Management of Severe Hypocalcemia
For severe symptomatic hypocalcemia, immediately administer intravenous calcium chloride 10% solution 5-10 mL (270 mg elemental calcium) over 2-5 minutes with continuous cardiac monitoring, as this is the preferred agent over calcium gluconate due to three times higher elemental calcium content and faster ionized calcium release. 1, 2
Immediate Assessment and Stabilization
Recognize Severe Hypocalcemia
- Severe hypocalcemia is defined as ionized calcium <0.9 mmol/L, with levels <0.8 mmol/L being particularly concerning for cardiac dysrhythmias 1
- Assess immediately for life-threatening symptoms: tetany, seizures, laryngospasm, bronchospasm, cardiac arrhythmias, or prolonged QT interval 1
- Obtain baseline 12-lead ECG before treatment to document QTc interval 1
Critical First Step: Check and Correct Magnesium
- Measure serum magnesium immediately—hypomagnesemia is present in 28% of hypocalcemic ICU patients and prevents calcium correction 1
- If hypomagnesemia is present, administer magnesium sulfate 1-2 g IV bolus immediately before or concurrent with calcium replacement 1
- Hypocalcemia cannot be fully corrected without adequate magnesium, as magnesium is required for PTH secretion and end-organ PTH response 1
Acute Intravenous Calcium Replacement
Preferred Agent: Calcium Chloride
- Calcium chloride 10% is superior to calcium gluconate: 10 mL contains 270 mg elemental calcium vs. only 90 mg in calcium gluconate 1, 2
- Calcium chloride releases ionized calcium more rapidly, especially critical in patients with liver dysfunction, hypothermia, or shock states where citrate metabolism is impaired 1
- Administer 5-10 mL of 10% calcium chloride IV over 2-5 minutes for adults 1, 3
- Pediatric dosing: 20 mg/kg (0.2 mL/kg) of calcium chloride IV 1
Alternative: Calcium Gluconate (if calcium chloride unavailable)
- Calcium gluconate 10% solution 15-30 mL IV over 2-5 minutes 1, 3
- Contains only 9.3 mg elemental calcium per mL (90 mg per 10 mL) 3
- FDA-approved for acute symptomatic hypocalcemia in pediatric and adult patients 3
Administration Precautions
- Use central venous access when possible to avoid severe tissue injury from extravasation 1
- Continuous cardiac monitoring is mandatory during IV calcium administration 1, 3
- Stop infusion immediately if symptomatic bradycardia occurs 1
- Never mix calcium with sodium bicarbonate or phosphate-containing solutions—precipitation will occur 1, 3
Continuous Calcium Infusion for Persistent Hypocalcemia
Infusion Protocol
- Initiate calcium gluconate infusion at 1-2 mg elemental calcium per kg body weight per hour, adjusted to maintain ionized calcium in normal range (1.15-1.36 mmol/L) 1
- Target maintaining ionized calcium >0.9 mmol/L minimum to support cardiovascular function and coagulation 1
- Optimal target range is 1.1-1.3 mmol/L 1
Monitoring During Infusion
- Measure ionized calcium every 4-6 hours initially during intermittent infusions 1, 3
- During continuous infusion, measure ionized calcium every 1-4 hours until stable 1, 3
- Once stable, monitor twice daily 1
Special Clinical Contexts
Massive Transfusion/Trauma Setting
- Hypocalcemia results from citrate-mediated chelation from blood products (each unit contains ~3g citrate) 1
- Citrate metabolism is impaired by hypoperfusion, hypothermia, or hepatic insufficiency—requiring more aggressive calcium replacement 1
- Colloid infusions independently contribute to hypocalcemia beyond citrate toxicity 1
- Maintain ionized calcium >0.9 mmol/L throughout massive transfusion 1
- Standard coagulation tests may appear normal despite significant hypocalcemia-induced coagulopathy because laboratory samples are citrated then recalcified before analysis 1
Cardiac Arrest with Hyperkalemia/Hypermagnesemia
- Consider calcium chloride 10% solution 5-10 mL or calcium gluconate 10% solution 15-30 mL IV over 2-5 minutes (Class IIb recommendation) 1
Tumor Lysis Syndrome
- Exercise extreme caution with calcium administration—only treat symptomatic patients 1
- Consider renal consultation if phosphate levels are elevated due to risk of calcium phosphate precipitation 1, 2
Transition to Oral Therapy
When to Transition
- When ionized calcium levels stabilize and oral intake is possible 1
- Typically after 24-48 hours of IV therapy with consistently normal ionized calcium 1
Oral Regimen
- Calcium carbonate 1-2 g three times daily (preferred due to high elemental calcium content) 1, 2
- Calcium citrate is superior in patients with achlorhydria or those taking acid-suppressing medications 1
- Limit individual doses to 500 mg elemental calcium to optimize absorption 1
- Total elemental calcium intake should not exceed 2,000 mg/day 1
Add Active Vitamin D
- Consider adding calcitriol up to 2 μg/day to enhance intestinal calcium absorption 1
- If 25-hydroxyvitamin D <30 ng/mL, plan for vitamin D supplementation once acute phase is managed 1
Critical Pitfalls to Avoid
Overcorrection
- Avoid overcorrection—iatrogenic hypercalcemia can result in renal calculi and renal failure 1, 2
- Monitor for severe hypercalcemia (ionized calcium >twice upper limit of normal) 1
Drug Interactions
- If patient is on cardiac glycosides, administer calcium slowly in small amounts with close ECG monitoring—synergistic arrhythmias may occur 3
- Calcium may reduce response to calcium channel blockers 3
Acidosis Correction
- Acidosis increases ionized calcium levels, so correction of acidosis may worsen hypocalcemia 1
- Anticipate need for increased calcium replacement when correcting acidosis 1
Phosphate Management
- If patient was previously on phosphate binders, these may need to be reduced or discontinued based on serum phosphorus levels 1
- Maintain calcium-phosphorus product <55 mg²/dL² 1
Prognostic Implications
- Low ionized calcium is associated with increased mortality, coagulopathy, and cardiovascular dysfunction—prompt correction is essential 1
- Severely hypocalcemic patients who fail to normalize ionized calcium by day 4 have double the mortality (38% vs. 19%) 4
- Even mild hypocalcemia impairs coagulation cascade (factors II, VII, IX, X activation) and platelet adhesion 1