Abstract: FR-PO567
Immobilization-Associated Hypercalcemia in the Hospital Setting: A Cohort Study
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Clinical
November 04, 2022 | Location: Exhibit Hall, Orange County Convention Center‚ West Building
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid‚ Electrolyte‚ and Acid-Base Disorders
- 1002 Fluid‚ Electrolyte‚ and Acid-Base Disorders: Clinical
Authors
- Park, Jacob, The University of Queensland Ochsner Clinical School, Herston, Queensland, Australia
- Lam, Walter, Department of Nephrology, Ochsner Health, New Orleans, Louisiana, United States
- Chalmers, Dustin, Department of Nephrology, Ochsner Health, New Orleans, Louisiana, United States
- Velez, Juan Carlos Q., Department of Nephrology, Ochsner Health, New Orleans, Louisiana, United States
Group or Team Name
- Ochsner Nephrology
Background
Immobility is an established cause of hypercalcemia. Supporting evidence is primarily derived from experimental studies and clinical case reports. Cohort studies are lacking. We examined the relative contribution of immobilization-associated hypercalcemia (Immob-HCa) to all causes of in-hospital hypercalcemia.
Methods
A retrospective review of medical records was conducted searching for cases of hypercalcemia at Ochsner Medical Center over a 1-year period. Hypercalcemia was defined as serum calcium > 11.0 mg/dL. Definite Immob-HCa was defined as presence of immobility by history combined with absence of disqualifying laboratory data (PTH > 60 ng/dL, 1,25 vitamin D > 70 pg/mL, 25 vitamin D > 80 ng/mL, PTH-related peptide > 2.5 pmol/L or monoclonal gammopathy), lytic lesion by imaging, or alternative etiology (malignancy, sarcoidosis, exposure to thiazide, end-stage kidney disease (ESKD) or calcium or vitamin D supplementation). Probable Immob-HCa was defined as documented immobility and absence of alternative etiology, but incomplete laboratory data.
Results
From a total of 364 patients with in-hospital hypercalcemia, 114 had elevated PTH, 83 had malignancy, 63 were on calcium or vitamin D supplements, 25 had ESKD, 22 were on a thiazide and 14 had sarcoidosis or elevated 1,25 vitamin D, adding to 321 cases excluded. The remaining 43 charts were manually reviewed. Among them, 5 cases were categorized as Definite Immob-HCa and 26 were categorized as Probable Immob-HCa. Twelve cases were undetermined. Thus, Immob-HCa accounted for up to 8.5% (31/364) of in-hospital hypercalcemia. Among the 31 Immob-HCa cases, median age was 72 (22-92), 35% women, 48% white, 29% self-identified black; median peak serum calcium was 12.2 (11.2-17.8) mg/dL. Corrected serum calcium was available in 20/31 (65%) of the cases, with a median of 12.8 (11.7-15.4) mg/dL. High ionized calcium was verified in 9 (29%) cases. Concomitant acute kidney injury (AKI) was present in 11 (35%) of the cases of Immob-HCa.
Conclusion
Immob-HCa accounts for approximately 1 in 12 of cases of in-hospital hypercalcemia and it is accompanied by AKI in one third of the cases. Incomplete diagnostic work up for hypercalcemia may underestimate its incidence. Raising awareness of this entity could lead to prevention and more prompt diagnosis and treatment.