To the Editor: Hip fracture is a commonly encountered clinical problem, with an annual estimated prevalence of 512,000 in the United States by 2040, at a cost of $16 billion.1 Hypovitaminosis D is commonly associated with hip fracture in older adults2,3 and is caused by multiple factors, such as decreased sun exposure with reduced skin production of vitamin D and low dietary D2/D3. This problem may result in proximal muscle weakness, pain, poorer dynamic balance, and slower performance speed,4 affecting rehabilitation during the acute postoperative and initial rehabilitation periods. Furthermore, symptomatic hypocalcemia may occur with intravenous bisphosphonate use, exacerbated by hypovitaminosis D, and may be life threatening and require hospitalization.5 In Australia, vitamin D supplementation is generally available only in an oral formulation at a dose of 1,000 IU (25 μg). The optimal dose and mode of replacement in vitamin D–deficient adults after hip fracture are not known. This study aimed to investigate the effectiveness of moderate-dose oral vitamin D replacement in improving 25-hydroxyvitamin D (25OHD) levels and rehabilitation outcomes after hip fracture surgery.
This study analyzed a cohort of older adults with a hip fracture requiring surgical intervention admitted to the orthopedic ward of a 450-bed metropolitan hospital in Sydney, Australia, over a 9-month period (February–October 2008). Junior orthopedic staff were provided with a protocol that included a suggested oral vitamin D replacement dose (2,000 U twice a day for 14 days). Exclusion criteria were hypercalcemia and severe renal impairment. Three independent assessors reviewed patient data retrospectively. Demographic, functional, and clinical data (including comorbidities) were collected for the two oral vitamin D replacement regimens: moderate dose (MD; 4,000 IU) and usual care (UC; 1,000 IU). The primary outcomes were improvement or maintenance of 25OHD level and change in 25OHD level at Day 14; secondary outcomes included time to mobilization, mobility and activity of daily living (ADL) status, length of stay, discharge destination, and mortality (inpatient, 6-month). Differences in 25OHD levels and rehabilitation outcomes between the two groups were identified using analysis of variance for continuous variables and chi-square for nominal variables.
One hundred thirty-four patients met the eligibility criteria for the study; 10 were excluded because of renal failure or medical instability. The 124 patients studied had a mean age of 80.3±8.6 (range 53–97); 75.8% were female and 74.2% lived in a private home before admission. A baseline analysis showed no significant imbalances between patients with the two vitamin D replacement regimens in terms of age, premorbid place of residence, dementia status, prior mobility and ADL status, and medical comorbidities. Vitamin D deficiency was prevalent in 76.7% of participants, with a mean 25OHD of 44.1±23.2 nmol/L (range 10–131), being severe (<12.5 nmol/L) in four participants (3.3%), moderate (12.5–24 nmol/L) in 18 (15.0%), and mild (25–49 nmol/L) in 70 (58.3%). Thirty-two percent had secondary hyperparathyroidism (parathyroid hormone >5.25 pmol/L in the presence of hypovitaminosis D). All patients were followed up, but it was possible to obtain a second 25OHD measurement on only 66 patients, mostly because of early release from the hospital. At 14 days (Figure 1), the MD group showed greater gains in serum 25OHD levels (22.4±18.3 vs 7.5±19.6 nmol/L, P=.002) than the UC group and was slightly more likely to improve (88.9% vs. 62.5%, P=.05) and less likely to worsen (11.1% vs 37.5%, P=.05). There were no significant differences in terms of symptomatic hypercalcemia, time to mobilization, change in mobility and ADL status, discharge destination, rehabilitation and total length of stay, or inpatient or 6-month postdischarge mortality.
This study confirms that hypovitaminosis D is common in patients presenting with hip fractures and reports the novel finding that 25OHD levels can decrease after hip fracture despite standard oral vitamin D treatment. A moderate oral dose (4,000 IU daily) replacement approach can significantly improve and maintain 25OHD levels within 2 weeks after a hip fracture. This approach may prevent hypovitaminosis D–related adverse effects after subsequent oral or intravenous bisphosphonate treatment, although this did not translate into detectable improvements in rehabilitation outcomes, which may have been because of insufficient responsiveness of these outcome measures and possibly because of the small doses of vitamin D supplemented and short duration of the study. With regard to the optimal dosage of vitamin D after hip fracture, a daily oral vitamin D replacement was shown to be more effective in improving 25OHD levels after 1 year than 300,000 IU D2 intramuscularly once yearly,6 suggesting the benefits of ongoing vitamin D supplementation. According to the results of the current study, we would advocate a vitamin D replacement protocol similar to that of a previous study,7 consisting of an initial parenteral loading dose (50,000–125,000 IU intramuscularly) within 10 days of hip fracture, followed by daily oral vitamin D (800–1,200 IU) and calcium (1,000–1,500 mg daily).7 We would also advocate for a large-dose parenteral vitamin D formation to be made available in Australia, because this is not currently available. Further studies are required to ascertain whether a larger initial loading dose of parenteral vitamin D can translate into improvements in rehabilitation outcomes.
We would like to thank all the clinical and administrative staff on Ward 3A (orthopedic ward) at Bankstown Lidcombe Hospital for their assistance in completing this “Improving the Care of HIp fractured patients at BANkstown hospital” project. We recognize the enormous contribution to patient care that our orthopedic services, nurses, physiotherapists, occupational therapists, social workers, speech pathologists, and dieticians provide to older patients after hip fractures.
Conflict of Interest: The editor in chief has reviewed the conflict of interest checklist provided by the authors and has determined that the authors have no financial or any other kind of personal conflicts with this paper.
Author Contributions: Jenson C. S. Mak: study design and concept, acquisition of subjects and data, analysis and interpretation of data, and preparation of manuscript. Jessica Stuart-Harris: acquisition of subjects and data, analysis and interpretation of data. Ian D. Cameron and Rebecca S. Mason: analysis and interpretation of data, and preparation of manuscript.
Sponsor's Role: None.