Magnesium plays a crucial role as an electrolyte in the human body, participating in numerous reactions and processes impacting cellular, nerve conduction, and other essential bodily functions. The typical range of serum magnesium levels is between 1.46 and 2.68 mg/dL. However, when the serum magnesium level falls below 1.46 mg/dL, it leads to an electrolyte disturbance called hypomagnesemia. Despite its significant impact, hypomagnesemia is usually asymptomatic until the serum magnesium concentration drops below 1.2 mg/dL.
A range of factors, including alcohol use disorder, chronic disease, gastrointestinal, renal loss, and other underlying medical conditions, can cause hypomagnesemia. The loss of magnesium in the body can result from various factors, including chronic diarrhea, vomiting, or malabsorption syndromes, leading to reduced magnesium intake. At the same time, the excessive use of certain medications like diuretics can increase the loss of magnesium. People who consume alcohol regularly or suffer from conditions impairing nutrient absorption may also risk developing hypomagnesemia.
Magnesium deficiency has several consequences, including muscle weakness, fatigue, and cardiac arrhythmias, which can lead to more severe complications if not appropriately addressed. Treatment of hypomagnesemia involves identifying and addressing the underlying cause of the condition, such as stopping the use of certain medications, addressing any underlying medical conditions, or administering magnesium supplements, depending on the severity of the deficiency.
Epidemiology
The prevalence of hypomagnesemia varies based on different characteristics and healthcare settings. In the general population, it has been reported to range from 2.5% to 15%. However, the prevalence is much higher in hospitalized patients, ranging from 12% to 20%. This prevalence is even more significant in critically ill patients, with one study estimating it as high as 65%.
A study conducted in India among 100 critically ill children with a mean age of 4.9 years showed a prevalence of approximately 55%. Similarly, another study found that patients with chronic alcohol use disorder had a 30% prevalence of hypomagnesemia. Although no recent studies have identified specific age groups that are more susceptible to hypomagnesemia, the condition can affect individuals of any age.
Anatomy
Pathophysiology
Magnesium is an essential mineral that plays a vital role in various biochemical reactions in the human body. It is the second most abundant intracellular cation after potassium. An average adult human body contains 1,000 millimoles of magnesium. Approximately 99% of this magnesium is found in bone and soft tissues. Magnesium is a crucial cofactor in many enzymatic reactions, including protein synthesis, DNA synthesis, and energy metabolism. It also plays an essential role in maintaining the body’s electrolyte balance, particularly concerning sodium, calcium and potassium.
The body regulates magnesium levels through a complex process involving the kidney, small bowel, and bone. The proximal tubule, thick ascending loop of Henle, and distal tubule of the kidney are primarily responsible for maintaining magnesium balance. The ileum and jejunum of the small bowel absorb magnesium, while bone serves as a reservoir of magnesium. Hypomagnesemia occurs due to various factors, such as renal or gastrointestinal losses or a disease condition. This alteration in magnesium homeostasis can result in various health problems, including neuromuscular hyperexcitability, cardiac arrhythmias, and seizures.
Several drugs can also cause hypomagnesemia by interfering with magnesium absorption or excretion. The condition is also caused by recessive mutations in the SLC12A3 gene that encodes the thiazide-sensitive sodium chloride cotransporter in the distal convoluted tubule. This mutation impairs the transcellular reabsorption of magnesium in the DCT, which causes an increase in calcium reabsorption. As a result, hypocalciuria and fluid loss occur, which can lower blood pressure.
Additionally, fluid loss triggers the renin-angiotensin-aldosterone system, leading to increased aldosterone levels, resulting in increased potassium secretion and subsequent hypokalemia. Mutations in this gene also affect the reabsorption of magnesium and calcium ions in the thick ascending limb of Henle, causing hypercalciuric hypomagnesemia that can eventually lead to nephrocalcinosis or chronic kidney disease. This condition can cause severe complications, including chronic kidney disease, renal failure, and electrolyte imbalances.
Etiology
Hypomagnesemia is a condition where the body has lower-than-normal levels of magnesium. There are several causes of hypomagnesemia, including decreased magnesium intake. This can happen in starvation, anorexia nervosa, terminal cancer, and alcohol use disorder. In such cases, the body may not receive adequate amounts of magnesium through the diet, leading to a deficiency.
Another cause of hypomagnesemia is the use of certain medications. Proton pump inhibitors, amphotericin B, digitalis, laxative abuse, and pentamidine are examples of drugs that can cause hypomagnesemia. These medications can interfere with the absorption, utilization, or excretion of magnesium in the body, leading to lower levels.
It is important to note that hypomagnesemia can also occur due to other factors, such as kidney disease, diabetes, and hyperthyroidism. In some cases, the cause may not be easily identifiable. The symptoms of hypomagnesemia can range from mild to severe and may include muscle cramps, weakness, nausea, vomiting, fatigue, and abnormal heart rhythms. If left untreated, hypomagnesemia can lead to serious complications such as seizures and cardiac arrest.
Genetics
Prognostic Factors
The prognosis for individuals with hypomagnesemia depends on the condition’s underlying cause. Patients whose hypomagnesemia can be attributed to a specific and identifiable factor tend to have a positive prognosis and are likely to experience a full recovery. On the other hand, hypomagnesemia in critically ill patients is associated with a range of negative outcomes, including a more extended stay in the intensive care unit, increased mortality rates, and a higher likelihood of requiring mechanical ventilation.
These factors can significantly impact a patient’s overall health and well-being, making it essential to address hypomagnesemia promptly and appropriately to prevent further complications. Given these findings, it is crucial to monitor magnesium levels closely in critically ill patients and provide appropriate interventions when necessary.
Early detection and treatment of hypomagnesemia can improve patient outcomes, decrease the length of hospital stays, and reduce the risk of adverse events associated with the condition. By working closely with healthcare providers, patients can receive the care and support needed to manage hypomagnesemia and improve their overall quality of life.
Clinical History
Clinical History
The clinical manifestations of this condition can be classified into neuromuscular and cardiovascular manifestations, as well as other electrolyte abnormalities. The early signs of hypomagnesemia include nausea, vomiting, loss of appetite, fatigue, and weakness. Patients may also experience dysphagia, as well as muscular weakness. Patients may develop tremors, seizures, delirium, and apathy in severe cases.
Neuromuscular manifestations of hypomagnesemia can affect the nerves and muscles throughout the body, leading to muscle cramps, spasms, and twitching. Cardiovascular manifestations can result in changes in heart rhythm and an increased risk of arrhythmias, cardiac arrest, and sudden death. Other electrolyte abnormalities, including hypocalcemia, hypokalemia, and hyponatremia, can also occur.
Physical Examination
Physical Examination
Changes in mental status are a possible manifestation of hypomagnesemia, including disorientation, irritability, depression, and even psychosis. Severe hypomagnesemia can also lead to cardiac arrhythmias and reversible respiratory muscle failure. It is important to note that, similar to hypermagnesemia, the pace at which hypomagnesemia develops may be more significant than the actual level of magnesium in the body regarding the onset of symptoms.
This means that symptoms may still appear if the magnesium level drops rapidly, even if it is not yet at a critically low level. Therefore, it is crucial to monitor magnesium levels closely in individuals at risk of hypomagnesemia, such as those with malnutrition, alcoholism, or certain medical conditions.
Hypomagnesemia can cause several neuromuscular manifestations, including muscular weakness, tremors, seizures, paresthesias, tetany, positive Chvostek, and Trousseau signs. In addition, hypomagnesemia can cause both vertical and horizontal nystagmus.
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Differential Diagnoses
Acrodysostosis
Blomstrand chondrodysplasia
Hypoparathyroidism
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
Hypomagnesemia requires treatment based on the kidney function, the severity of the symptoms, and hemodynamic stability. In cases where patients are hemodynamically volatile in an acute hospital setting, 1-2 grams of magnesium sulfate can be administered over 15 minutes. For stable patients with severe and symptomatic hypomagnesemia, 1-2 grams of magnesium sulfate can be given over an hour. Adult patients requiring non-emergent repletion generally receive 4-8 grams of magnesium sulfate administered gradually over 12 to 24 hours.
Pediatric patients are given 25 to 50 mg/kg, with a maximum dose of 2 grams. For asymptomatic patients who are not hospitalized and can endure oral medication, sustained-release oral replacement should be attempted first. Magnesium chloride containing 64-71.5 mg or magnesium L-lactate containing 84 mg elemental magnesium are two examples of oral sustained-release magnesium preparations that can be used in such cases. Following repletion, it is important to recheck serum electrolyte levels to ensure that the treatment has been effective.
Although serum magnesium levels rise rapidly with treatment, it takes longer to deplete intracellular magnesium. As a result, patients with normal renal function should continue magnesium repletion for two days after their levels have normalized. Caution should be exercised when replenishing magnesium levels in patients with atypical kidney function, as defined by a creatinine clearance of less than 30 mL/min. Such patients risk developing hypermagnesemia, a condition characterized by excess magnesium in the blood, which can lead to potentially severe complications.
To minimize the risk of hypermagnesemia, studies suggest decreasing the magnesium dose by 50% and thoroughly monitoring magnesium levels. Additionally, it is crucial to address and treat the underlying cause of persistent hypomagnesemia, such as renal losses. In some cases, patients with chronic renal magnesium wasting or diuretic-induced hypomagnesemia may benefit from using potassium-sparing diuretics like triamterene or amiloride.
These diuretics can help preserve magnesium and potassium levels while managing fluid retention. It is also important to note that calcium replacement should be prioritized in patients with concurrent hypocalcemia before initiating magnesium replacement. This approach helps to avoid the increased urinary excretion of calcium caused by sulfate from magnesium sulfate, which can form a complex with ionized calcium.
Administer 15 to 30 mL (1,500 to 3,000 mg) one to three times a day.
It is contraindicated in severe renal impairment.
Dietary recommendations
19 to 30 years:
Females: Administer 310 mg/day
Pregnancy: Administer 350 mg/day
Lactation: Administer 310 mg/day
Males: Administer 400 mg/day
≥31 years:
Females: Administer 320 mg/day
Pregnancy: Administer 360 mg/day
Lactation: Administer 320 mg/day
Males: Administer 420 mg/day
25-50 mg/kg intravenous/intraosseous (IV/IO) medication over a period of 10-20 minutes (or faster if the patient has torsades de pointes), with a maximum dose of 2 g
Administer 10 to 20 mg/kg/dose four times a day; Administer 300 mg four times a day.
Note: Due to the potential of magnesium to cause diarrhea, achieving adequate magnesium levels with oral therapy may be challenging; an Intravenous supplement may be more appropriate, particularly in cases of severe shortfall.
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References
https://www.ncbi.nlm.nih.gov/books/NBK500003/
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Magnesium plays a crucial role as an electrolyte in the human body, participating in numerous reactions and processes impacting cellular, nerve conduction, and other essential bodily functions. The typical range of serum magnesium levels is between 1.46 and 2.68 mg/dL. However, when the serum magnesium level falls below 1.46 mg/dL, it leads to an electrolyte disturbance called hypomagnesemia. Despite its significant impact, hypomagnesemia is usually asymptomatic until the serum magnesium concentration drops below 1.2 mg/dL.
A range of factors, including alcohol use disorder, chronic disease, gastrointestinal, renal loss, and other underlying medical conditions, can cause hypomagnesemia. The loss of magnesium in the body can result from various factors, including chronic diarrhea, vomiting, or malabsorption syndromes, leading to reduced magnesium intake. At the same time, the excessive use of certain medications like diuretics can increase the loss of magnesium. People who consume alcohol regularly or suffer from conditions impairing nutrient absorption may also risk developing hypomagnesemia.
Magnesium deficiency has several consequences, including muscle weakness, fatigue, and cardiac arrhythmias, which can lead to more severe complications if not appropriately addressed. Treatment of hypomagnesemia involves identifying and addressing the underlying cause of the condition, such as stopping the use of certain medications, addressing any underlying medical conditions, or administering magnesium supplements, depending on the severity of the deficiency.
The prevalence of hypomagnesemia varies based on different characteristics and healthcare settings. In the general population, it has been reported to range from 2.5% to 15%. However, the prevalence is much higher in hospitalized patients, ranging from 12% to 20%. This prevalence is even more significant in critically ill patients, with one study estimating it as high as 65%.
A study conducted in India among 100 critically ill children with a mean age of 4.9 years showed a prevalence of approximately 55%. Similarly, another study found that patients with chronic alcohol use disorder had a 30% prevalence of hypomagnesemia. Although no recent studies have identified specific age groups that are more susceptible to hypomagnesemia, the condition can affect individuals of any age.
Magnesium is an essential mineral that plays a vital role in various biochemical reactions in the human body. It is the second most abundant intracellular cation after potassium. An average adult human body contains 1,000 millimoles of magnesium. Approximately 99% of this magnesium is found in bone and soft tissues. Magnesium is a crucial cofactor in many enzymatic reactions, including protein synthesis, DNA synthesis, and energy metabolism. It also plays an essential role in maintaining the body’s electrolyte balance, particularly concerning sodium, calcium and potassium.
The body regulates magnesium levels through a complex process involving the kidney, small bowel, and bone. The proximal tubule, thick ascending loop of Henle, and distal tubule of the kidney are primarily responsible for maintaining magnesium balance. The ileum and jejunum of the small bowel absorb magnesium, while bone serves as a reservoir of magnesium. Hypomagnesemia occurs due to various factors, such as renal or gastrointestinal losses or a disease condition. This alteration in magnesium homeostasis can result in various health problems, including neuromuscular hyperexcitability, cardiac arrhythmias, and seizures.
Several drugs can also cause hypomagnesemia by interfering with magnesium absorption or excretion. The condition is also caused by recessive mutations in the SLC12A3 gene that encodes the thiazide-sensitive sodium chloride cotransporter in the distal convoluted tubule. This mutation impairs the transcellular reabsorption of magnesium in the DCT, which causes an increase in calcium reabsorption. As a result, hypocalciuria and fluid loss occur, which can lower blood pressure.
Additionally, fluid loss triggers the renin-angiotensin-aldosterone system, leading to increased aldosterone levels, resulting in increased potassium secretion and subsequent hypokalemia. Mutations in this gene also affect the reabsorption of magnesium and calcium ions in the thick ascending limb of Henle, causing hypercalciuric hypomagnesemia that can eventually lead to nephrocalcinosis or chronic kidney disease. This condition can cause severe complications, including chronic kidney disease, renal failure, and electrolyte imbalances.
Hypomagnesemia is a condition where the body has lower-than-normal levels of magnesium. There are several causes of hypomagnesemia, including decreased magnesium intake. This can happen in starvation, anorexia nervosa, terminal cancer, and alcohol use disorder. In such cases, the body may not receive adequate amounts of magnesium through the diet, leading to a deficiency.
Another cause of hypomagnesemia is the use of certain medications. Proton pump inhibitors, amphotericin B, digitalis, laxative abuse, and pentamidine are examples of drugs that can cause hypomagnesemia. These medications can interfere with the absorption, utilization, or excretion of magnesium in the body, leading to lower levels.
It is important to note that hypomagnesemia can also occur due to other factors, such as kidney disease, diabetes, and hyperthyroidism. In some cases, the cause may not be easily identifiable. The symptoms of hypomagnesemia can range from mild to severe and may include muscle cramps, weakness, nausea, vomiting, fatigue, and abnormal heart rhythms. If left untreated, hypomagnesemia can lead to serious complications such as seizures and cardiac arrest.
The prognosis for individuals with hypomagnesemia depends on the condition’s underlying cause. Patients whose hypomagnesemia can be attributed to a specific and identifiable factor tend to have a positive prognosis and are likely to experience a full recovery. On the other hand, hypomagnesemia in critically ill patients is associated with a range of negative outcomes, including a more extended stay in the intensive care unit, increased mortality rates, and a higher likelihood of requiring mechanical ventilation.
These factors can significantly impact a patient’s overall health and well-being, making it essential to address hypomagnesemia promptly and appropriately to prevent further complications. Given these findings, it is crucial to monitor magnesium levels closely in critically ill patients and provide appropriate interventions when necessary.
Early detection and treatment of hypomagnesemia can improve patient outcomes, decrease the length of hospital stays, and reduce the risk of adverse events associated with the condition. By working closely with healthcare providers, patients can receive the care and support needed to manage hypomagnesemia and improve their overall quality of life.
Clinical History
The clinical manifestations of this condition can be classified into neuromuscular and cardiovascular manifestations, as well as other electrolyte abnormalities. The early signs of hypomagnesemia include nausea, vomiting, loss of appetite, fatigue, and weakness. Patients may also experience dysphagia, as well as muscular weakness. Patients may develop tremors, seizures, delirium, and apathy in severe cases.
Neuromuscular manifestations of hypomagnesemia can affect the nerves and muscles throughout the body, leading to muscle cramps, spasms, and twitching. Cardiovascular manifestations can result in changes in heart rhythm and an increased risk of arrhythmias, cardiac arrest, and sudden death. Other electrolyte abnormalities, including hypocalcemia, hypokalemia, and hyponatremia, can also occur.
Physical Examination
Changes in mental status are a possible manifestation of hypomagnesemia, including disorientation, irritability, depression, and even psychosis. Severe hypomagnesemia can also lead to cardiac arrhythmias and reversible respiratory muscle failure. It is important to note that, similar to hypermagnesemia, the pace at which hypomagnesemia develops may be more significant than the actual level of magnesium in the body regarding the onset of symptoms.
This means that symptoms may still appear if the magnesium level drops rapidly, even if it is not yet at a critically low level. Therefore, it is crucial to monitor magnesium levels closely in individuals at risk of hypomagnesemia, such as those with malnutrition, alcoholism, or certain medical conditions.
Hypomagnesemia can cause several neuromuscular manifestations, including muscular weakness, tremors, seizures, paresthesias, tetany, positive Chvostek, and Trousseau signs. In addition, hypomagnesemia can cause both vertical and horizontal nystagmus.
Differential Diagnoses
Acrodysostosis
Blomstrand chondrodysplasia
Hypoparathyroidism
Hypomagnesemia requires treatment based on the kidney function, the severity of the symptoms, and hemodynamic stability. In cases where patients are hemodynamically volatile in an acute hospital setting, 1-2 grams of magnesium sulfate can be administered over 15 minutes. For stable patients with severe and symptomatic hypomagnesemia, 1-2 grams of magnesium sulfate can be given over an hour. Adult patients requiring non-emergent repletion generally receive 4-8 grams of magnesium sulfate administered gradually over 12 to 24 hours.
Pediatric patients are given 25 to 50 mg/kg, with a maximum dose of 2 grams. For asymptomatic patients who are not hospitalized and can endure oral medication, sustained-release oral replacement should be attempted first. Magnesium chloride containing 64-71.5 mg or magnesium L-lactate containing 84 mg elemental magnesium are two examples of oral sustained-release magnesium preparations that can be used in such cases. Following repletion, it is important to recheck serum electrolyte levels to ensure that the treatment has been effective.
Although serum magnesium levels rise rapidly with treatment, it takes longer to deplete intracellular magnesium. As a result, patients with normal renal function should continue magnesium repletion for two days after their levels have normalized. Caution should be exercised when replenishing magnesium levels in patients with atypical kidney function, as defined by a creatinine clearance of less than 30 mL/min. Such patients risk developing hypermagnesemia, a condition characterized by excess magnesium in the blood, which can lead to potentially severe complications.
To minimize the risk of hypermagnesemia, studies suggest decreasing the magnesium dose by 50% and thoroughly monitoring magnesium levels. Additionally, it is crucial to address and treat the underlying cause of persistent hypomagnesemia, such as renal losses. In some cases, patients with chronic renal magnesium wasting or diuretic-induced hypomagnesemia may benefit from using potassium-sparing diuretics like triamterene or amiloride.
These diuretics can help preserve magnesium and potassium levels while managing fluid retention. It is also important to note that calcium replacement should be prioritized in patients with concurrent hypocalcemia before initiating magnesium replacement. This approach helps to avoid the increased urinary excretion of calcium caused by sulfate from magnesium sulfate, which can form a complex with ionized calcium.
Administer 15 to 30 mL (1,500 to 3,000 mg) one to three times a day.
It is contraindicated in severe renal impairment.
Dietary recommendations
19 to 30 years:
Females: Administer 310 mg/day
Pregnancy: Administer 350 mg/day
Lactation: Administer 310 mg/day
Males: Administer 400 mg/day
≥31 years:
Females: Administer 320 mg/day
Pregnancy: Administer 360 mg/day
Lactation: Administer 320 mg/day
Males: Administer 420 mg/day
25-50 mg/kg intravenous/intraosseous (IV/IO) medication over a period of 10-20 minutes (or faster if the patient has torsades de pointes), with a maximum dose of 2 g
Administer 10 to 20 mg/kg/dose four times a day; Administer 300 mg four times a day.
Note: Due to the potential of magnesium to cause diarrhea, achieving adequate magnesium levels with oral therapy may be challenging; an Intravenous supplement may be more appropriate, particularly in cases of severe shortfall.
https://www.ncbi.nlm.nih.gov/books/NBK500003/
medtigo
Hypomagnesemia
Updated :
August 30, 2023
Magnesium plays a crucial role as an electrolyte in the human body, participating in numerous reactions and processes impacting cellular, nerve conduction, and other essential bodily functions. The typical range of serum magnesium levels is between 1.46 and 2.68 mg/dL. However, when the serum magnesium level falls below 1.46 mg/dL, it leads to an electrolyte disturbance called hypomagnesemia. Despite its significant impact, hypomagnesemia is usually asymptomatic until the serum magnesium concentration drops below 1.2 mg/dL.
A range of factors, including alcohol use disorder, chronic disease, gastrointestinal, renal loss, and other underlying medical conditions, can cause hypomagnesemia. The loss of magnesium in the body can result from various factors, including chronic diarrhea, vomiting, or malabsorption syndromes, leading to reduced magnesium intake. At the same time, the excessive use of certain medications like diuretics can increase the loss of magnesium. People who consume alcohol regularly or suffer from conditions impairing nutrient absorption may also risk developing hypomagnesemia.
Magnesium deficiency has several consequences, including muscle weakness, fatigue, and cardiac arrhythmias, which can lead to more severe complications if not appropriately addressed. Treatment of hypomagnesemia involves identifying and addressing the underlying cause of the condition, such as stopping the use of certain medications, addressing any underlying medical conditions, or administering magnesium supplements, depending on the severity of the deficiency.
The prevalence of hypomagnesemia varies based on different characteristics and healthcare settings. In the general population, it has been reported to range from 2.5% to 15%. However, the prevalence is much higher in hospitalized patients, ranging from 12% to 20%. This prevalence is even more significant in critically ill patients, with one study estimating it as high as 65%.
A study conducted in India among 100 critically ill children with a mean age of 4.9 years showed a prevalence of approximately 55%. Similarly, another study found that patients with chronic alcohol use disorder had a 30% prevalence of hypomagnesemia. Although no recent studies have identified specific age groups that are more susceptible to hypomagnesemia, the condition can affect individuals of any age.
Magnesium is an essential mineral that plays a vital role in various biochemical reactions in the human body. It is the second most abundant intracellular cation after potassium. An average adult human body contains 1,000 millimoles of magnesium. Approximately 99% of this magnesium is found in bone and soft tissues. Magnesium is a crucial cofactor in many enzymatic reactions, including protein synthesis, DNA synthesis, and energy metabolism. It also plays an essential role in maintaining the body’s electrolyte balance, particularly concerning sodium, calcium and potassium.
The body regulates magnesium levels through a complex process involving the kidney, small bowel, and bone. The proximal tubule, thick ascending loop of Henle, and distal tubule of the kidney are primarily responsible for maintaining magnesium balance. The ileum and jejunum of the small bowel absorb magnesium, while bone serves as a reservoir of magnesium. Hypomagnesemia occurs due to various factors, such as renal or gastrointestinal losses or a disease condition. This alteration in magnesium homeostasis can result in various health problems, including neuromuscular hyperexcitability, cardiac arrhythmias, and seizures.
Several drugs can also cause hypomagnesemia by interfering with magnesium absorption or excretion. The condition is also caused by recessive mutations in the SLC12A3 gene that encodes the thiazide-sensitive sodium chloride cotransporter in the distal convoluted tubule. This mutation impairs the transcellular reabsorption of magnesium in the DCT, which causes an increase in calcium reabsorption. As a result, hypocalciuria and fluid loss occur, which can lower blood pressure.
Additionally, fluid loss triggers the renin-angiotensin-aldosterone system, leading to increased aldosterone levels, resulting in increased potassium secretion and subsequent hypokalemia. Mutations in this gene also affect the reabsorption of magnesium and calcium ions in the thick ascending limb of Henle, causing hypercalciuric hypomagnesemia that can eventually lead to nephrocalcinosis or chronic kidney disease. This condition can cause severe complications, including chronic kidney disease, renal failure, and electrolyte imbalances.
Hypomagnesemia is a condition where the body has lower-than-normal levels of magnesium. There are several causes of hypomagnesemia, including decreased magnesium intake. This can happen in starvation, anorexia nervosa, terminal cancer, and alcohol use disorder. In such cases, the body may not receive adequate amounts of magnesium through the diet, leading to a deficiency.
Another cause of hypomagnesemia is the use of certain medications. Proton pump inhibitors, amphotericin B, digitalis, laxative abuse, and pentamidine are examples of drugs that can cause hypomagnesemia. These medications can interfere with the absorption, utilization, or excretion of magnesium in the body, leading to lower levels.
It is important to note that hypomagnesemia can also occur due to other factors, such as kidney disease, diabetes, and hyperthyroidism. In some cases, the cause may not be easily identifiable. The symptoms of hypomagnesemia can range from mild to severe and may include muscle cramps, weakness, nausea, vomiting, fatigue, and abnormal heart rhythms. If left untreated, hypomagnesemia can lead to serious complications such as seizures and cardiac arrest.
The prognosis for individuals with hypomagnesemia depends on the condition’s underlying cause. Patients whose hypomagnesemia can be attributed to a specific and identifiable factor tend to have a positive prognosis and are likely to experience a full recovery. On the other hand, hypomagnesemia in critically ill patients is associated with a range of negative outcomes, including a more extended stay in the intensive care unit, increased mortality rates, and a higher likelihood of requiring mechanical ventilation.
These factors can significantly impact a patient’s overall health and well-being, making it essential to address hypomagnesemia promptly and appropriately to prevent further complications. Given these findings, it is crucial to monitor magnesium levels closely in critically ill patients and provide appropriate interventions when necessary.
Early detection and treatment of hypomagnesemia can improve patient outcomes, decrease the length of hospital stays, and reduce the risk of adverse events associated with the condition. By working closely with healthcare providers, patients can receive the care and support needed to manage hypomagnesemia and improve their overall quality of life.
Clinical History
The clinical manifestations of this condition can be classified into neuromuscular and cardiovascular manifestations, as well as other electrolyte abnormalities. The early signs of hypomagnesemia include nausea, vomiting, loss of appetite, fatigue, and weakness. Patients may also experience dysphagia, as well as muscular weakness. Patients may develop tremors, seizures, delirium, and apathy in severe cases.
Neuromuscular manifestations of hypomagnesemia can affect the nerves and muscles throughout the body, leading to muscle cramps, spasms, and twitching. Cardiovascular manifestations can result in changes in heart rhythm and an increased risk of arrhythmias, cardiac arrest, and sudden death. Other electrolyte abnormalities, including hypocalcemia, hypokalemia, and hyponatremia, can also occur.
Physical Examination
Changes in mental status are a possible manifestation of hypomagnesemia, including disorientation, irritability, depression, and even psychosis. Severe hypomagnesemia can also lead to cardiac arrhythmias and reversible respiratory muscle failure. It is important to note that, similar to hypermagnesemia, the pace at which hypomagnesemia develops may be more significant than the actual level of magnesium in the body regarding the onset of symptoms.
This means that symptoms may still appear if the magnesium level drops rapidly, even if it is not yet at a critically low level. Therefore, it is crucial to monitor magnesium levels closely in individuals at risk of hypomagnesemia, such as those with malnutrition, alcoholism, or certain medical conditions.
Hypomagnesemia can cause several neuromuscular manifestations, including muscular weakness, tremors, seizures, paresthesias, tetany, positive Chvostek, and Trousseau signs. In addition, hypomagnesemia can cause both vertical and horizontal nystagmus.
Differential Diagnoses
Acrodysostosis
Blomstrand chondrodysplasia
Hypoparathyroidism
Hypomagnesemia requires treatment based on the kidney function, the severity of the symptoms, and hemodynamic stability. In cases where patients are hemodynamically volatile in an acute hospital setting, 1-2 grams of magnesium sulfate can be administered over 15 minutes. For stable patients with severe and symptomatic hypomagnesemia, 1-2 grams of magnesium sulfate can be given over an hour. Adult patients requiring non-emergent repletion generally receive 4-8 grams of magnesium sulfate administered gradually over 12 to 24 hours.
Pediatric patients are given 25 to 50 mg/kg, with a maximum dose of 2 grams. For asymptomatic patients who are not hospitalized and can endure oral medication, sustained-release oral replacement should be attempted first. Magnesium chloride containing 64-71.5 mg or magnesium L-lactate containing 84 mg elemental magnesium are two examples of oral sustained-release magnesium preparations that can be used in such cases. Following repletion, it is important to recheck serum electrolyte levels to ensure that the treatment has been effective.
Although serum magnesium levels rise rapidly with treatment, it takes longer to deplete intracellular magnesium. As a result, patients with normal renal function should continue magnesium repletion for two days after their levels have normalized. Caution should be exercised when replenishing magnesium levels in patients with atypical kidney function, as defined by a creatinine clearance of less than 30 mL/min. Such patients risk developing hypermagnesemia, a condition characterized by excess magnesium in the blood, which can lead to potentially severe complications.
To minimize the risk of hypermagnesemia, studies suggest decreasing the magnesium dose by 50% and thoroughly monitoring magnesium levels. Additionally, it is crucial to address and treat the underlying cause of persistent hypomagnesemia, such as renal losses. In some cases, patients with chronic renal magnesium wasting or diuretic-induced hypomagnesemia may benefit from using potassium-sparing diuretics like triamterene or amiloride.
These diuretics can help preserve magnesium and potassium levels while managing fluid retention. It is also important to note that calcium replacement should be prioritized in patients with concurrent hypocalcemia before initiating magnesium replacement. This approach helps to avoid the increased urinary excretion of calcium caused by sulfate from magnesium sulfate, which can form a complex with ionized calcium.
https://www.ncbi.nlm.nih.gov/books/NBK500003/
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