Research Article

Hypomagnesemia: A Clinical Approach in Chronically Ill Patients

with Multiple Comorbidities
Hassan Nagy1*, Sara Ersoezlue2, Raveena Kataria3, Harendra Kumar4, Ayush Anand5
1FM Resident at MidHudson- Institute for Family Health, NY, USA

24th Year MBBS Student at Dow University of Health Sciences, Karachi, Pakistan
3Clinical Microbiology Tutor at MIMER Medical College, Pune, India

4BP Koirala Institute of Health Sciences, Dharan, Nepal

5Cardiologist, Attending at University Hospital Zurich, Department of Internal Medicine, Switzerland

*Correspondence author: Hassan Nagy, FM Resident at MidHudson- Institute for Family Health, NY, USA; Email: hassmnagy@gmail.com

Citation: Nagy H, et al.
Hypomagnesemia: A Clinical
Approach in Chronically Ill Patients
with Multiple Comorbidities. Jour
Clin Med Res.. 2023;4(1):1-14.
http://dx.doi.org/10.46889/JCMR.20
23.4103
Received Date: 14-01-2023
Accepted Date: 05-02-2023
Published Date: 12-02-2023
Copyright: © 2023 by the authors.
Submitted for possible open access
publication under the terms and
conditions of the Creative Commons
Attribution (CCBY) license
(https://creativecommons.org/li
censes/by/4.0/).
Abstract
Magnesium (Mg) is vital for many biochemical and physiological metabolic processes in the
normally functioning human body physiology. Hypomagnesemia in hospitalized patients is
particularly common among those with chronic illnesses with preexisting comorbidities and
maybe other electrolyte abnormalities. Hypomagnesemia can cause fatal complications that lead
to severe symptoms or death. However, it is often underdiagnosed. Hypomagnesemia in this
cohort of patients prompts proper diagnosis and adequate correction.
Mg deficiency in chronically ill patients can be caused by multiple etiologies mainly due to
gastrointestinal and/or renal disorders or is associated with other electrolyte abnormalities like
hypokalemia and hypocalcemia. Consequently, it could lead to possible severe neuromuscular
and cardiovascular complications. Magnesium levels in the serum can be easily assessed and
corrected by repletion therapy. More clinical trials and investigations on the repletion therapy
and treatment strategies are warranted.
Hospitalized patients with chronic illnesses and comorbidities are at higher risks of
hypomagnesemia whether they present with low Magnesium serum levels only or associated
with clinical manifestations. Those patients should receive Magnesium repletion therapy and
continue to be monitored for serum Magnesium levels until it becomes within the normal range.
Keywords: Magnesium Deficiency; Hypomagnesemia; Electrolyte Abnormalities; Chronically
Ill Patients; Cardiac Arrhythmias; ICU Hypomagnesemia; High Magnesium Containing Foods;
Magnesium Repletion Therapy

Introduction
Magnesium is a divalent intracellular cation that is vital for many biochemical and physiological metabolic processes in the
human body including neuromuscular conduction, muscle and myocardial contraction, energy production, bone development,
immunological functions, as well as glycemic control and blood pressure regulation [1]. Therefore, the body requires a
maintained serum magnesium level within the physiologic range of 0.7-2.4 mg/dL (0.7-1.0 mmol/L), which is mainly regulated
by gastrointestinal uptake and renal excretion [2,3].

However, compared to other electrolytes magnesium disbalances are underdiagnosed, which is why magnesium is also referred
to as the “forgotten electrolyte” [4,5].

Hypomagnesaemia can be attributed to a wide variety of chronic and acute illnesses including gastrointestinal and renal diseases
that lead to loss of magnesia, alcohol abuse, certain drugs such as amphotericin, diuretics, proton-pump inhibitors and digitoxin
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as well as redistribution in acute severe diseases, cardiopulmonary surgeries, or refeeding syndrome [6].

Hospital-acquired hypomagnesaemia is a common phenomenon that is associated with a wide range of disorders and can cause
severe symptoms and fatal complications, in particular cardiac arrhythmias. It is particularly common among critically ill
patients [5]. Importantly, hypomagnesemia has recently been shown to be associated with a significantly higher in-hospital
mortality (4%) compared to patients with normal magnesium levels (1.5%) [6].

Epidemiology
The prevalence of hypomagnesemia in the general population is approximately 2% [6]. However, among hospitalized patients’
higher rates were reported [5,6]. Recently, Cheungpasitporn, et al., 2020, found that 15% of patients with normal magnesium
levels on admission developed hospital-acquired hypomagnesemia in their large study on 26,020 adult hospitalized patients at
the Mayo Clinic [5]. In another recent large single-center study of 12,696 hospitalized patients in Italy, the overall prevalence was
found to be 8%, with a higher frequency among females (53%) and patients over 65 years (59%) [7]. Previous smaller studies
reported hypomagnesemia rates ranging from 9-65%. Particularly high rates were found in critically ill ICU patients [5].

Pathoetiology
A negative magnesium balance brought on by a reduction in oral intake, an increase in gastrointestinal or renal losses, or a
transfer of magnesium from the extracellular to the intracellular compartment leads to hypomagnesemia. Rarely does
hypomagnesemia have a genetic etiology; instead, it is often an acquired disease [1,8,9]. Magnesium is a cofactor in several
biological processes. Sodium, calcium and potassium are just a few of the other electrolytes that magnesium has an instant impact
on. Low magnesium levels may be caused by renal and gastrointestinal losses as previously mentioned [10-13].

Magnesium homeostasis includes the kidneys (mainly via the proximal tubule, the thick ascending loop of Henle and the distal
tubule), the small bowel (mostly through the jejunum and ileum) and the bones. Hypomagnesemia occurs when any factor a
drug or a clinical situation disturbs the magnesium homeostasis. Table 1 shows a list of common causes. Magnesium and calcium
are related; hence, a magnesium deficit may produce hypocalcemia. Magnesium shortage reduces the production of Parathyroid
Hormone (PTH) via inhibiting the magnesium-dependent adenyl cyclase, which produces Cyclic Adenosine Monophosphate
(cAMP) (PTH). Consequently, there is a decrease in calcium levels since PTH controls calcium levels. Magnesium is also involved
in the regulation of the vascular tone and cardiac rhythm, which is why hypomagnesemia increases the risk of cardiac
arrhythmias.

Low Intake Medications Gastrointestinal Losses Renal Losses Redistribution

• Dietary • Loop and thiazide • Acute diarrhea • Familial • Refeeding
intake diuretics • Chronic diarrhea disorders (e.g., syndrome
• Starvation • Proton pump • Nasogastric Bartter • Acute
• Alcohol use inhibitors suction syndrome) pancreatitis
disorder • Aminoglycoside Fistulas • Drugs (see
• Critically ill antibiotics • Malabsorption above)
patients • Amphotericin B • Acute pancreatitis • Hypercalcemia
receiving • Digitalis • Gastric bypass • Alcohol abuse
total • Chemotherapeutic surgery
parenteral drugs, such as • Drugs
nutrition cisplatin,
cyclosporine,
tacrolimus
Table 1: Common causes of hypomagnesemia.

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Clinical Encounter
Although clinically relevant signs and symptoms do not develop until serum levels fall below 0.5 mmol/L (1.2 mg/dL),
hypomagnesemia is commonly defined as blood magnesium concentrations below 0.66 mmol/L (1.6 mg/dL), with or without
associated total body depletion [14]. However, as magnesium is involved in several structural and physiological processes,
unfavorable consequences linked to hypomagnesemia may manifest clinically as acute and apparent symptoms or persistent and
subtle symptoms in almost every organ system.

Clinical signs of hypomagnesemia that need medical treatment include neuropsychiatric disorders including apathy, delirium
and even coma, as well as neuromuscular hyperexcitability, which may include tremors, fasciculation, tetany and convulsions.
Hypomagnesemia may also result in atrial and ventricular arrhythmias, torsades de pointes in the presence of preexisting long-
QT-syndrome, an increased risk of digoxin overdose and sudden death, among other potentially fatal consequences. Alterations
in glucose homeostasis, hypertension, atherosclerosis, osteoporosis, asthma, migraines and other end-organ damage are long-
term negative effects that are less often linked to hypomagnesemia.

Symptomatic magnesium deficiency in patients may manifest itself in many different ways. Electrolyte abnormalities,
neuromuscular complaints and cardiovascular symptoms are the most frequent clinical signs. Table 2 discusses certain
symptoms and indicators [15].

Food Milligrams (mg) per serving Percent DV*

Pumpkin seeds, roasted, 1 ounce 156 37
Almonds, dry roasted, 1 ounce 80 19
Spinach, boiled, ½ cup 78 19
Cashews, dry roasted, 1 ounce 74 18
Peanuts, oil roasted, ¼ cup 63 15
Cereal, shredded wheat, 2 large biscuits 61 15
Black beans, cooked, ½ cup 60 14
Potato, baked with skin, 3.5 ounces 43 10
Rice, brown, cooked, ½ cup 42 10
Yogurt, plain, low fat, 8 ounces 42 10
Breakfast cereals, fortified with 10% of the DV for magnesium, 1 serving 42 10
Table 2: Clinical Manifestation.

The following tests need to be carried out on a patient who has hypomagnesemia suspicions [15]:
● Serum magnesium, phosphate, calcium level
● Basic metabolic panel, including serum creatinine/kidney function, glucose levels
● Electrocardiogram

The cause of hypomagnesemia is often determined from the patient's medical history. If in doubt, magnesium excretion in the
urine over a 24-hour period should be monitored to see if gastrointestinal or renal losses are present. The following formula,
where U and P stand for urine and plasma concentrations of magnesium (Mg) and creatinine (Cr), may also be used to compute
the fractional excretion of magnesium (on a random urine sample) (Cr).

FEMg = [(UMg x PCr) / (PMg x UCr x 0.7)] x 100

If a person with normal renal function has a fractional excretion of magnesium more than 2%, renal magnesium wasting from
drugs like diuretics, aminoglycosides, or cisplatin is most likely the cause of the hypomagnesemia.

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Complications and Prognosis of Hypomagnesemia in Chronically Ill Patients

Hypomagnesemia can lead to a wide array of complications in chronically ill patients with comorbidities. It can involve various
body systems and can lead to an increased risk of chronic diseases. A study by Arinzon, et al., among the geriatric age group
reported a significant association between hypomagnesemia and various comorbidities such as chronic kidney disease, heart
failure and T2DM [16].

Cardiovascular
Hypomagnesemia is well known to increase the risk of arrhythmias, most likely through impairments of the cell membrane
physiology resulting in abnormal cardiac repolarization [1]. Typical electrocardiographic findings include QRS complex
widening, ST-segment depression and peaked T-waves as well as frequent premature atrial and ventricular beats. Severe
hypomagnesemia can further result in PR prolongation, progressive QRS prolongation and diminished T waves and predispose
to ventricular tachycardia and cardiac death [17]. Various studies have examined the relationship between hypomagnesemia
and electrophysiological changes. Ceremuzynski, et al., found that there is a statistically significant association with complex
arrhythmias in patients with serum magnesium levels that are reduced by 0.15 mg% compared to patients with a normal
magnesium level [18]. They further found that approximately three-fifths of patients with complex arrhythmias and three-fourths
of patients with benign arrhythmias had hypomagnesaemia [18]. Moreover, increased risk for ventricular tachycardia and
ventricular fibrillation was reported in patients with myocardial infarction and hypomagnesemia [19]. Misialek, et al., found that
serum magnesium levels below 1.55 mq/L were associated with a 1.6 times increased risk of atrial fibrillation compared to
patients with a magnesium level above 1.55 mq/L [20].

Conflicting data have been found for a possible association of heart failure and hypomagnesaemia. While Helte, et al., did not
find a significant association other study found links between hypomagnesemia and heart failure [21]. For instance, Kunutsor,
et al., who conducted a cohort study in Finland to assess chronic disease risk factors among middle-aged men (aged 42-61 years),
found with hypomagnesaemia to be an independent risk factor for future heart failure in a median follow-up of 25 years [22].
Similarly, Wannamethee, et al., reported an increased risk of heart failure in older men (aged 60-79 years) in Great Britain in a
15-year follow-up period [23]. Furthermore, the Atherosclerosis Risk in Communities Cohort study cohort revealed 1.71 times
increased for heart failure independent of gender over a median follow-up of 21 years in patients with a serum magnesium level
below 1.4 meq/L [24].

Kafka, et al., reported an increased incidence of hypomagnesemia in patients with myocardial infarction and Shiyovich, et al.,
found that patients with T2DM and myocardial infarction have a statistically significant higher incidence of hypomagnesemia
[25,26]. Moreover, a meta-analysis revealed that the increased risk of coronary artery disease was 1.18 times increased in patients
with low serum magnesium levels [27].

Menez, et al., assessed the association between hypomagnesemia and peripheral artery disease. They reported a statistically
significant increase in the risk of peripheral artery disease in patients with an eGFR ≥ 60 mL/min/1.73 m 2, but not in those with a
eGFR ≤ 60 mL/min/1.73 m2 [28]. In line with this, a cohort study by Sun, et al., reported a 30 percent increase in the occurrence of
peripheral artery disease in participants with a magnesium level ≤ 1.4 mq/L [29].

Moreover, hypomagnesemia is associated with the occurrence of aortic valve calcifications [30]. Additionally, patients with
T2DM and chronic kidney disease were found to have a higher incidence of mitral valve calcifications [31].

Endocrinology
Orlova, et al., reported 1.4 times increase in the prevalence of hypomagnesemia in women with osteoporosis, women with
climacteric syndrome and those requiring hormone replacement therapy [32].

Hypomagnesemia strongly predicts Type 2 Diabetes Mellitus (T2DM) [33]. Alswat, et al., reported an increased prevalence of
diabetic foot at 11 % in patients with hypomagnesemia compared to 3% in those with normomagnesemia [34]. Additionally,
fasting blood glucose levels were found to be elevated at 12 mmol/L in hypomagnesemia patients compared to 9 mmol/L (p-
value = 0.017) in normomagnesemia patients. In line with this HbA1c was around 8.8% in patients with hypomagnesemia

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compared to 8.0% in those with normomagnesemia [34]. Similarly, Dasgupta, et al., reported statistically significant increased
fasting blood glucose and HbA1c levels and diabetic foot in T2DM patients with hypomagnesemia [35]. Moreover, Batar, et al.,
reported a significant increase in the development of neuropathy, nephropathy, retinopathy and cardiovascular disease in
patients with T2DM in the presence of hypomagnesemia [36]. Agrawal, et al., conducted a case-control study to assess the
relation between serum magnesium levels and macrovascular complications of T2DM. They reported significantly lower
magnesium levels in patients with T2DM and coronary atherosclerosis compared to those with uncomplicated diabetes [37].
Also, a statistically significant negative correlation was reported between serum magnesium levels vs fasting blood glucose and
HbA1c in T2DM patients with coronary atherosclerosis or peripheral avascular disease [37]. In contrast to these findings,
Chanchlani, et al., did not find a significant association of hypomagnesemia with hyperglycemia or diabetes in pediatric post-
transplant patients [38].

Neurology
Naidech, et al., did not find a significant relation between magnesium level and hematoma volume in intracerebral hemorrhage
patients [39]. Alam, et al., assessed the relation between hypomagnesemia and dementia and found a 24% to 34% increased risk
of dementia in patients in the lowest quintile of serum magnesium levels compared to those in the highest quintile [40].

Prognostic Value
The promise study did not find a significant relationship between hypomagnesemia and prognosis in heart failure patients [41].
Similarly, Marten, et al., found that hypomagnesemia is not significantly associated with a higher risk of cardiovascular events
affecting the prognosis of cardiac patients [42]. In contrast, Li, et al., found a significant association between low serum
magnesium levels and hemodialysis patients' mortality [43]. A meta-analysis by Upala, et al., revealed a 1.9 times increased
mortality risk in patients admitted to ICU who were found to have hypomagnesemia compared to patients with normal
magnesium levels [44].

Patient Education
A Daily Intake (DI) of 3.6 mg/kg, with an Acceptable Daily Intake (ADI) of 320 to 420 mg/day (13-17 mmol/day) is recommended
for adults [45]. This can be achieved through consumption of magnesium rich foods such as green leafy vegetables, whole grain
cereals, legumes, nuts and seafood [45].

Consultation with a dietician and formulating a dietary plan taking into account the sources and potential inhibitors of
magnesium intake is the recommended first line treatment in mild asymptomatic hypomagnesemia [46].

Hypoalbuminemia has been associated with spurious cases of hypomagnesemia [47]. Adequate protein intake with sufficient
protein supplementation, especially in malnourished patients, is recommended [48].

With the insidious long-term complications and overall higher mortality undiagnosed hypomagnesemia carries, such a dietary
approach should be recommended to all high-risk patients [4,48-57].

The significant rate of hypomagnesemia in the general population (up to 2%-4.6%, based on previous studies), is closely tied
with a decreasing dietary intake, both due to an overall decrease in soil magnesium content and an increased consumption of
processed foods which impairs magnesium intestinal absorption [56-59].

Other dietary habits that can impair uptake include consumption of carbonated beverages, a low protein diet (<30 mg/day) and
a diet rich in rice and nuts containing phytates, polyphenols and oxalic acid. Moreover, ingestion of caffeine and alcohol increases
renal excretion of magnesium [60-64]. Solid meals can be beneficial in enhancing magnesium absorption by prolonging the GI
transit time while an increase in dietary fiber leads to increased magnesium loss in feces (Table 3) [65].

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Neuromuscular Manifestations Cardiovascular Manifestations Other Electrolyte and

Hormonal Abnormalities
• Tremors • Electrocardiogram changes, including • Hypocalcemia
• Tetany, including positive widening of the QRS complex, peaked T • Hypoparathyroidism
Trousseau and Chvostek signs, waves, prolongation of the PR interval • Hypokalemia
muscle spasms, muscle • Atrial and ventricular premature
cramps systoles
• Seizures • Atrial fibrillation
• Vertical nystagmus • Ventricular arrhythmias, including
• Apathy torsades de pointes
• Delirium • Cardiac ischemia
Table 3: High magnesium containing foods [45].

Though commonly asymptomatic, severe hypomagnesemia can present with warning signs, such as neuromuscular irritability
and cardiac arrhythmias [66].

Role of the Interdisciplinary Medical Team

Due to the number of potential causes of hypomagnesemia, management warrants an interdisciplinary team involvement [64-
81]. The underling contributors to hypomagnesemia must be elucidated to avoid treatment failure and recurrences [64,81].
Among patients with chronic illnesses, drug induced hypomagnesemia features commonly and extensively [66,82,83].

PPI induced hypomagnesemia is reversible within 2 weeks of PPI cessation and should be avoided thereafter due to rapid fall in
magnesium levels when reintroduced [84-89]. A tapered discontinuation and switch to an alternative acid suppressant such as
H2 Receptor Antagonists (H2RAs) should be considered for persistent gastro-intestinal complaints [90,91].

The myriad of gastrointestinal conditions that can lead to hypomagnesemia call for detailed consultation with a GI specialist, to
manage the underlying conditions along with IV magnesium replenishment to counter the decreased intestinal magnesium
absorption [82-84,92].

On the cardiac service, chronic thiazide-induced dose dependent hypomagnesemia can be avoided by the concurrent use of a
potassium-sparing agent [93]. It is recommended to routinely assess magnesium levels in patients on a long-term thiazide
diuretic, particularly those on more than one year of treatment and elderly patients [93,94]. The use of Loop diuretics has not
shown to increase the risk of hypomagnesemia [93]. Due to the established correlation between hypomagnesemia and the risk
of cardiac arrhythmias and sudden cardiac death, it has been suggested to measure serum Mg levels on admission [71,95-99].
Additionally, hypomagnesemia should be on the differentials for acute arrhythmias [100]. Concerning ECG abnormalities such
as QTc prolongation and global T-wave inversions, which could be due to isolated hypomagnesemia, have shown to resolve
after IV magnesium sulfate infusion [101]. In the case of antibiotic-induced hypomagnesemia, monitoring of serum magnesium
levels should be performed based on the suspicion of hypomagnesemia (cardiac arrhythmias, neuromuscular symptoms and
other electrolyte abnormalities) and in such cases, management with magnesium supplementation should be administered as
needed [80,89-92].

In cases with mild to moderate renal derangements, it is important to dose magnesium according to the GFR to avoid
hypomagnesemia [93]. While magnesium therapy is not recommended for critically ill patients with severe renal failure, patients
with severe chronic kidney disease can be given magnesium supplementation at 25-50% dose reduction and careful monitoring
[82].

Also, to note, acute renal insufficiency in combination with the decreased clearance of Intravenous drugs in ICU patients leads
to potential interactions that affect magnesium levels. This should be considered in critically ill patients with chronic renal disease
[60,80].

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Oncology services bear a considerable burden of hypomagnesemia. Not only have lower serum levels been correlated with
increased incidence of certain cancers, but many chemotherapeutic agents have also shown to cause hypomagnesemia [93-102].
Importantly, chemotherapy-induced hypomagnesemia was found to be associated with a higher mortality [103]. Therefore
currently, routine monitoring and prophylactic magnesium therapy is recommended for patients undergoing platin-based
chemotherapy and therapy with cetuximab/panitumumab [97,104].

Overall, hypomagnesemia is often missed among differentials although it is an easily treatable deficiency with important clinical
implications [65]. Particularly in patients with non-specific neurologic and/or cardiac complaints especially with underlying GI
comorbidities or extensive drug history, there should be a high degree of clinical suspicion [100].

It should be noted that magnesium also aids in maintaining physiologic levels of other ions such as potassium, calcium,
phosphate and that correcting hypomagnesemia in addition to potassium and calcium supplementation, leads to correction of
refractory or unexplained hypokalemia /hypocalcemia’s states [105-108]. Magnesium may be empirically given to patients at
high-risk for hypomagnesemia who are presenting with unexplained hypokalemia and/or hypocalcemia.

Data strongly supports testing for baseline serum magnesium on inpatient admission. However, due to the risk of
hypermagnesemia there should be caution against the indiscriminate use of magnesium [71].

Recommendations and Limitations

Because of the complex intracellular distribution of magnesium, serum levels may not reflect the true magnesium status. A
normal magnesium level may still warrant treatment for patients at risk of deficiency or with symptomatic hypomagnesaemia
[80].

If dietary approach and correction of underlying conditions fails to correct serum levels, magnesium supplementation should be
considered [63].

Oral magnesium salts (e.g., Mg oxide, Mg lactate or Mg chloride) may be used independently for chronic or mild
hypomagnesemia with mild or no symptoms or is used as maintenance therapy after intravenous replacement [80,108].

Six to eight tablets (60-96 mg per tablet) for severe hypomagnesemia and two to four tablets for mild asymptomatic disease are
recommended to be taken daily in divided doses [61].

Mg salts are not all well absorbed in the GI tract especially in large doses and can cause GI symptoms such as vomiting or
diarrhea [109]. Magnesium oxide is commonly used due to its low cost, but it is also associated with more GI side effects [82].
Mg gluconate, sulfate, or aspartate could be alternative options. If a particular magnesium salt is not effective or is tolerated
poorly, another one should be considered [62,110]. Sustained-release magnesium preparations are less likely to cause diarrhea
and create a gradual up rise in serum magnesium that leads to reduced urinary magnesium excretion [68].

Dietary supplements alone are not sufficient to stabilize magnesium levels in the setting of underlying conditions such as
malnutrition or heavy alcohol consumption [112].

Symptomatic hypomagnesemia warrants more emergent and aggressive management. Intravenous magnesium
supplementation is considered for severe hypomagnesemia < 0.5 mmol/L (1mg/dl) or significant symptomatic presentation [80].
1 gram of magnesium sulfate (MgSO4) contains 100 mg (4 mmol or 8 mEq) of elemental magnesium. IV magnesium is available
as MgSO4 formulations of 10%, 20%, or 50% (0.1g, 0.2 or 0.5g MgSO 4/1 ml) solutions.

General consensus recommends administering 8-12 grams (64 to 96 mEq [32 to 48 mmol]) of IV MgSO 4 over the initial 24 hours,
followed by 4-6 grams/day (32 to 48 mEq [16 to 24 mmol]) for 3 or 4 days [92].

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For acute hemodynamically unstable patients (torsade de pointes, seizures or hypomagnesemia hypokalemia), IV MgSO 4 can be
administered as 1 - 2 grams (8 to 16 mEq [4 to 8 mmol]) in 100 ml of D5W over 2 - 15 minutes, repeating if necessary. This is
followed by IV MgSO4 6g (50 mEq [25 mmol])/day as maintenance [82,113].

In hemodynamically stable patients with severe (≤1 mg/dL [0.4 mmol/L or 0.8 mEq/L]) and/or symptomatic hypomagnesemia, 1
- 2 grams (8 - 16 mEq [4 - 8 mmol]) of IV MgSO4 in 50-100 mL of 5 % DW can be given initially over 5-60 minutes; followed by a
nonemergency repletion infusion of 4 - 8 grams of MgSO4 (32 - 64 mEq [16 - 32 mmol]) given slowly over 12 to 24 hours [114].
This dose can be repeated to maintain the plasma magnesium concentration above 1 mg/dL (0.4 mmol/L or 0.8 mEq/L).

Alternatively, in severe but not life-threatening hypomagnesemia, an infusion of 1-2 grams/hour (8 to 16 mEq [4 to 8 mmol]) of
MgSO4 can be administered for 3-6 hours, decreasing to a rate of 0.5-1 grams/hour (4 to 8 mEq [2 to 4 mmol]) as maintenance
infusion [115].

For hospitalized patients with mild to moderate hypomagnesemia, oral formulations are not well tolerated and parenteral
infusion is given at an estimated repletion dose:
1. For mild (1.6-1.9 mg/dL [0.7-0.8 mmol/L or 1.4-1.6 mEq/L] and combined with suspicion of magnesium depletion), give
1 to 2 grams (8 to 16 mEq [4 to 8 mmol]) of IV MgSO 4 over 1-2 hours [114]
2. For moderate hypomagnesemia (1-1.5 mg/dL [0.4-0.6 mmol/L or 0.8-1.2 mEq/L]), give 2 to 4 grams (16 to 32 mEq [8 to 16
mmol]) of IV MgSO4 over 4 - 12 hours

Repeat doses are given based on the follow-up measurement.

The target serum magnesium concentrations for critically ill ICU patients are 1.5 mg/dL or higher, due to the high risk of mortality
associated with this population [116,118].

For those lacking intravenous access, IV MgSO4 can be injected intra-muscularly as a last resort. 1-2 g of MgSO4 can be given
intramuscularly every 6 hours for 24 hours in a total of 4 doses [114].

In the pediatric population, 25 to 50 mg/kg (0.2 to 0.4 mEq/kg [0.1 to 0.2 mmol/kg]) MgSO 4 is given as a slow infusion with a
maximum single dose of 2 grams (16 mEq [8 mmol]) [115].

In general, MgSO4 in doses less than 6 grams can be given over a period of 8-12 hours, whereas higher doses should be
administrated over a time period greater than 25 hours to account for the slow distribution and initial renal excretion [119,120].
Rapid intravenous administration and high levels of Mg (> 4-5 mmol/L) can lead to cardiac arrhythmia, muscular depression,
respiratory irregularities and/or hypotension [45]. Cardiac monitoring and regular clinical assessment should be done, especially
with high doses and in elderly patients. In case of intolerable intoxication; IV calcium (100-200 mg over 5-10 min) can be given
[119].

Monitoring serum levels and assessing clinical resolution provides information on the effectiveness of magnesium
supplementation [114]. However, testing magnesium levels immediately following an infusion may give a falsely elevated value,
as magnesium is slow to equilibrate between serum and intracellular spaces. This does not indicate repletion of body stores and
further supplementation with oral magnesium salts is often necessary [45].

Research Limitations
The empirical results reported in this study should be considered in the light of some limitations. Firstly, this review article has
cited sources that are geographically distributed and the samples studied represented a singular population subgroup. Therefore,
any confounding differences based on nationality may have been missing.

Secondly, the burden of hypomagnesemia is still poorly understood, as it is not routinely tested for and considered clinically as

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other electrolyte imbalances. Some of the studies reviewed had smaller sample sizes; prospective studies with large study
populations would provide a better understanding of this condition.

There is still some uncertainty as to the accuracy of serum magnesium levels in reflecting true magnesium stores; however, in
our review we have based the diagnosis and treatment on these values. Potential future research could help to understand the
scope of inaccuracies in diagnosis and suggest more reliable testing parameters.

The presence of rare genetic hypomagnesemia and its treatment was not focused on this review, as we focused more on
hypomagnesemia secondary to chronic conditions. There is a wide scope for understanding and elucidating genetic causes in
further studies.

Conflict of Interest
The authors have no conflict of interest to declare.

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