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Magnesium - hypermagnesemia

Key points

The kidney is crucial in maintaining the normal plasma magnesium (Mg) concentration in the narrow range of 0.8 to 1.0 mmol/L.

Hypermagnesemia is an uncommon problem in the absence of magnesium administration or kidney failure. When it occurs, the elevation in the plasma magnesium concentration is usually mild (<3 mEq/L, 3.6 mg/dL, or 1.5 mmol/L) and patients are asymptomatic. However, clinical symptoms may be seen when the plasma magnesium concentration exceeds 4 mEq/L (4.8 mg/dL or 2 mmol/L).

Background:

Hypermagnesaemia is caused by either excessive intake (usually iatrogenic causes), poor excretion (renal failure), release from cells (rhabdomyolysis, tumour lysis) or in other disease states.

Below is a list of aetiologies that may precipitate hypermagnesemia:

  • Patients with end-stage kidney disease, or on dialysis.
  • Medication use such as lithium, laxatives, antacids, rectal enemas and PPIs
  • Patients receiving Parenteral nutrition.
  • Newborns to mothers receiving IV Mg. Therapy for pre-eclampsia.
  • DKA
  • Hyperparathyroidism
  • Hypothyroidism
  • Addisons disease
  • Familial hypocalciuric hypocalcaemia
  • Perforated viscus with continued oral intake
  • Tumour lysis syndrome (increased potassium, Mg, and phosphate. Decreased calcium)
  • Rhabdomyolysis

Assessment

History and examination

The clinical presentation of hypermagnesaemia will depend upon the plasma concentrations (see table 1 for a summary).

The overall concerning effects are exhibited on the muscles (including the heart).

Other nonspecific effects including autonomic symptoms, pruritis and inhibition of parathyroid hormone.

Neuromuscular effects — Neuromuscular toxicity is the most consistently observed complication of hypermagnesemia. The clinical manifestation exists on a spectrum from diminished deep tendon reflexes, somnolence; loss of deep tendon reflexes; muscle paralysis, flaccid quadriplegia, decreased function of muscles of respiration and apnoea. Parasympathetic blockade inducing fixed and dilated pupils, mimicking a central brainstem herniation syndrome, are also manifestations of hypermagnesaemia.

Cardiovascular effects — Magnesium is an effective cardiac potassium and calcium channel blocker both extracellularly and intracellularly. These changes combine to impair cardiovascular function resulting in hypotension, conduction defects, bradycardia, complete heart block and cardiac arrest. ECG changes include prolongation of the PR interval, an increase in QRS duration, an increase in the QT interval.

Hypocalcaemia — Moderate hypermagnesemia can inhibit the secretion of parathyroid hormone (PTH), leading to a reduction in the plasma calcium concentration. In the long term, hypermagnesemia can contribute to osteomalacia renal osteodystrophy and adynamic bone disease, especially in patients with kidney disease.

Other symptoms — Hypermagnesemia may be associated with nonspecific early symptoms such as nausea, vomiting, and flushing. Hypermagnesemia can also cause and/or exacerbate pruritus in dialysis patients.

Plasma magnesium concentration

Clinical signs and symptoms

4 to 6 mEq/L (2 to 3 mmol/L)

Nausea, flushing, headache, lethargy, drowsiness, and diminished deep tendon reflexes.

6 to 10 mEq/L (3 to 5 mmol/L)

Somnolence, hypocalcaemia, absent deep tendon reflexes, hypotension, bradycardia, and electrocardiogram (ECG) changes.

>10 mEq/L (>5 mmol/L)

Muscle paralysis leading to flaccid quadriplegia, apnoea and respiratory failure, complete heart block, and cardiac arrest. In most cases, respiratory failure precedes cardiac collapse.

Table 1: Summary of the relationship between plasma magnesium concentration and resultant clinical signs.

Management

Investigations

  • Serum magnesium levels
  • Calcium levels
  • TFTs
  • ECG

Treatment

Treatment is dependent on renal function:

KIDNEY FUNCTION

TREATMENT

Normal

Medical management:

- Cessation Mg containing medications

- IV N saline

+/- loop diuretic to increase renal excretion

- Aim for a urine output of at least 60 mL per hour

Moderate impairment

- mild acute kidney injury (AKI)

- Chronic kidney disease (CKD) eGFR 15-45mL/min/1.73m2

- +/- symptomatic hyper Mg

Medical management:

- Cessation Mg containing medications

- IV N saline

- loop diuretic ie furosemide

- Aim for a urine output of at least 60 mL per hour

(if above measures fail and severe neurological/cardiovascular manifestations present – may require dialysis)

Severe impairment

- Moderate/Severe AKI

- Advanced CKD – eGFR <15 mL/min/1.73m2

- Severe/symptomatic hyperMg

1. Dialysis

If symptomatic, whilst waiting for dialysis:

2. IV calcium – 100-200mg elemental Ca over 5-10mins

3. Medical management: (UNLESS ANURIC)

- Cessation Mg containing medications

- IV N saline

- loop diuretic ie furosemide

- Aim for a urine output of at least 60 mL per hour

References

eTG

UPTODATE

LITFL

Patient UK

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