Treatment of Hypocalcemia
For symptomatic hypocalcemia with ionized calcium <1.0 mmol/L, administer calcium chloride 10 mL of 10% solution (270 mg elemental calcium) intravenously over 2-5 minutes with continuous ECG monitoring, but only after correcting concurrent hypomagnesemia with magnesium sulfate 1-2 g IV bolus first. 1
Acute Management of Symptomatic Hypocalcemia (Ionized Ca <1.0 mmol/L)
Step 1: Correct Magnesium Deficiency FIRST
- Check serum magnesium immediately in all patients with symptomatic hypocalcemia, as hypomagnesemia is present in 28% of hypocalcemic patients and prevents effective calcium correction through impaired PTH secretion and end-organ PTH resistance. 1, 2
- Administer magnesium sulfate 1-2 g IV bolus immediately before any calcium replacement if magnesium is low, as calcium supplementation will fail without adequate magnesium levels. 1
- Magnesium acts as a cofactor for PTH secretion and facilitates calcium release from bone in the presence of adequate vitamin D and parathormone. 2
Step 2: Intravenous Calcium Administration
- Calcium chloride is strongly preferred over calcium gluconate because 10 mL of 10% calcium chloride contains 270 mg elemental calcium versus only 90 mg in calcium gluconate—three times more calcium per volume. 1
- Administer calcium chloride 10 mL of 10% solution IV over 2-5 minutes for symptomatic patients with tetany, seizures, laryngospasm, bronchospasm, or cardiac arrhythmias. 1
- If calcium chloride is unavailable, use calcium gluconate 10% solution 15-30 mL IV over 2-5 minutes as an alternative. 1
- Administer via central line when possible to avoid severe tissue necrosis if extravasation occurs. 1
Step 3: Continuous Monitoring During Acute Treatment
- Continuous ECG monitoring is mandatory during IV calcium administration to detect QT interval changes, arrhythmias, and torsades de pointes. 1
- Obtain baseline 12-lead ECG before treatment and document QTc interval every 8-12 hours after calcium replacement. 1
- If ionized calcium falls below 0.9 mmol/L post-parathyroidectomy, start calcium gluconate infusion at 1-2 mg elemental calcium per kg per hour, titrating to maintain ionized calcium 1.15-1.36 mmol/L. 1
Critical Safety Considerations
- Never administer calcium through the same IV line as sodium bicarbonate to prevent precipitation. 1
- Use extreme caution when serum phosphorus exceeds 5.5 mg/dL (1.62 mmol/L), as high phosphate markedly increases calcium-phosphate precipitation risk in tissues and kidneys. 1
- Do not administer calcium supplements until phosphate is reduced below 5.5 mg/dL when the calcium-phosphorus product exceeds 55 mg²/dL². 1
Chronic Management of Mild Asymptomatic Hypocalcemia
Indications for Treatment
- Initiate oral calcium supplementation when corrected total calcium is <8.4 mg/dL (2.10 mmol/L) AND intact PTH is above the target range for the patient's CKD stage. 3, 1
- In CKD stages 3-4, treat when PTH >70 pg/mL (stage 3) or >110 pg/mL (stage 4); in stage 5 dialysis, treat when PTH >300 pg/mL. 1
Oral Calcium Regimen
- Calcium carbonate 1-2 g three times daily (providing 1,200-2,400 mg elemental calcium) is the preferred first-line oral supplement due to high elemental calcium content (40%), low cost, and wide availability. 3, 1
- Limit individual doses to 500 mg elemental calcium and divide throughout the day with meals to optimize absorption and minimize gastrointestinal side effects. 1
- Total elemental calcium intake (dietary plus supplements) must not exceed 2,000 mg/day to prevent hypercalciuria, nephrocalcinosis, and renal calculi. 3, 1
- Calcium citrate is superior in patients with achlorhydria or those taking acid-suppressing medications. 1
Vitamin D Supplementation
- Measure 25-hydroxyvitamin D at the initial visit; if <30 ng/mL, start ergocalciferol 50,000 IU orally once monthly for 6 months. 1
- Daily vitamin D₃ supplementation 400-800 IU/day is recommended for all adults with chronic hypocalcemia to maintain adequate stores. 1
- Active vitamin D metabolites (calcitriol 0.25-2 µg/day) are reserved for severe or refractory cases when PTH remains >300 pg/mL (stage 5 CKD) despite adequate vitamin D repletion, and should be used under endocrinologist guidance. 1
Target Calcium Levels
- Maintain corrected total calcium in the low-normal range (8.4-9.5 mg/dL or 2.10-2.37 mmol/L) to minimize hypercalciuria while preventing symptoms and reducing vascular calcification risk. 3, 1
- In CKD stages 3-4, maintain calcium within the normal laboratory range; in stage 5 dialysis, aim for the lower end of normal. 3, 1
Addressing Concurrent Magnesium Deficiency
Magnesium Replacement Protocol
- Administer magnesium sulfate 1-2 g IV bolus immediately for symptomatic patients with concurrent hypomagnesemia, followed by calcium replacement. 1
- Oral magnesium oxide 12-24 mmol daily is the preferred oral formulation for chronic magnesium deficiency or malabsorption. 1
- Magnesium supplementation is indicated for all patients with documented hypomagnesemia, as it is necessary for PTH secretion and end-organ PTH response. 1
Why Magnesium Must Be Corrected First
- Hypomagnesemia causes hypocalcemia through two mechanisms: impaired PTH secretion and end-organ resistance to PTH. 1
- Calcium supplementation alone will fail without magnesium correction, as magnesium facilitates calcium release from bone. 2
- Pharmacological doses of vitamin D (ergocalciferol or dihydrotachysterol) do not correct hypocalcemia in the presence of magnesium deficiency. 2
Monitoring Requirements
- Measure corrected total calcium and phosphorus at least every 3 months during chronic calcium supplementation. 3, 1
- Monitor pH-corrected ionized calcium, magnesium, PTH, and creatinine concentrations regularly for patients with chronic hypocalcemia. 1
- Keep the calcium-phosphorus product below 55 mg²/dL² to prevent soft-tissue and vascular calcification. 3, 1
- Measure ionized calcium every 4-6 hours for the first 48-72 hours post-parathyroidectomy, then twice daily until stable. 1
Contraindications and Safety Thresholds
- Discontinue all calcium-based therapy when corrected serum calcium exceeds 10.2 mg/dL (2.54 mmol/L) to prevent hypercalcemia. 3, 1
- Do not use calcium-based phosphate binders when plasma PTH <150 pg/mL on 2 consecutive measurements or when severe vascular calcifications are present. 1
- Avoid calcium administration when serum phosphorus exceeds 5.5 mg/dL due to calcium-phosphate precipitation risk. 1
- Avoid over-correction, which can result in iatrogenic hypercalcemia, renal calculi, nephrocalcinosis, and renal failure. 1
Special Clinical Scenarios
Massive Transfusion
- Monitor ionized calcium continuously during massive transfusion, as each unit of blood products contains approximately 3 g of citrate that binds calcium. 1
- Citrate metabolism may be impaired by hypoperfusion, hypothermia, and hepatic insufficiency, requiring more aggressive calcium replacement. 1
Post-Parathyroidectomy
- Use of active vitamin D metabolites (calcitriol) before and after parathyroidectomy reduces the incidence of severe postoperative hypocalcemia. 1
- Once oral intake is feasible, resume calcium carbonate 1-2 g three times daily together with calcitriol up to 2 µg per day. 1
Dialysis Patients
- For intensive hemodialysis regimens, use dialysate calcium ≥1.50 mmol/L (3.0 mEq/L) to maintain neutral or positive calcium balance. 1
- Higher dialysate calcium (1.75 mmol/L or 3.5 mEq/L) is required if PTH is elevated and increasing or if alkaline phosphatase is rising. 1
Common Pitfalls to Avoid
- Never attempt calcium correction without first checking and correcting magnesium, as 28% of hypocalcemic patients have concurrent hypomagnesemia. 1
- Do not aggressively correct mild asymptomatic hypocalcemia without evaluating PTH, phosphorus, and the calcium-phosphorus product. 1
- Avoid calcium-based phosphate binders when phosphorus is elevated (>4.6 mg/dL in CKD stages 3-4, >5.5 mg/dL in stage 5). 1
- Do not exceed 2,000 mg/day total elemental calcium intake to prevent nephrocalcinosis. 3, 1
Recent Paradigm Shift
- The 2025 KDIGO Controversies Conference shifted away from permissive hypocalcemia, particularly in patients on calcimimetics, due to severe hypocalcemia occurring in 7-9% of such patients with associated muscle spasms, paresthesia, and myalgia. 1
- This represents a paradigm shift toward more aggressive correction of hypocalcemia while carefully monitoring for vascular calcification risk. 1