Management of insufficiency fractures associated with long-term bisphosphonate therapy in a cat

Abstract

Case summary A 10-year-old spayed female domestic medium hair cat presented after sustaining atraumatic insufficiency fractures of the right calcaneus and the left tibia approximately 6 weeks apart. Chronic alendronate therapy had been ongoing for 9 years for the management of previously diagnosed idiopathic hypercalcemia. The right calcaneal fracture was managed non-operatively due to minimal functional impairment. The left tibial fracture was managed via open reduction and internal fixation with orthogonal plating. Alendronate therapy was discontinued at the time of the fracture repair with prednisolone being used to manage the hypercalcemia. Despite rapid clinical improvement, the tibial fracture had a protracted healing course, with clinical union only being achieved 22 weeks postoperatively. At 17 months postoperatively, the idiopathic hypercalcemia remained well controlled. Gait assessment, orthopedic examination and orthogonal radiographs performed at this time revealed resolution of left pelvic limb lameness, a normal orthopedic examination of the left pelvic limb and no evidence of implant-associated complications. Monitoring is ongoing but at the time of publication, no further fractures have occurred. Relevance and novel information As reported in humans, this case report gathers evidence of associations between bisphosphonate treatment and the occurrence of insufficiency fractures in cats, and provides evidence that stress reactions may precede their development. If bisphosphonate therapy is utilized in the long term, serial radiographic monitoring for signs of impending fracture may be warranted. Fracture repair can be successful in cats that have received long-term bisphosphonate therapy, but delayed healing should be anticipated and implant choices made accordingly.

Ionized hypercalcemia can resolve with nutritional modification in cats with idiopathic hypercalcemia or chronic kidney disease

“…27,28 The long-term use of oral alendronate has been associated with osteo necrosis of the jaw and increased cortical bone thickness leading to pathological fractures. [29][30][31][32] The long-term use of glucocorticoids can contribute to adverse effects ratio >1.0:1 to reduce the risk of nutritional hyperparathyroidism. Adverse renal effects have been observed in studies where cats were fed high-phosphate diets with Ca:P ratios of <1.0:1.…”

“… 27 , 28 The long-term use of oral alendronate has been associated with osteonecrosis of the jaw and increased cortical bone thickness leading to pathological fractures. 29 – 32 The long-term use of glucocorticoids can contribute to adverse effects on bone health and may also increase the risk of the development of diabetes mellitus secondary to insulin antagonism. 33 , 34 …”