1. Clinical Assessment

Summary: Early recognition of neuromuscular and cardiovascular signs guides laboratory evaluation and prevents progression to severe toxicity.

History

• Medications: Diuretics, bisphosphonates, citrate anticoagulation, proton-pump inhibitors, aminoglycosides, magnesium-containing laxatives or supplements.
• Comorbidities: Renal dysfunction, pancreatitis, sepsis, massive transfusion, endocrine disorders (e.g., primary hyperparathyroidism).
• Symptoms: Perioral paresthesia, muscle cramps, weakness, polyuria, confusion, hypotension.

Physical Examination

• Hypocalcemia signs: Hyperactive reflexes, Chvostek sign (facial nerve tap), Trousseau sign (inflated cuff-induced carpal spasm), prolonged QT interval on ECG.
• Hypomagnesemia clues: Refractory cramps, tremor, arrhythmias despite calcium correction.
• Hypercalcemia signs: Lethargy, signs of volume depletion, shortened QT interval, hypertension.
• Hypermagnesemia signs: Diminished deep-tendon reflexes, bradycardia, hypotension, respiratory depression.

2. Laboratory Diagnostics

Summary: Integrate total and ionized calcium measurements, magnesium levels, and ancillary labs for accurate assessment.

Total vs. Ionized Calcium

• Total Calcium: Represents both protein-bound and free (ionized) calcium. It must be corrected for albumin levels, especially in patients with hypoalbuminemia. The standard formula is: Corrected Ca (mg/dL) = measured Ca + 0.8 × (4.0 – albumin [g/dL]).
• Ionized Calcium: Represents the physiologically active form. It is the preferred measurement in critically ill patients, those with significant acid-base disturbances, or after massive transfusions with citrate.

Serum Magnesium

• Reference range: 1.8–2.4 mg/dL
• Hypomagnesemia: <1.5 mg/dL; symptoms often appear <1.2 mg/dL
• Hypermagnesemia: >2.4 mg/dL; moderate symptoms >4.0 mg/dL; severe toxicity >6.0 mg/dL

Ancillary Tests & Acid-Base Influences

• Key Labs: Phosphate, intact parathyroid hormone (PTH), 25-OH and 1,25-OH vitamin D, creatinine/eGFR.
• PTH Interpretation: PTH is appropriately high in primary hyperparathyroidism but suppressed in malignancy- or vitamin D–mediated hypercalcemia.
• Acid-Base Effects: Alkalosis increases protein binding of calcium, which lowers the ionized fraction even if total calcium is normal. Conversely, acidosis decreases binding, increasing the ionized fraction.

3. Imaging and Specialized Modalities

Summary: Use imaging to detect end-organ calcifications and the electrocardiogram (ECG) to identify life-threatening conduction abnormalities.

Renal Imaging

Renal ultrasound or a noncontrast CT scan can be used to evaluate for nephrocalcinosis (calcium deposits in the kidney parenchyma) and nephrolithiasis (kidney stones). The presence of cortical calcifications is particularly suggestive of a chronic hypercalcemic state, such as primary hyperparathyroidism.

ECG Interpretation

Electrolyte disturbances directly impact cardiac myocyte action potentials, leading to characteristic ECG changes:

• Hypocalcemia / Hypomagnesemia: Prolongation of the QT interval, which increases the risk for torsades de pointes.
• Hypercalcemia: Shortening of the QT interval.
• Hypermagnesemia: PR interval prolongation, QRS complex widening, and bradyarrhythmias.

4. Severity Classification

Summary: Stratifying mild, moderate, and severe electrolyte disturbances based on lab values and clinical signs is crucial for guiding the urgency and route of intervention.

5. Clinical Decision Points

Summary: The severity of the disorder and the presence of symptoms dictate the choice between oral versus intravenous repletion and determine when to engage specialist consultation.

IV vs. Oral Repletion Criteria

• Calcium: Use IV calcium gluconate for any symptomatic patient or if corrected calcium is <8.0 mg/dL. Reserve oral calcium carbonate or citrate for mild, asymptomatic cases with a functioning GI tract.
• Magnesium: Administer IV magnesium sulfate for levels <1.2 mg/dL, any ECG changes, or severe symptoms like seizures. Oral magnesium oxide or other supplements are suitable for mild, chronic hypomagnesemia but are limited by poor absorption and diarrhea.

Specialist Consultation Thresholds

• Endocrinology: Consult for persistent or severe hypercalcemia (e.g., >14 mg/dL), especially when the etiology (PTH vs. non-PTH mediated) is unclear.
• Nephrology: Consult for severe hypermagnesemia (>6.0 mg/dL) or any hypermagnesemia associated with hemodynamic instability or oliguria, as emergent dialysis may be required.