The name “magnesium” comes from the Greek district of Magnesia. This element is useful in improving the strength of aluminum and is often used in airplane and car construction. It also has other applications, such as acting as a mordant for dyes, making plastics fire retardant, and is used in electronics and heat-resistant cookware.
Magnesium is also used in medicine to treat various conditions, such as ventricular arrhythmia and eclampsia. Plants need magnesium for chlorophyll, while animals require it for enzymatic action, transporters, and nucleic acid synthesis. Magnesium and calcium play an essential role in neuromuscular functions, myocardial electrical activity, and vascular tone.
Magnesium absorption can be improved by factors such as parathormone, vitamin D, and sodium in the diet, while fats, calcium, phosphates, and phytic acid can decrease it. Most of the body’s magnesium is found in the bones and muscles, with only a small amount in extracellular fluids. The normal range of serum magnesium levels is 0.7 to 1.0 mmol/L.
Epidemiology
Hypermagnesemia is a rare electrolyte disorder that is observed in around 10-15% of hospitalized patients with renal failure. In addition, research indicates that high serum magnesium levels are prevalent in certain healthy populations, with an overall prevalence of 3.0% reported in Iranian subjects, particularly in males (p < 0.05).
Investigating hypermagnesemia as a potential risk factor for other illnesses could be worthwhile. For example, the researchers discovered that individuals with cardiovascular disease often have elevated magnesium concentrations, and 2.3 mg/dL or higher values are linked to increased hospital mortality rates.
Anatomy
Pathophysiology
Renal function has vital participation in the metabolism of magnesium, as the majority of the filtered magnesium is inertly reabsorbed in the ascending limb of the loop of Henle. This results in a high resorbent capacity of the kidney, which usually provides magnesium equilibrium till the creatinine clearance falls less than 20 ml/min.
Therefore, an increase in plasma magnesium levels is unlikely due to diet alone unless mega-doses of magnesium are taken. However, additional laxative use can overwhelm the excretory mechanism, especially in underlying subclinical renal failure, leading to hypermagnesemia.
Magnesium acts as a physiologic calcium blocker, and increased levels can cause significant hemodynamic and electrophysiological effects. Additionally, the risk of cardiac arrhythmias and cardiac arrest is increased when hyperkalemia is concomitant. Neurologic manifestations inhibit acetylcholine delivery from the neuromuscular endplate due to increased extracellular magnesium levels.
Etiology
Hypermagnesemia primarily affects patients with kidney disease. Certain factors such as alcoholism, malnourishment, and the use of proton pump inhibitors, can increase the risk of developing this condition. Hypothyroidism and cortico-adrenal insufficiency are also recognized causes. Another possible cause of hypermagnesemia is hyperparathyroidism and variations in calcium metabolism, which can lead to increased calcium-induced magnesium absorption in the tubule.
Additionally, patients with familial hypocalciuric hypercalcemia (FHH), a rare autosomal dominant condition, may develop hypermagnesemia. Finally, lithium-based psychotropic drugs may also cause hypermagnesemia by reducing excretion. Hyper-magnesemia can occur in the elderly population, even in the absence of kidney problems. This is often due to decreased gut motility caused by underlying bowel conditions, and those taking anticholinergics or opioids and those with inflammatory bowel diseases are at a higher risk.
Some medications containing magnesium, such as antacids and laxatives, can also increase magnesium levels, particularly in elderly patients with kidney problems. While relatively safe, long-term use of magnesium oxide can increase the risk of hyper-magnesemia and requires periodic evaluation in geriatric patients. Severe hyper-magnesemia can occur after taking bowel preparation agents or excessive oral intake in patients on hemodialysis.
Milk-alkali syndrome, caused by consuming large amounts of absorbable alkali and milk, can also increase the risk of hyper-magnesemia. Iatrogenic hyper-magnesemia can result from excessive magnesium infusion used to manage eclampsia. Newborns of mothers who receive parenteral magnesium sulfate during labor may also develop toxicity, despite having normal serum magnesium levels.
Genetics
Prognostic Factors
The outcome of hypermagnesemia is determined by the severity of magnesium levels and the underlying medical condition that caused it. Mild hypermagnesemia, without any exacerbating factors such as renal impairment, is typically harmless.
However, severe hypermagnesemia, with significantly elevated magnesium levels, poses a significant risk to the patient’s health and increases the likelihood of mortality.
Clinical History
Clinical History
Patients with symptomatic hypermagnesemia may exhibit various clinical symptoms based on the severity and timing of the electrolytic disturbance. In general, hypermagnesemia is well-managed. Patients with abnormal readings (less than 4 mg/dL) may be silent or paucisymptomatic.
The most common symptoms and indications are weakness, nausea, and disorientation. Hypermagnesemia (below 7 mg/dL) is considered mild. Asymptomatic or paucisymptomatic symptoms include fatigue, nausea, disorientation, and bewilderment.
Moderate hypermagnesemia (7 to 12 mg/dL), reduced responses, increasing disorientation and drowsiness, bladder immobility, flushing, headache, and constipation.
Physical Examination
Physical Examination
Weakness, nausea, disorientation, and confusion are the most common symptoms. Elevated levels (7 to 12 mg/dL) cause reduced responses, increasing disorientation, drowsiness, bladder immobility, constipation flushing, and headache. A small drop in blood pressure and impaired vision can occur due to decreased accommodation and confluence.
Higher values (greater than 12.0 mg/dL) may cause paralytic ileus, muscular paralysis, reduced breathing rate, low blood pressure, electrocardiogram (ECG) alterations such as increased PR and QRS interval with, atrioventricular block and sinus bradycardia, coma, and cardiac death.
Hypermagnesemia, when combined with hypocalcemia, can cause choreiform motions and convulsions. The clinical picture worsens, and there are few cases of people surviving higher hypermagnesaemia levels.
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
Eliminating all sources of exogenous magnesium is necessary for patients with moderate silent hypermagnesemia and good renal function (GFR over 60 ml/min). The half-time of magnesium removal must be considered; it is roughly 28 hours. In more serious instances, early intervention and careful tracking of the ECG, blood pressure, and neuromuscular function are required: Calcium chloride or gluconate is given intravenously 1 g in 2 to 5 minutes, repeated over five minutes.
The theory suggests that calcium interferes with magnesium’s effects on muscle and cardiac performance. Systemic saline (for instance, at 150 ml/hour). Diuretics must be used in conjunction with saline solution infusions to prevent further electrolyte changes (e.g., hypokalemia) and metabolic alkalosis. The physician must take serial calcium and magnesium values. Supporting cardiorespiratory exercise is frequently required in conjunction with electrolytic rectification.
As a result, therapy for this electrolyte imbalance may frequently necessitate intensive care unit (ICU) admission. Certain clinical situations necessitate a unique strategy. For example, in the treatment of eclampsia, the magnesium infusion is discontinued if urine production falls below 80 mL (in 4 hours), deep tendon reflexes are missing, or the respiratory rate falls below 12 breaths/minute. A remedy is a 10% calcium gluconate or chloride solution (10 mL intravenously repetitive over 5 minutes).
The name “magnesium” comes from the Greek district of Magnesia. This element is useful in improving the strength of aluminum and is often used in airplane and car construction. It also has other applications, such as acting as a mordant for dyes, making plastics fire retardant, and is used in electronics and heat-resistant cookware.
Magnesium is also used in medicine to treat various conditions, such as ventricular arrhythmia and eclampsia. Plants need magnesium for chlorophyll, while animals require it for enzymatic action, transporters, and nucleic acid synthesis. Magnesium and calcium play an essential role in neuromuscular functions, myocardial electrical activity, and vascular tone.
Magnesium absorption can be improved by factors such as parathormone, vitamin D, and sodium in the diet, while fats, calcium, phosphates, and phytic acid can decrease it. Most of the body’s magnesium is found in the bones and muscles, with only a small amount in extracellular fluids. The normal range of serum magnesium levels is 0.7 to 1.0 mmol/L.
Hypermagnesemia is a rare electrolyte disorder that is observed in around 10-15% of hospitalized patients with renal failure. In addition, research indicates that high serum magnesium levels are prevalent in certain healthy populations, with an overall prevalence of 3.0% reported in Iranian subjects, particularly in males (p < 0.05).
Investigating hypermagnesemia as a potential risk factor for other illnesses could be worthwhile. For example, the researchers discovered that individuals with cardiovascular disease often have elevated magnesium concentrations, and 2.3 mg/dL or higher values are linked to increased hospital mortality rates.
Renal function has vital participation in the metabolism of magnesium, as the majority of the filtered magnesium is inertly reabsorbed in the ascending limb of the loop of Henle. This results in a high resorbent capacity of the kidney, which usually provides magnesium equilibrium till the creatinine clearance falls less than 20 ml/min.
Therefore, an increase in plasma magnesium levels is unlikely due to diet alone unless mega-doses of magnesium are taken. However, additional laxative use can overwhelm the excretory mechanism, especially in underlying subclinical renal failure, leading to hypermagnesemia.
Magnesium acts as a physiologic calcium blocker, and increased levels can cause significant hemodynamic and electrophysiological effects. Additionally, the risk of cardiac arrhythmias and cardiac arrest is increased when hyperkalemia is concomitant. Neurologic manifestations inhibit acetylcholine delivery from the neuromuscular endplate due to increased extracellular magnesium levels.
Hypermagnesemia primarily affects patients with kidney disease. Certain factors such as alcoholism, malnourishment, and the use of proton pump inhibitors, can increase the risk of developing this condition. Hypothyroidism and cortico-adrenal insufficiency are also recognized causes. Another possible cause of hypermagnesemia is hyperparathyroidism and variations in calcium metabolism, which can lead to increased calcium-induced magnesium absorption in the tubule.
Additionally, patients with familial hypocalciuric hypercalcemia (FHH), a rare autosomal dominant condition, may develop hypermagnesemia. Finally, lithium-based psychotropic drugs may also cause hypermagnesemia by reducing excretion. Hyper-magnesemia can occur in the elderly population, even in the absence of kidney problems. This is often due to decreased gut motility caused by underlying bowel conditions, and those taking anticholinergics or opioids and those with inflammatory bowel diseases are at a higher risk.
Some medications containing magnesium, such as antacids and laxatives, can also increase magnesium levels, particularly in elderly patients with kidney problems. While relatively safe, long-term use of magnesium oxide can increase the risk of hyper-magnesemia and requires periodic evaluation in geriatric patients. Severe hyper-magnesemia can occur after taking bowel preparation agents or excessive oral intake in patients on hemodialysis.
Milk-alkali syndrome, caused by consuming large amounts of absorbable alkali and milk, can also increase the risk of hyper-magnesemia. Iatrogenic hyper-magnesemia can result from excessive magnesium infusion used to manage eclampsia. Newborns of mothers who receive parenteral magnesium sulfate during labor may also develop toxicity, despite having normal serum magnesium levels.
The outcome of hypermagnesemia is determined by the severity of magnesium levels and the underlying medical condition that caused it. Mild hypermagnesemia, without any exacerbating factors such as renal impairment, is typically harmless.
However, severe hypermagnesemia, with significantly elevated magnesium levels, poses a significant risk to the patient’s health and increases the likelihood of mortality.
Clinical History
Patients with symptomatic hypermagnesemia may exhibit various clinical symptoms based on the severity and timing of the electrolytic disturbance. In general, hypermagnesemia is well-managed. Patients with abnormal readings (less than 4 mg/dL) may be silent or paucisymptomatic.
The most common symptoms and indications are weakness, nausea, and disorientation. Hypermagnesemia (below 7 mg/dL) is considered mild. Asymptomatic or paucisymptomatic symptoms include fatigue, nausea, disorientation, and bewilderment.
Moderate hypermagnesemia (7 to 12 mg/dL), reduced responses, increasing disorientation and drowsiness, bladder immobility, flushing, headache, and constipation.
Physical Examination
Weakness, nausea, disorientation, and confusion are the most common symptoms. Elevated levels (7 to 12 mg/dL) cause reduced responses, increasing disorientation, drowsiness, bladder immobility, constipation flushing, and headache. A small drop in blood pressure and impaired vision can occur due to decreased accommodation and confluence.
Higher values (greater than 12.0 mg/dL) may cause paralytic ileus, muscular paralysis, reduced breathing rate, low blood pressure, electrocardiogram (ECG) alterations such as increased PR and QRS interval with, atrioventricular block and sinus bradycardia, coma, and cardiac death.
Hypermagnesemia, when combined with hypocalcemia, can cause choreiform motions and convulsions. The clinical picture worsens, and there are few cases of people surviving higher hypermagnesaemia levels.
Eliminating all sources of exogenous magnesium is necessary for patients with moderate silent hypermagnesemia and good renal function (GFR over 60 ml/min). The half-time of magnesium removal must be considered; it is roughly 28 hours. In more serious instances, early intervention and careful tracking of the ECG, blood pressure, and neuromuscular function are required: Calcium chloride or gluconate is given intravenously 1 g in 2 to 5 minutes, repeated over five minutes.
The theory suggests that calcium interferes with magnesium’s effects on muscle and cardiac performance. Systemic saline (for instance, at 150 ml/hour). Diuretics must be used in conjunction with saline solution infusions to prevent further electrolyte changes (e.g., hypokalemia) and metabolic alkalosis. The physician must take serial calcium and magnesium values. Supporting cardiorespiratory exercise is frequently required in conjunction with electrolytic rectification.
As a result, therapy for this electrolyte imbalance may frequently necessitate intensive care unit (ICU) admission. Certain clinical situations necessitate a unique strategy. For example, in the treatment of eclampsia, the magnesium infusion is discontinued if urine production falls below 80 mL (in 4 hours), deep tendon reflexes are missing, or the respiratory rate falls below 12 breaths/minute. A remedy is a 10% calcium gluconate or chloride solution (10 mL intravenously repetitive over 5 minutes).
500-1000 mg intravenously for 2-5 minutes
Monitor the patient for any signs of recovery
Repeat the dose if CNS depression stays
medtigo
Hypermagnesemia
Updated :
August 30, 2023
The name “magnesium” comes from the Greek district of Magnesia. This element is useful in improving the strength of aluminum and is often used in airplane and car construction. It also has other applications, such as acting as a mordant for dyes, making plastics fire retardant, and is used in electronics and heat-resistant cookware.
Magnesium is also used in medicine to treat various conditions, such as ventricular arrhythmia and eclampsia. Plants need magnesium for chlorophyll, while animals require it for enzymatic action, transporters, and nucleic acid synthesis. Magnesium and calcium play an essential role in neuromuscular functions, myocardial electrical activity, and vascular tone.
Magnesium absorption can be improved by factors such as parathormone, vitamin D, and sodium in the diet, while fats, calcium, phosphates, and phytic acid can decrease it. Most of the body’s magnesium is found in the bones and muscles, with only a small amount in extracellular fluids. The normal range of serum magnesium levels is 0.7 to 1.0 mmol/L.
Hypermagnesemia is a rare electrolyte disorder that is observed in around 10-15% of hospitalized patients with renal failure. In addition, research indicates that high serum magnesium levels are prevalent in certain healthy populations, with an overall prevalence of 3.0% reported in Iranian subjects, particularly in males (p < 0.05).
Investigating hypermagnesemia as a potential risk factor for other illnesses could be worthwhile. For example, the researchers discovered that individuals with cardiovascular disease often have elevated magnesium concentrations, and 2.3 mg/dL or higher values are linked to increased hospital mortality rates.
Renal function has vital participation in the metabolism of magnesium, as the majority of the filtered magnesium is inertly reabsorbed in the ascending limb of the loop of Henle. This results in a high resorbent capacity of the kidney, which usually provides magnesium equilibrium till the creatinine clearance falls less than 20 ml/min.
Therefore, an increase in plasma magnesium levels is unlikely due to diet alone unless mega-doses of magnesium are taken. However, additional laxative use can overwhelm the excretory mechanism, especially in underlying subclinical renal failure, leading to hypermagnesemia.
Magnesium acts as a physiologic calcium blocker, and increased levels can cause significant hemodynamic and electrophysiological effects. Additionally, the risk of cardiac arrhythmias and cardiac arrest is increased when hyperkalemia is concomitant. Neurologic manifestations inhibit acetylcholine delivery from the neuromuscular endplate due to increased extracellular magnesium levels.
Hypermagnesemia primarily affects patients with kidney disease. Certain factors such as alcoholism, malnourishment, and the use of proton pump inhibitors, can increase the risk of developing this condition. Hypothyroidism and cortico-adrenal insufficiency are also recognized causes. Another possible cause of hypermagnesemia is hyperparathyroidism and variations in calcium metabolism, which can lead to increased calcium-induced magnesium absorption in the tubule.
Additionally, patients with familial hypocalciuric hypercalcemia (FHH), a rare autosomal dominant condition, may develop hypermagnesemia. Finally, lithium-based psychotropic drugs may also cause hypermagnesemia by reducing excretion. Hyper-magnesemia can occur in the elderly population, even in the absence of kidney problems. This is often due to decreased gut motility caused by underlying bowel conditions, and those taking anticholinergics or opioids and those with inflammatory bowel diseases are at a higher risk.
Some medications containing magnesium, such as antacids and laxatives, can also increase magnesium levels, particularly in elderly patients with kidney problems. While relatively safe, long-term use of magnesium oxide can increase the risk of hyper-magnesemia and requires periodic evaluation in geriatric patients. Severe hyper-magnesemia can occur after taking bowel preparation agents or excessive oral intake in patients on hemodialysis.
Milk-alkali syndrome, caused by consuming large amounts of absorbable alkali and milk, can also increase the risk of hyper-magnesemia. Iatrogenic hyper-magnesemia can result from excessive magnesium infusion used to manage eclampsia. Newborns of mothers who receive parenteral magnesium sulfate during labor may also develop toxicity, despite having normal serum magnesium levels.
The outcome of hypermagnesemia is determined by the severity of magnesium levels and the underlying medical condition that caused it. Mild hypermagnesemia, without any exacerbating factors such as renal impairment, is typically harmless.
However, severe hypermagnesemia, with significantly elevated magnesium levels, poses a significant risk to the patient’s health and increases the likelihood of mortality.
Clinical History
Patients with symptomatic hypermagnesemia may exhibit various clinical symptoms based on the severity and timing of the electrolytic disturbance. In general, hypermagnesemia is well-managed. Patients with abnormal readings (less than 4 mg/dL) may be silent or paucisymptomatic.
The most common symptoms and indications are weakness, nausea, and disorientation. Hypermagnesemia (below 7 mg/dL) is considered mild. Asymptomatic or paucisymptomatic symptoms include fatigue, nausea, disorientation, and bewilderment.
Moderate hypermagnesemia (7 to 12 mg/dL), reduced responses, increasing disorientation and drowsiness, bladder immobility, flushing, headache, and constipation.
Physical Examination
Weakness, nausea, disorientation, and confusion are the most common symptoms. Elevated levels (7 to 12 mg/dL) cause reduced responses, increasing disorientation, drowsiness, bladder immobility, constipation flushing, and headache. A small drop in blood pressure and impaired vision can occur due to decreased accommodation and confluence.
Higher values (greater than 12.0 mg/dL) may cause paralytic ileus, muscular paralysis, reduced breathing rate, low blood pressure, electrocardiogram (ECG) alterations such as increased PR and QRS interval with, atrioventricular block and sinus bradycardia, coma, and cardiac death.
Hypermagnesemia, when combined with hypocalcemia, can cause choreiform motions and convulsions. The clinical picture worsens, and there are few cases of people surviving higher hypermagnesaemia levels.
Eliminating all sources of exogenous magnesium is necessary for patients with moderate silent hypermagnesemia and good renal function (GFR over 60 ml/min). The half-time of magnesium removal must be considered; it is roughly 28 hours. In more serious instances, early intervention and careful tracking of the ECG, blood pressure, and neuromuscular function are required: Calcium chloride or gluconate is given intravenously 1 g in 2 to 5 minutes, repeated over five minutes.
The theory suggests that calcium interferes with magnesium’s effects on muscle and cardiac performance. Systemic saline (for instance, at 150 ml/hour). Diuretics must be used in conjunction with saline solution infusions to prevent further electrolyte changes (e.g., hypokalemia) and metabolic alkalosis. The physician must take serial calcium and magnesium values. Supporting cardiorespiratory exercise is frequently required in conjunction with electrolytic rectification.
As a result, therapy for this electrolyte imbalance may frequently necessitate intensive care unit (ICU) admission. Certain clinical situations necessitate a unique strategy. For example, in the treatment of eclampsia, the magnesium infusion is discontinued if urine production falls below 80 mL (in 4 hours), deep tendon reflexes are missing, or the respiratory rate falls below 12 breaths/minute. A remedy is a 10% calcium gluconate or chloride solution (10 mL intravenously repetitive over 5 minutes).
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