Magnesium Disorders Nursing Guide

Magnesium — Key Facts

Normal serum Mg²⁺: 0.7–1.0 mmol/L (1.7–2.4 mg/dL). Magnesium is the second most abundant intracellular cation. 99% is intracellular (bone, muscle) — serum levels can be normal even when total body Mg²⁺ is depleted.

Roles of Magnesium

Co-factor for >300 enzyme reactions (ATP synthesis, DNA/protein production)
Essential for Na/K-ATPase pump (maintains K⁺ inside cells)
Regulates NMDA receptor (neuroprotection in eclampsia)
Cardiac membrane stabilisation
Bronchodilation (in severe asthma)

Hypomagnesaemia causes refractory hypokalaemia — always check Mg²⁺ when K⁺ fails to correct. Mg²⁺ is needed for Na/K-ATPase which keeps K⁺ inside cells and out of urine.

Hypomagnesaemia (Mg²⁺ < 0.7 mmol/L)

Causes

GI Losses

Diarrhoea (most common)
NG suctioning, vomiting
Malabsorption, Crohn's, short bowel

Drugs

PPIs (omeprazole, pantoprazole) — reduce Mg²⁺ absorption; significant cause in long-term PPI use
Loop and thiazide diuretics — renal wasting
Gentamicin, amphotericin — tubular toxicity
Cisplatin — renal wasting
Alcohol — renal wasting + poor intake

Renal Losses

Bartter/Gitelman syndrome
Post-obstructive diuresis
Hyperaldosteronism

Other

Diabetic ketoacidosis (osmotic diuresis)
Hungry bone syndrome (post-parathyroidectomy)
Poor intake (malnutrition, alcoholism)

Clinical Features

Neuromuscular: tremor, tetany (Chvostek's sign, Trousseau's sign), muscle cramps, weakness
Cardiac: tachyarrhythmias, Torsades de Pointes (QT prolongation), ventricular fibrillation
Refractory hypokalaemia and hypocalcaemia (both resist correction without Mg²⁺ correction)

Treatment

IV magnesium sulphate 2–4g over 15–30 minutes for symptomatic or severe (<0.5 mmol/L)
Maintenance: 4–8g/day IV or oral magnesium glycerophosphate/oxide (oral preparations cause diarrhoea — Mg²⁺ is a laxative)
Oral: Magnesium glycerophosphate 4 mmol TDS is better tolerated than magnesium oxide
Treat underlying cause (stop PPI if possible, treat diarrhoea)

Hypermagnesaemia (Mg²⁺ > 1.0 mmol/L)

Rare in patients with normal renal function — kidneys efficiently excrete excess Mg²⁺.

Causes

Renal failure (most common) — inability to excrete Mg²⁺
Excessive Mg²⁺ supplementation (iatrogenic)
Magnesium-containing antacids/laxatives in renal failure patients
Eclampsia treatment overdose
Adrenal insufficiency

Clinical Features by Level

Mg²⁺ (mmol/L)	Clinical Effects
1.5–2.5	Nausea, flushing, drowsiness, headache
2.5–5.0	Loss of deep tendon reflexes (earliest sign of toxicity), hypotension, bradycardia
5.0–7.5	Muscle paralysis, respiratory depression
> 7.5	Cardiac arrest, complete heart block

ANTIDOTE for hypermagnesaemia = Calcium gluconate 10% 10–20 mL IV over 5–10 minutes
Calcium antagonises magnesium's effects on neuromuscular junctions and cardiac conduction. This is also used to rapidly reverse Mg²⁺ toxicity during eclampsia treatment.

Management

Stop all magnesium-containing products and IV Mg²⁺ infusions
IV calcium gluconate for symptomatic hypermagnesaemia
IV fluids + furosemide (increases renal Mg²⁺ excretion)
Haemodialysis in severe cases or renal failure patients
Mechanical ventilation if respiratory depression

Magnesium Sulphate in Eclampsia & Pre-eclampsia

MgSO₄ is the first-line treatment and prevention of eclamptic seizures. It is NOT an antihypertensive — it works by blocking NMDA receptors (cerebral vasodilation and neuroprotection).

Standard Magnesium Sulphate Protocol (Parkland Regimen)

Loading dose: 4g IV over 15–20 minutes (add 4g MgSO₄ 50% to 100 mL 0.9% NaCl → infuse over 15–20 min)
Maintenance: 1–2g/hour IV infusion for 24 hours after last seizure (or delivery)

Monitoring During Magnesium Infusion

MANDATORY monitoring every 30–60 minutes:

Deep tendon reflexes (DTR) — patellar reflex MUST be present. Loss of DTR = first sign of Mg²⁺ toxicity (Mg²⁺ ~ 2.5–5 mmol/L). STOP infusion if reflexes lost.
Respiratory rate ≥ 12 breaths/min. Stop if RR < 12 (Mg²⁺ ~ 5+ mmol/L)
Urine output ≥ 25 mL/hr (Mg²⁺ excreted renally)
Level of consciousness

If Signs of Toxicity

STOP magnesium infusion immediately
Calcium gluconate 10% 10 mL IV over 3 minutes (antidote)
High-flow oxygen
Ventilatory support if required
Senior obstetric/anaesthetic team immediately

Antihypertensive Management in Severe Pre-eclampsia (alongside MgSO₄)

Target BP: SBP <160 mmHg, DBP <110 mmHg (higher thresholds are associated with maternal stroke)
First-line: IV labetalol, oral nifedipine modified release, or IV hydralazine
Labetalol: 50mg IV over 1 minute; repeat every 15 min (max 200mg)

GCC obstetric nursing note: MgSO₄ is WHO-essential medicine and widely available in GCC obstetric units. Nurses administering MgSO₄ must be trained in toxicity recognition, DTR assessment, and calcium gluconate administration. These are frequently tested in GCC nursing licensure exams.

MCQ Practice — Magnesium Disorders

Q1. During a magnesium sulphate infusion for eclampsia, the nurse finds the patellar reflex is absent and the respiratory rate is 8 breaths/min. What is the IMMEDIATE action?

A) Increase the magnesium infusion rate to treat the seizures

B) Administer IV furosemide to increase magnesium excretion

C) Stop the magnesium infusion and give IV calcium gluconate 10% 10 mL immediately

D) Give oral magnesium antacid to counteract intravenous excess

✅ C — Absent deep tendon reflexes + respiratory depression = magnesium toxicity. STOP infusion immediately. Calcium gluconate is the antidote — antagonises magnesium's effects. High-flow O₂ and ventilatory support as needed. This is a nursing emergency requiring immediate action.

Q2. A patient with hypokalaemia (K⁺ 3.0 mmol/L) fails to correct despite adequate potassium replacement. The nurse should suspect and check:

A) Serum phosphate

B) Serum calcium

C) Serum magnesium

D) Thyroid function tests

✅ C — Hypomagnesaemia causes refractory hypokalaemia. Mg²⁺ is required for Na/K-ATPase which retains K⁺ inside cells. Without correcting Mg²⁺, K⁺ replacement will continue to leak into urine. Always check Mg²⁺ in resistant hypokalaemia.

Q3. Which drug class is a significant cause of hypomagnesaemia through reduced intestinal magnesium absorption?

A) Calcium channel blockers

B) Beta-blockers

C) Proton pump inhibitors (omeprazole, pantoprazole)

D) ACE inhibitors

✅ C — Long-term PPIs reduce intestinal Mg²⁺ absorption through inhibition of TRPM6/7 transient receptor potential channels. This is an increasingly recognised cause of hypomagnesaemia, especially in patients on long-term acid suppression. Check Mg²⁺ in patients on PPIs with unexplained symptoms.

Q4. IV magnesium sulphate 2g is given in the emergency treatment of which ventricular arrhythmia?

A) Atrial fibrillation with rapid ventricular response

B) Monomorphic ventricular tachycardia

C) Complete heart block

D) Torsades de Pointes (polymorphic VT with prolonged QT)

✅ D — IV magnesium sulphate 2g is the first-line treatment for Torsades de Pointes. It stabilises the cardiac membrane and shortens the QT interval. Amiodarone is CONTRAINDICATED in Torsades as it further prolongs QT. MgSO₄ is also used as an adjunct in refractory VF.

Magnesium Disorders — Nursing Guide

Magnesium — Key Facts

Roles of Magnesium

Hypomagnesaemia (Mg²⁺ < 0.7 mmol/L)

Causes

GI Losses

Drugs

Renal Losses

Other

Clinical Features

Treatment

Hypermagnesaemia (Mg²⁺ > 1.0 mmol/L)

Causes

Clinical Features by Level

Management

Magnesium Sulphate in Eclampsia & Pre-eclampsia

Standard Magnesium Sulphate Protocol (Parkland Regimen)

Monitoring During Magnesium Infusion

If Signs of Toxicity

Antihypertensive Management in Severe Pre-eclampsia (alongside MgSO₄)

MCQ Practice — Magnesium Disorders