20, or 50 mL Premade bags: 1, 2 and 4 g Capsules: 70 and 140 mg |
| Magnesium carbonate | 10.5 | 254.77 | 21 | Liquid: 54 mg/5 mL |
| Magnesium citrate | 6.59 | 160 | 13.7 | 1.745 g/30 mL; 296 mL bottle |
Note. IV, intraveneous.
ADVERSE REACTIONS
Although normal magnesium levels are 1.5–2.2 mg/100 mL in pediatric patients, children typically do not experience symptoms of hypermagnesemia until serum levels are greater than or equal to 4 mg/dL. Once serum magnesium levels are greater than 4 mg/dL, patients may start to experience symptoms such as nausea, vomiting, flushing, and headaches. As serum magnesium levels increase above 6 mg/dL, patients may begin to experience more serious adverse reactions such as loss of deep tendon reflexes, hypotension, electrocardiogram changes, and muscle paralysis (
Jhang et al., 2013
; Kraft, Btaiche, Sacks and Kudsk, 2005
). These high serum levels are most common in patients with renal failure taking supplemental magnesium; however, case reports exist of pediatric patients experiencing fatal overdoses of magnesium without known renal impairment (McGuire, Kulkarni and Baden, 2000
). A summary of magnesium levels and associated symptoms can be located in Table 3.TABLE 3Manifestations of altered serum magnesium concentrations
| Magnesium level | |||
|---|---|---|---|
| Mg/dL | mEq/L | Mmol/L | Manifestations |
| < 1.2 | < 1 | < 0.5 | Tetany Seizures Arrhythmias |
| 1.2–1.8 | 1–1.5 | 0.5–0.75 | Neuromuscular irritability Hypocalcemia Hypokalemia |
| 1.8–2.5 | 1.5–2.1 | 0.75–1.05 | Normal magnesium level |
| 2.5–5 | 2.1–4.2 | 1.05–2.1 | Typically asymptomatic |
| 5–7 | 4.2–5.8 | 2.1–2.9 | Lethargy Drowsiness Flushing Nausea and vomiting Diminished deep tendon reflexes |
| 7–12 | 5.8–10 | 2.9–5 | Somnolence Loss of deep tendon reflexes Hypotension ECG changes |
| > 12 | > 10 | > 5 | Complete heart block Cardiac arrest Apnea Paralysis Coma |
Note. ECG, electrocardiogram.
Oral magnesium is generally well tolerated when given within a normal dosing range, with the most common adverse effect being gastrointestinal disturbances (
Taketomo, hodding and Kraus, 2020
). For IV administration of magnesium, most studies assessing high-dose IV magnesium infusions have shown few adverse effects. Out of 53 patients receiving an IV magnesium sulfate infusion in a retrospective review by Kokotajlo et al., 2014
, only one patient (receiving 40 mg/kg over 1 hr) experienced an adverse reaction. This patient became hypotensive; however, once the IV infusion rate was subsequently decreased from 1 to 5 hr, the hypotension resolved (Kokotajlo et al., 2014
). In another study assessing a higher dosing strategy in asthma patients, magnesium sulfate 100 mg/kg over 35 min only resulted in minor adverse effects of epigastric warmth (12.5%), pain (16.6%), and tingling and numbness (12.5%) at the infusion site. Each of these side effects started within 2–3 min after initiating the infusion and then subsided soon after the infusion started. No other significant side effects (hypotension or respiratory depression) were noted in this study (Devi et al., 1997
). Another study by Pruikkonen et al., 2018
assessed magnesium sulfate 40 mg/kg over 20 min versus placebo in pediatric patients with severe wheezing. Out of 31 patients receiving magnesium sulfate, only one patient experienced a minor adverse effect of facial redness and infusion site erythema (Prukkoinen et al., 2018). Finally, in a study by Irazuzta, Paredes, Pavlicich and Domínguez, 2016
in which patients received high-dose magnesium infusions up to 50 mg/kg/hr over 4 hr (maximum 8,000 mg/4 hr), no adverse effects, including hypotension, were reported (Irazuzta, Paredes, Pavlicich and Domínguez, 2016
).FORMULATIONS
When using different formulations of magnesium, it is imperative to know how much elemental magnesium the patient is receiving. In addition, when interpreting dosing recommendations, it is crucial to know whether the provided dose is referencing total milligrams of the formulation or milligrams or milliequivalents of elemental magnesium. Table 2 contains a list of common formulation of magnesium and their respective amounts of elemental magnesium.
HYPERMAGNESEMIA
Hypermagnesemia is defined as a serum magnesium concentration greater than 2.4 mg/dL. Elevated magnesium is rare; the most common causes are renal insufficiency and iatrogenic causes such as over-replacement, treatment of eclampsia, laxative abuse, and lithium toxicity. Adrenal insufficiency and hyperparathyroidism may also contribute to hypermagnesemia. Common symptoms of hypermagnesemia (Table 3) include nausea, vomiting, paresthesia, dysarthria, loss of deep tendon reflexes, altered mental status, and seizures. Treatment of hypermagnesemia depends on the underlying cause. For asymptomatic end-stage renal disease patients who have missed a treatment session (hemodialysis) or have been nonadherent with home peritoneal dialysis, the initial treatment is magnesium restriction, loop diuretics, and dialysis. In severe hypermagnesemia, administration of IV calcium can reverse the loss of deep tendon reflexes, hypotension, and respiration depression. IV calcium can be given as either calcium chloride (20 mg/kg/dose; maximum dose 1 g) or calcium gluconate (100 mg kg/dose; maximum 3 g/dose) intravenously over 5–10 min. Doses may be repeated every 10 min until symptoms resolve (
Taketomo, hodding and Kraus, 2020
).Magnesium is an essential element as it plays an important role in muscle contraction and relaxation, cell membrane stabilization, heart rhythm, vascular tone, and a cofactor in many enzymatic reactions (
Hansen & Bruserud, 2018
). Magnesium replacement is warranted in pediatric patients that show symptoms of hypomagnesemia or with serum magnesium levels < 1.5 mEq/L. Pediatric patients may also receive magnesium for torsades de pointe and asthma exacerbations. As the amount of elemental magnesium varies among differing magnesium formulations, it is imperative for the provider to ensure that the amount of elemental magnesium being given aligns with the dosing recommendation. Correction of magnesium deficits should precede attempts to correct hypocalcemia or hypokalemia. Hypermagnesemia is rare, but its causes are frequently iatrogenic. Stopping the offending agent and administration of rescue doses of IV calcium allow for renal elimination of magnesium, or the use of renal replacement therapies can be used in patients with renal dysfunction if medically necessary.- Hansen B.A.
- Bruserud O.
Hypomagnesemia in critically ill patients.
Journal ofIntensive Care. 2018; 621https://doi.org/10.1186/s40560-018-0291-y
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Biography
Sarah Anderson, Pharmacy Resident, New Hanover Regional Medical Center, Wilmington, NC.
Elizabeth Farrington, Clinical Pharmacist, Pediatrics, New Hanover Regional Medical Center, Wilmington, NC.
Article info
Footnotes
Conflicts of interest: None to report.
The authors of this paper declare no concerning possible financial or personal relationships with commercial entities (or their competitors) that may be referenced in this presentation.
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Copyright
Copyright © 2021 by the National Association of Pediatric Nurse Practitioners. Published by Elsevier Inc. All rights reserved.
