Can Hypercalcemia Cause Paraplegia?
No, hypercalcemia does not cause paraplegia—the relationship is reversed: immobilization from paraplegia causes hypercalcemia. 1, 2
The Actual Causal Relationship
Paraplegia leads to hypercalcemia, not the other way around. When you become immobilized due to spinal cord injury or severe neuropathy causing paraplegia, the lack of weight-bearing activity triggers increased bone resorption, which releases calcium into the bloodstream and causes hypercalcemia. 1, 2
Mechanism of Immobilization-Induced Hypercalcemia
- Immobilization from paraplegia increases bone turnover, with elevated bone resorption markers indicating accelerated calcium release from bone into the circulation. 1
- This typically develops weeks to months after the onset of immobilization, not immediately—one case showed profound hypercalcemia appearing 3 months after paraplegia onset. 2
- The hypercalcemia can be severe and persistent, sometimes reaching extreme levels that require aggressive treatment beyond standard bisphosphonates and fluids. 1
Clinical Presentation of Hypercalcemia
While hypercalcemia itself does not cause paraplegia, it does cause other serious neurological symptoms when severe:
- Mild hypercalcemia (total calcium <12 mg/dL) is usually asymptomatic but may cause fatigue and constipation in approximately 20% of patients. 3
- Severe hypercalcemia (total calcium ≥14 mg/dL or ionized calcium ≥10 mg/dL) causes nausea, vomiting, dehydration, confusion, somnolence, and coma—but not paralysis or paraplegia. 3
- Neurological symptoms of hypermagnesemia (not hypercalcemia) include muscular weakness and paralysis, which is a different electrolyte disorder. 4
Diagnostic Approach for Immobilization Hypercalcemia
This diagnosis is challenging because no specific laboratory test confirms it—it is a diagnosis of exclusion. 2
- Measure serum PTH first: In immobilization hypercalcemia, PTH is suppressed (low-normal), distinguishing it from primary hyperparathyroidism where PTH would be elevated or inappropriately normal. 2, 5
- Urinary calcium excretion is markedly elevated due to the calcium load from bone resorption. 2
- Serum 1,25-dihydroxyvitamin D is typically decreased, not elevated, ruling out vitamin D-mediated causes. 2
- Rule out malignancy (the most common cause of hypercalcemia in hospitalized patients), primary hyperparathyroidism, sarcoidosis, and myeloma through appropriate imaging and laboratory evaluation. 3, 6, 2
Treatment of Immobilization Hypercalcemia
Standard treatment with IV fluids and bisphosphonates may be insufficient for severe cases. 1
- Initial therapy: Intravenous hydration plus bisphosphonates (zoledronic acid or pamidronate) are first-line for symptomatic or severe hypercalcemia. 3
- Subcutaneous calcitonin provides rapid calcium lowering when conventional treatment fails, and may need to be continued for 8 weeks or longer. 1
- Resumption of weight-bearing activity is the definitive treatment—as physical therapy progresses and mobility improves, hypercalcemia typically resolves and remains normal after calcitonin discontinuation. 2
- Glucocorticoids are not effective for immobilization hypercalcemia (they work for vitamin D-mediated causes like sarcoidosis). 3, 6
Critical Clinical Pitfall
Do not assume hypercalcemia is causing neurological deficits in a patient with paraplegia. The paraplegia came first and is causing the hypercalcemia through immobilization, not vice versa. 1, 2 The hypercalcemia may cause altered mental status, confusion, or coma if severe enough, but it will not cause or worsen the paralysis itself. 3