HYPERMAGNESEMIA 

Definition

Hypermagnesemia is defined as a serum magnesium concentration > 2.4 mg/dL
(> 1.0 mmol/L or > 2.0 mEq/L)

Severity

Serum Mg (mg/dL)

mmol/L

Mild

2.5–4

1.0–1.6

Moderate

4–6

1.6–2.5

Severe

>6

>2.5

Life-threatening

>10–12

>5


Normal Magnesium Physiology 

Distribution

  • Total body Mg ≈ 25 g
  • Bone: 60%
  • Muscle/soft tissue: 39%
  • Extracellular fluid: <1%

Normal Serum Magnesium

  • 1.7–2.4 mg/dL (0.7–1.0 mmol/L)

Intestinal Absorption

  • Passive + active (TRPM6 channels)
  • Increased when Mg deficient

Renal Handling

  • Primary regulator of Mg balance
  • 70% reabsorbed in thick ascending limb (TAL)
  • PTH enhances reabsorption
  • Loop diuretics Mg reabsorption

👉 Hypermagnesemia almost always implies renal failure or excess intake


Etiology of Hypermagnesemia

1. Renal Causes (MOST COMMON)

Condition

Mechanism

Acute kidney injury

Mg excretion

CKD (GFR <30 mL/min)

Accumulation

ESRD

Severe hypermagnesemia with intake

Hyporeninemic hypoaldosteronism

distal Mg excretion

📌 Hypermagnesemia without renal failure is rare


2. Excess Magnesium Intake

Iatrogenic

  • Magnesium sulfate (eclampsia, torsades)
  • Mg-containing IV fluids
  • TPN with excess Mg

Oral / GI Sources

  • Antacids (Mg hydroxide)
  • Laxatives (milk of magnesia)
  • Bowel prep solutions
  • Herbal medications

⚠️ Elderly + constipation + renal dysfunction = classic risk


3. Increased GI Absorption

Condition

Mechanism

Ileus / bowel obstruction

Prolonged contact

Inflammatory bowel disease

absorption

Chronic constipation

Increased uptake


4. Endocrine / Metabolic Causes

Condition

Mechanism

Hypothyroidism

renal clearance

Adrenal insufficiency

Mg excretion

Hyperparathyroidism

intestinal absorption


5. Cellular Release / Shifts (Rare)

  • Tumor lysis syndrome
  • Rhabdomyolysis
  • Hemolysis
  • Acidosis (Mg shifts extracellularly)


Pathophysiology

Magnesium is a physiologic calcium antagonist and neuromuscular depressant.

Key Mechanisms

  1. Inhibits presynaptic acetylcholine release
  2. Blocks calcium channels
  3. Suppresses PTH secretion
  4. Decreases Na-K-ATPase activity
  5. Vasodilation ( SVR)

👉 Results in:

  • Neuromuscular paralysis
  • Cardiac conduction defects
  • Hypotension
  • Respiratory failure


Clinical Features (Mg Level-Based)

Neuromuscular

Mg level

Manifestation

3–4 mg/dL

Nausea, flushing

4–6 mg/dL

DTRs, lethargy

6–10 mg/dL

Loss of reflexes, muscle weakness

>10 mg/dL

Flaccid paralysis, respiratory depression

>12–15 mg/dL

Coma

📌 Loss of deep tendon reflexes = early and sensitive sign


Cardiovascular

Mg level

Effect

4–6

Bradycardia

6–10

Hypotension, PR prolongation

>10

Heart block

>15

Cardiac arrest (asystole)


Respiratory

  • Hypoventilation
  • Respiratory muscle paralysis
  • Apnea (severe)


CNS

  • Confusion
  • Somnolence
  • Coma


ECG Changes

Mg Level

ECG Findings

Mild

PR prolongation

Moderate

QRS widening

Severe

Complete heart block

Extreme

Asystole


Laboratory Findings

  • Serum magnesium
  • Hypocalcemia (Mg suppresses PTH)
  • Hyperkalemia (renal failure)
  • Creatinine / urea

📌 Always check Ca²⁺, K⁺, ABG


Diagnosis

Confirmatory

  • Serum magnesium level

Supportive

  • Renal function tests
  • ECG monitoring
  • Neurological examination (DTRs)


Differential Diagnosis

Condition

Key Difference

Hyperkalemia

Peaked T waves

Hypocalcemia

Tetany (opposite of Mg)

Guillain–Barré

Ascending paralysis

Myasthenia gravis

Preserved reflexes


MANAGEMENT OF HYPERMAGNESEMIA 

Principles

  1. Stop magnesium intake
  2. Stabilize myocardium
  3. Enhance magnesium elimination
  4. Provide ventilatory support if needed


Step-Wise Management

1. Asymptomatic / Mild (Mg <4 mg/dL)

  • Stop Mg-containing drugs
  • Monitor levels
  • Ensure hydration
  • Normal renal function usually self-limited


2. Symptomatic or Mg ≥4–6 mg/dL

A. IV Calcium – FIRST LINE ANTIDOTE

Drug

Dose

Calcium gluconate 10%

10–20 mL IV over 5–10 min

Calcium chloride

5–10 mL (central line only)

📌 Mechanism: Antagonizes Mg at neuromuscular junction & myocardium
📌 Effect lasts 30–60 minutes may need repeat dosing


B. Enhance Renal Excretion (If kidneys working)

  • IV isotonic saline
  • Loop diuretics (furosemide)

👉 Increases urinary Mg loss


3. Severe Hypermagnesemia / Renal Failure

C. Hemodialysis – DEFINITIVE TREATMENT

Indications:

  • Mg >6–8 mg/dL with symptoms
  • Renal failure
  • Life-threatening arrhythmias
  • Respiratory depression
  • Refractory to medical therapy

📌 Mg is small, water-soluble, minimally protein bound dialyzable


4. ICU Support

  • Continuous ECG monitoring
  • Ventilatory support if respiratory depression
  • Vasopressors if hypotension