Uncommon clinical finding, and symptomatic process is even less common.

Uncommon problem in the absence of magnesium administration or renal failure.

Has a low incidence because the kidney is able to eliminate excess magnesium by rapidly reducing its tubular reabsorption to almost negligible amount.

Plasma magnesium ranges from 1.7-2.3 mg/dL.

Approximately 30% of total plasma magnesium is protein-bound.

Approximately of magnesium 70% is filterable.

Normally, only 3% of filtered magnesium appears in urine and 97% is reabsorbed by the renal tubules.

Approximately 25-30% of filtered magnesium is reabsorbed in the proximal tubule, and 60-65% of filtered magnesium is reabsorbed in the thick ascending loop of Henle and 5% is reabsorbed in the distal nephron.

The most common cause of hypermagnesemia is renal failure, and other causes include excessive intake, lithium treatment, hypothyroidism, adrenal insufficiency, Familial hypocalciuric hypercalcemia, Milk alkali syndrome and depression.

Patients with end-stage renal disease often have mild hypermagnesemia, and ingestion of magnesium-containing medications can exacerbate the process.

In patients on dialysis, the serum magnesium level directly relates to the dialysate magnesium concentration.

Associated with increased mortality attribute to greater neurohormonal activation, parathyroid hormone suppression, renal dysfunction, and hyperphosphatemia

With acute renal failure, hypermagnesemia usually presents during the oliguric phase, and levels returns to normal during the diuretic phase.

Exogenous magnesium during the oliguric phase can lead to severe hypermagnesemia.

People often take magnesium-containing medications (eg, antacids, laxatives, rectal enemas).

Hypermagnesemia can develop after treatment of drug overdoses with magnesium-containing cathartics, and it also occurs in patients taking magnesium-containing medications for therapeutic purposes.

Most of the above patients have normal renal function.

With ingestion of a large amount of magnesium with a gastrointestinal disorder such as I gastritis, colitis, gastric dilation, absorption may increase.

Monitoring serum magnesium levels in patients taking magnesium-containing medications is prudent.

Excessive tissue breakdown as is seen with sepsis, shock, large burns, especially with concurrent renal failure, can deliver a large amount of magnesium from the intracellular space, along with a massive elevation of phosphorus and potassium.

In the treatment of eclampsia, hypermagnesemia is induced deliberately and can be symptomatic.

Occasionally, can occur in the newborn infant, as a result of maternal magnesium therapy.

Magnesium-containing phosphorus binders are rarely used in end-stage renal disease patients but can lead to elevated magnesium levels.

Lithium therapy causes hypermagnesemia by decreasing urinary excretion, although the mechanism for this is not completely clear.

Familial hypocalciuric hypercalcemia may cause modest elevations in serum magnesium.

This autosomal dominant disorder is characterized by very low excretion of calcium and magnesium and by a normal parathyroid hormone level.

Abnormalities of calcium and magnesium handling are due to mutations in the calcium-sensing receptor, resulting in increased magnesium reabsorption in the loop of Henle.

Hypothyroidism, adrenal insufficiency, milk-alkali syndrome and theophylline intoxication occasionally produce mild elevations of serum magnesium.

Three types of symptoms may be seen when the plasma magnesium concentration exceeds 4 meq/L (4.8 mg/dL or 2 mmol/L): neuromuscular; cardiovascular; and hypocalcemia.

Plasma magnesium concentration 4 to 6 meq/L (4.8 to 7.2 mg/dL or 2 to 3 mmol/L) is associated with nausea, flushing, headache, lethargy, drowsiness, and diminished deep tendon reflexes.

Plasma magnesium concentration 6 to 10 meq/L (7.2 to 12 mg/dL or 3 to 5 mmol/L) associated with somnolence, hypocalcemia, absent deep tendon reflexes, hypotension, bradycardia, and ECG changes.

Plasma magnesium concentration above 10 meq/L (12 mg/dL or 5 mmol/L) associated with muscle paralysis, respiratory paralysis, complete heart block, and cardiac arrest.

Increased magnesium levelsvdecreases impulse transmission across the neuromuscular junction producing a curare-like effect.

Diminished deep tendon reflexes that is usually first noted when the plasma magnesium concentration reaches 4 to 6 meq/L (4.8 to 7.2 mg/dL or 2 to 3 mmol/L).

More severe hypermagnesemia can result in somnolence, loss of deep tendon reflexes, muscle paralysis, flaccid quadriplegia and, since smooth muscle function impairment with decreased respiration and eventual apnea.

Parasympathetic blockade can induce fixed and dilated pupils.

Magnesium is an effective calcium channel blocker both extracellularly and intracellularly.

Intracellular magnesium profoundly blocks several cardiac potassium channels.

Bradycardia and hypotension begin to appear at a plasma magnesium concentration above 4 to 5 meq/L (4.8 to 6 mg/dL or 2 to 2.5 mmol/L).


ECG changes can be seen at a concentration of 5 to 10 meq/L (6 to 12 mg/dL or 2.5 to 5 mmol/L), including prolongation of the P-R interval, an increase in QRS duration, and an increase in Q-T interval. 

Complete heart block and cardiac arrest may occur at a plasma magnesium concentration above 15 meq/L (18 mg/dL or 7.5 mmol/L).

Inhibits the secretion of parathyroid hormone, leading to a reduction in the plasma calcium concentration

The fall in the plasma calcium concentration is usually transient and produces no symptoms.

Symptoms of drowsiness, signs of hyporeflexia with neuromuscular, respiratory, and cardiovascular collapse can occur.

Can lead to hypocalcemia.

Seen in severe renal failure with the administration of magnesium containing antacids, and following intravenous magnesium sulfate for eclampsia or preeclampsia.

Mild elevations common in patients on dialysis.

Symptoms of hypermagnesemia usually are not apparent unless the serum magnesium level is greater than 2 mmol/L.

Concomitant hypocalcemia, hyperkalemia, or uremia exaggerate the symptoms at any given level.

Neuromuscular symptoms are the most common presenting problems.

Hypermagnesemia causes blockage of neuromuscular transmission by preventing presynaptic acetylcholine release and by competitively inhibiting calcium influx into the presynaptic nerve channels via the voltage-dependent calcium channel.

One of the earliest symptoms, is deep-tendon reflex attenuation.

Facial paresthesias also may occur at moderate serum levels.

Muscle weakness is a more severe manifestation, occurring at levels greater than 5 mmol/L.

Muscle weakness can result in flaccid muscle paralysis and depressed respiration and can eventually progress to apnea.

Depresses the conduction system of the heart and sympathetic ganglia.

A moderate increase in serum magnesium can lead to a mild decrease in blood pressure, and a greater concentration may cause severe symptomatic hypotension.

Magnesium is also cardiotoxic and, in high concentrations, can cause bradycardia.

Occasionally, complete heart block and cardiac arrest may occur at levels greater than 7 mmol/L.

Hypocalcemia results from a decrease in the secretion of parathyroid hormone (PTH) or from end-organ resistance to PTH.

Paralytic ileus may develop from smooth-muscle paralysis.

In mothers being treated with magnesium for preterm labor suppression are at risk for smooth-muscle paralysis.

May interfere with blood clotting through interference with platelet adhesiveness, thrombin generation time, and clotting time.

Nonspecific symptoms include nausea, vomiting, and cutaneous flushing.

Usually a result of a combination of excess magnesium intake and a coexisting impairment of renal function.

Diagnosis involves measuring serum magnesium levels.

Diagnosis in many cases is unsuspected, but its existence should be suspected in the context of preeclampsia, renal failure, the presence of magnesium-containing preparations, or a decreased anion gap.

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