Urgent considerations
See Differentials for more details
Hypomagnesaemia
Generally defined as serum magnesium <0.75 mmol/L (<1.5 mEq/L).
Severe magnesium deficiency
Patients with severe magnesium depletion (<0.5 mmol/L [<1 mEq/L]) are symptomatic.[40] Symptoms include hallucinations, seizures, muscle spasms, swallowing difficulty or inability (spasms of oesophageal muscles), and irregular heart beats. The condition can be life-threatening due to recurring seizures or irregular heart beats that can progress towards arrhythmias, extrasystoles, torsades de pointes, ventricular tachycardia, or ventricular fibrillation.
Intravenous magnesium replacement is indicated if the serum magnesium is <0.5 mmol/L (<1 mEq/L), or if the patient is symptomatic.[40] Local protocols should be consulted and followed. Higher infusion rates may be required in emergencies (e.g., seizures). The underlying cause should also be treated.
Mild magnesium deficiency
Patients with mild magnesium depletion (serum magnesium 1-1.5 mEq/L) are usually asymptomatic and can be managed with oral magnesium replacement.[40] Local dosing recommendations may vary and should be followed.
Cardiac arrhythmias
Magnesium depletion produces characteristic changes in the ECG. Modest depletion causes widening of the QRS complex, with resultant prolongation of the QT interval, and peaking of T waves. If the depletion worsens, the QRS complex continues to widen, prolongation of the PR interval occurs, and the T wave is diminished.[41] Ventricular arrhythmias result, usually in patients with concurrent ischaemic heart disease; these include ventricular extrasystolic beats, ventricular tachycardia (particularly torsades de pointes), and ventricular fibrillation. It is not clear whether these arrhythmias are due to hypomagnesaemia, associated hypokalaemia, or both.
Patients with ECG changes require oral magnesium replacement. Patients with arrhythmias require intravenous magnesium sulfate. Local protocols for adult dosing may vary and should be consulted. Specialist advice should be sought for dosing in children. Patients with a sustained ventricular tachycardia that does not respond to initial therapy require cardioversion. Defibrillation is required in cases of ventricular fibrillation, in accordance with advanced life support algorithms. See Sustained ventricular tachycardias and Cardiac arrest.
Prolonged QT intervals are often observed in severe hypomagnesaemia. Prolonged QT intervals due to inherited channelopathies can be complicated or aggravated by underlying hypomagnesaemia, especially if severe.[42] Restoration of proper serum magnesium level by oral supplementation for mild hypomagnesaemia or with intravenous magnesium for severe hypomagnesaemia is recommended to attenuate incidence of prolonged QT intervals and prevent occurrence of torsades de pointes.
Eclampsia
Eclampsia is characterised by the occurrence of seizures in a patient with pre-eclampsia in the absence of any other identified cause. Eclampsia is treated with intravenous magnesium sulfate.[14] Local protocols may vary and should be consulted. Any woman who presents with seizures in pregnancy requires immediate treatment, even if the diagnosis is not yet established. The diagnosis is confirmed by the presence of hypertension and proteinuria, and exclusion of other causes of seizures. See Pre-eclampsia (Management).
Diabetic ketoacidosis
An acute and potentially fatal metabolic complication of diabetes mellitus caused by absolute insulin deficiency. Symptoms usually develop rapidly over one day or less, and include polyuria, polydipsia, weakness, weight loss, nausea, vomiting, and occasionally abdominal pain. Signs of volume depletion, Kussmaul's respiration, and acetone breath are also present. Ketoacidosis is often precipitated by suboptimal insulin therapy or an acute medical illness in people with known diabetes, but is also a common first presentation of type 1 diabetes mellitus. Treatment involves immediate fluid replacement and intravenous insulin.[43] Potassium, phosphate, magnesium, and bicarbonate may also be required, depending on the degree of electrolyte and acid-base disturbance that is present. See Diabetic ketoacidosis (Management).
Metabolic alkalosis
Some causes of hypomagnesaemia, such as renal disease, chronic diuretic use, or hyperaldosteronism, may produce a concomitant severe metabolic alkalosis (arterial pH >7.6). Rapid reduction of arterial pH can be achieved by controlled hypoventilation, sedation, and mechanical ventilation. Volume depletion should be corrected with normal saline, and associated electrolyte abnormalities should be corrected. If normal saline is contraindicated (due to volume overload or severe renal failure), hydrogen chloride (HCl) or ammonium chloride can be used to correct the alkalosis. However, these treatments carry a high risk of complications (haemolysis and tissue necrosis with HCl, and ammonia toxicity with ammonium chloride). If a diuretic is suspected as the cause, the dose should be reduced, or the drug discontinued. Hyperaldosteronism requires treatment with spironolactone and/or resection of the aldosterone-secreting tumour.
Refractory hypocalcaemia
Hypocalcaemia in the presence of hypomagnesaemia will not resolve unless the magnesium level is normalised. Appropriate magnesium supplementation should be given. Normomagnesaemic magnesium deficiency should always be considered as a cause of refractory hypocalcaemia; a therapeutic trial of magnesium supplementation improves calcium level in this condition.
Refractory hypokalaemia
Hypokalaemia in the presence of hypomagnesaemia will not resolve unless the magnesium level is normalised. Appropriate magnesium supplementation should be given. Normomagnesaemic magnesium deficiency should always be considered as a cause of refractory hypokalaemia; a therapeutic trial of magnesium supplementation improves potassium levels in this condition.
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