Hypermagnesemia symptoms - Hypermagnesemia treatment - causes

Hypermagnesemia causes - Hypermagnesemia symptoms and treatment
Hypermagnesemia is a rare disorder of electrolyte balance caused by elevated levels of serum magnesium. Early symptoms of hypermagnesemia are general lethargy and hypotension.
Treatment of the disorder is essentially by immediate discontinuation of magnesium intake and haemodialysis. Elevated serum magnesium level is of rare occurrence, as in healthy individuals excess amounts of the mineral is eliminated by the kidneys in the urine.

Hypermagnesemia symptoms

Depending upon the level of increase in serum magnesium, symptoms of hypermagnesemia progress in severity. Some of the symptoms are listed below:
  • Lethargy,
  • nausea,
  • hypotension,
  • hyporeflexia,
  • hypoventilation,
  • vasodilatation,
  • arrhythmia,
  • hypoxic encephalopathy,
  • bradycardia,
  • asystole and
  • cardiac arrest.

Hypermagnesemia causes

Intake of very large doses of magnesium-containing supplements, laxatives or antacids by persons with renal insufficiency can cause hypermagnesemia.
Absence of hemodialysis in the event of acute renal failure, causes elevated magnesium levels in the blood serum.
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Intestinal hypomotility causes decreased elimination of the mineral as well as its increased absorption from the gastrointestinal tract.
Adrenal insufficiency is known to cause secondary hypermagnesemia.
Pregnant women under preeclampsia or eclampsia treatment, are given magnesium sulfate infusion to prevent eclamptic seizures and to control blood pressure. Close monitoring is necessary to prevent rise in serum levels of magnesium.
Neonates may receive excess magnesium from their eclamptic mother who has undergone magnesium sulfate infusion.
An episode of diabetic ketoacidosis and dehydration can cause hypermagnesemia.
Release of massive amounts of intracellular magnesium in conditions such as rhabdomyolysis, hemolysis or tumor lysis syndrome can contribute to elevated levels of the mineral in the blood serum.
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Endocrine system impairment as in hypothyroidism or hyperparathyroidism can cause this disorder.
Excessive consumption of magnesium compounds as supplements or laxatives can cause hypermagnesemia in constipated individuals.
Kutsal E et al reported a case of severe hypermagnesemia as a result of excessive purgative ingestion in a child without renal failure. She was given magnesium hydroxide cathartic tablets for seven days for relieving constipation. The serum magnesium levels reached 14.9 mg/dL and the child had symptoms of lethargy and hypotension when referred to hospital. Immediate hemodialysis improved her condition and the magnesium level was brought under control with the resolution of symptoms.
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In another case reported by Weng YM et al, a 70 years old women suffering from constipation, had the magnesium oxide tablets retained in the gastrointestinal tract without evacuation. It caused continuous absorption and rebound of hypermagnesemia leading to prolonged hypotension and hypoxic encephalopathy.

Hypermagnesemia treatment

The first step in treatment is withdrawing magnesium supplementation in all forms.
In patients suffering from persistent bowel hypomotility (constipation) even after the use magnesium based laxatives, gastrointestinal tract evacuation or decontamination must be carried out to stop continued absorption of the mineral.
Intravenous calcium gluconate is administered as treatment to negate the effect of hypermagnesemia on the neuromuscular and cardiac functions.
In case of renal sufficiency intravenous diuretics are administered to speedup the elimination of the excess mineral.
In case of hypermagnesemia induced by other diseases, simultaneous treatments must carried out.
In cases of renal insufficiency or failure, hemodialysis is the only treatment option available to remove excess magnesium.

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1.Kutsal E, Aydemir C, Eldes N, Demirel F, Polat R, Taspnar O, Kulah E. Severe hypermagnesemia as a result of excessive cathartic ingestion in a child without renal failure. Pediatr Emerg Care. 2007 Aug;23(8):570-2.
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