Hypermagnesemia is defined as an abnormally elevated concentration of magnesium in the blood. It is a rare laboratory and clinical finding. The symptoms depend on the serum concentration of magnesium and may include muscle weakness, facial paresthesias, and in severe cases, cardiac arrest.
Hypermagnesemia remains asymptomatic until serum magnesium levels rise above 2mmol/L. The presence of co-existing hypocalcemia, hyperkalemia, and uremia may worsen the clinical presentation at any given serum level. The clinical features of hypermagnesemia depend on the serum concentration of magnesium.
Hypermagnesemia commonly presents with neuromuscular blockade. This results from the inhibition of presynaptic acetylcholine release and presynaptic calcium influx via the voltage-gated calcium channels . Other features of hypermagnesemia include reduced or absent deep tendon reflexes, facial paresthesias, muscle weakness, flaccid paralysis, hypotension, respiratory depression which may eventually progress to apnea, and bradycardia . The smooth muscle paralysis caused by hypermagnesemia may result in paralytic ileus . However, the effects of hypermagnesemia on the muscle usually occur at mild to moderate elevations of serum magnesium levels.
Excess serum magnesium inhibits the sympathetic outflow to the heart and causes hyperpolarization of the conduction fibers, thereby causing bradycardia. In severe cases, hypermagnesemia may result in a complete heart block and cardiac arrest. These usually occur at moderate to severe elevations of serum magnesium levels. Hypermagnesemia at higher concentrations may also result in depressed consciousness and ultimately, death.
Hypermagnesemia may also impair platelet adhesion, thrombin production time, and clotting time, therefore resulting in bleeding disorders. Other non-specific symptoms of hypermagnesemia include nausea, vomiting, headache, and dizziness. Mothers being treated for pre-eclampsia are at a considerable risk of hypermagnesemia .
ECG changes are observed at serum magnesium levels of 6-12mg/dL. These changes include a prolonged PR interval and QRS complex, delayed intraventricular depolarization, and heightened T wave. The ECG may also reveal features of other electrolyte imbalances.
Serum magnesium levels of 9-12 mg/dL present with somnolence, hyporeflexia, and hypotension. Serum levels above 12mg/dL results in sinoatrial and atrioventricular block, muscle paralysis, hypoventilation, ventricular arrhythmias, and stupor. Cardiac asystole, coma, and respiratory depression usually occur at serum magnesium levels above 15.6 mg/dL    .
Diagnosis of hypermagnesemia involves blood investigation to determine its serum concentration in a suspected case . In cases where analysis of serum magnesium concentration is not immediately possible, a clue to the diagnosis may be given by the history: treatment for a recent or concomitant disease such as pre-eclampsia, renal failure, or intestinal hypomotility, or certain medications including vitamins, antacids, and cathartics.
Serum levels of other electrolytes including potassium, calcium, and magnesium could also aid the diagnosis because hypermagnesemia is rarely the sole electrolytic anomaly  . Hyperkalemia and hypocalcemia are usually concurrent findings.
Other necessary investigations include renal function tests: BUN, creatine levels, and creatinine clearance tests, serum creatine phosphokinase, urine myoglobin, and arterial blood gases. Urine myoglobulin and creatine phosphokinase levels are needed if myoglobinuria is suspected. An arterial blood gas analysis may reveal respiratory acidosis.
Thyroid function tests are also necessary to rule out hypothyroidism, which is an uncommon cause of hypermagnesemia.
The ECG shows certain changes including a prolonged PR interval, widened QRS complex, and an elevated T wave at serum magnesium levels of 5-10mEq/L.
The treatment of hypermagnesemia depends on the presentation, renal function, and the serum magnesium concentration. However, the principles of management include the inhibition of magnesium effects and the elimination of excess magnesium while correcting the underlying disease, if any . Management generally consists of treatment of the underlying cause, cardiorespiratory support, diuretic therapy, intravenous infusion of calcium gluconate, and hemodialysis  .
Being an antagonist of magnesium, calcium reverses the muscular, respiratory, and cardiac effects of hypermagnesemia and also increases the renal excretion of magnesium . It is administered as 10% calcium gluconate 10-20 ml IV slowly. Intravenous furosemide helps to increase the renal excretion of magnesium in cases of renal insufficiency. However, hemodialysis could be essential in very severe cases of hypermagnesemia with a normal or severely impaired renal function . This is because up to 70% of serum magnesium are not protein-bound, hence can be eliminated by hemodialysis. Hemodialysis is more effective than peritoneal dialysis in terms of reducing the magnesium concentration to safer levels. However, peritoneal dialysis is a good alternative if hemodialysis is unavailable or impractical. Indications for hemodialysis include renal failure, hypermagnesemia unresponsive to diuretic therapy, arrhythmias, and persistent hemodynamic instability.
Cases with hypotension and hemodynamic instability require fluid resuscitation. In patients with depressed levels of consciousness, intubation may be necessary.
The outcome is generally good if magnesium levels are normalized.
The most common cause of hypermagnesemia is renal failure. Other causes include excessive iatrogenic administration of drugs containing magnesium, lithium therapy, familial hypocalciuric hypercalcemia, depression, hypoparathyroidism, hypothyroidism, diabetic ketoacidosis, milk-alkali syndrome, skeletal muscle neoplasms, and Addison's disease   . Familial hypocalciuric hypercalcemia is an autosomal dominant disorder characterized by reduced excretion of calcium and magnesium in the presence of normal parathyroid activity. It is a common cause of mild hypermagnesemia. Individuals with renal impairment are generally more prone to hypermagnesemia from iatrogenic causes. Diabetic ketoacidosis causes hypermagnesemia by reducing extracellular fluid volume content from dehydration.
End-stage renal disease causes hypermagnesemia if the patient is not on dialysis. In acute renal failure, hypermagnesemia is observed during the phase of oliguria with the serum magnesium levels normalizing in the polyuric phase. In patients undergoing dialysis, the serum level of magnesium is proportional to the magnesium concentration in the dialysate .
Hypermagnesemia can be caused or exacerbated by per os ingestion of normal or high doses of magnesium-containing drugs such as antacids, laxatives, and cathartics    .
Diseases associated with excessive tissue breakdown including extensive burns, sepsis, rhabdomyolysis, tumor lysis syndrome, and shock, can also lead to hypermagnesemia. These conditions cause electrolytes including magnesium to flow from the intracellular space into the blood .
Hypothyroidism, milk-alkali syndrome, and theophylline overdose are also common causes of hypermagnesemia  . Iatrogenic causes include intravenous administration of magnesium at therapeutic or excessive doses for certain conditions such as asthma, pre-eclampsia or eclampsia, and cardiac arrhythmias .
Less common causes include increased GI absorption or reduced GI loss of magnesium due to GI hypomotility which may result from the use of anticholinergic medications or opioids, chronic constipation, and bowel obstruction.
Hypermagnesemia is rare in the United States. Furthermore, the elderly are more prone to hypermagnesemia because of the use of magnesium-containing laxatives and antacids and also due to the high incidence of ESRD in this age group.
The reference range of total serum magnesium is 1.7-2.4mg/dL. The kidney is the main organ involved in magnesium homeostasis. The proximal tubule absorbs 10% of the filtered magnesium, while 50-70% of the remaining filtered magnesium is absorbed by the thick ascending limb of the loop of Henle .
Generally, hypermagnesemia occurs via three mechanisms: decreased excretion (as in renal failure), excessive intake (oral or intravenous administration of magnesium or magnesium-containing drugs for therapeutic purposes), or increased GI absorption (GI hypomotility).
Hypermagnesemia has several effects on the CNS, cardiovascular systems, and the neuromuscular junctions.
Prevention of hypermagnesemia can be achieved by restriction of magnesium intake in susceptible patients, such as withdrawal of treatment once certain symptoms such as muscle weakness and loss of deep tendon reflexes start to emerge, and renal replacement therapy in those with end-stage renal disease.
Hypermagnesemia is a rare disorder which is most commonly associated with iatrogenic administration of magnesium and renal failure. The laboratory diagnosis is made when serum magnesium exceeds 2.1 mEq/L (1.05mmol/L). The reference range for serum magnesium is 1.5-2.1 mEq/L (1.7-2.4mg/dL). Most of the serum magnesium is detected in the blood in its ionized form.
Magnesium is contained in all green plants, and in a lot of seeds and fruits. Magnesium is one of the most vital electrolytes in the body, necessary for DNA synthesis, protein synthesis, and in many metabolic processes.
There are a number of causes of hypermagnesemia and these include renal impairment, administration of therapeutic or excessive doses of magnesium-containing medications, diseases which cause tissue breakdown, such as rhabdomyolysis, burns, sepsis, and intestinal hypomotility.
Hypermagnesemia is unusual in individuals with normal renal function because the healthy kidneys are usually able to maintain magnesium homeostasis by rapidly inhibiting its tubular reabsorption when serum magnesium is high. In patients with chronic renal failure or end-stage renal disease (ESRD), dialysis performs this function of eliminating excess magnesium, the rate of which depends on the dialysis solution employed .
The clinical presentation of hypermagnesemia depends on the serum magnesium level and renal capacity. However, symptomatic or clinical cases of hypermagnesemia are a rare occurrence. Clinical features generally include nausea, vomiting, muscle weakness, lowered blood pressure, bradycardia, and reduced or absent deep tendon reflexes. In severe cases, flaccid paralysis, paresthesias, altered mental status, respiratory depression, atrioventricular heart block, and cardiac arrest occur.
Diagnosis of hypermagnesemia can be made via laboratory tests including serum magnesium, serum potassium, and serum calcium levels, as hypermagnesemia rarely occurs in isolation without derangements in these electrolytes. Arterial blood gas analysis and an ECG are also important in the diagnosis of hypermagnesemia.
Hypermagnesemia is a condition in which the level of magnesium in the blood is higher than it should be. The normal range of magnesium in the blood is 1.7-2.4 mg/dL. Magnesium is one of the key substances in the body called electrolytes which play a number of critical roles. Magnesium is needed to produce certain hormones, DNA, and other proteins in the body.
Magnesium can be found richly in vegetables, fruits, and seeds. The kidney is the main organ which maintains the balance of magnesium in the body by excreting excess magnesium. Therefore, kidney failure is a very common cause of hypermagnesemia.
Excess blood magnesium is commonly seen in patients with kidney failure, because in this case, the kidneys can no longer excrete magnesium, so it accumulates in the blood. Other causes include receiving treatment with magnesium or drugs which contain magnesium, such as vitamins and antacids. Some pregnant women diagnosed with a condition called pre-eclampsia (a disorder characterized by very high blood pressure and protein in the urine during pregnancy) may be treated with magnesium sulfate infusion to prevent seizures; therefore, these women are at a high risk of hypermagnesemia. Patients with asthma and an irregular heart rhythm may also be treated with magnesium, posing a risk of hypermagnesemia to these patients.
Other causes of hypermagnesemia include a less active thyroid function (hypothyroidism), decreased activity of the parathyroid glands (hypoparathyroidism), tumors of the skeletal muscles, increased intestinal absorption of magnesium (resulting from slowed intestinal movement and delayed transit of food through the gut), insufficiency of the adrenal glands, and certain diseases characterized by breakdown of cells such as sepsis, burns, crush injuries, and cancer.
Hypermagnesemia is a rare disorder and it rarely produces symptoms. Symptoms depend on the level of magnesium in the blood. However, in cases where it produces symptoms, it results in muscle weakness or paralysis, lowered blood pressure, reduced heart rate, lowered rate of breathing, and in severe cases, cardiac arrest and coma.
Doctors can make a diagnosis of hypermagnesemia by testing for blood levels of magnesium and other substances like potassium and calcium. Other tests include kidney function tests and an electrocardiogram (ECG); the latter demonstrates the electrical activity of the heart. Thyroid gland function can also be tested by certain blood investigations to rule out hypothyroidism as the culprit.
Treatment of hypermagnesemia involves the treatment or correction of the underlying cause and reversal of the effects of excess magnesium in the body. The reversal can be achieved by administering calcium intravenously. Calcium antagonizes the effects of magnesium. Eliminating excess magnesium can be achieved by administering diuretics such as furosemide: these are drugs which increase the excretion of water and salt by the kidneys. Hemodialysis is a very important method of eliminating the excess magnesium from the blood in patients with severe kidney disease.