Stroke survivors face substantially increased hip fracture incidence and elevated mortality compared to non-stroke populations.

This narrative review explores the epidemiological, pathophysiological, and clinical interrelationships between stroke and hip fractures, focusing specifically on stroke survivors. The study covers a 5-year follow-up period and compares outcomes against non-stroke populations. Key secondary outcomes include bone density loss, falls, motor impairments, healthcare burden, osteoporosis screening, exercise-based rehabilitation, and lifestyle modifications. The review synthesizes existing literature to highlight the unique vulnerabilities of this patient group.

The primary results demonstrate that the incidence of hip fracture post-stroke is 7.6% within the 5-year follow-up window. This rate is significantly higher than the 2.8% observed in non-stroke populations. Furthermore, hip fractures in stroke patients are associated with a 2.1- to 4.8-fold increased risk compared to baseline expectations. In terms of acute outcomes, 30-day postoperative mortality in stroke patients with hip fractures reaches up to 14.8%. Functional recovery is also notably reduced in this cohort compared to non-stroke counterparts.

Safety and tolerability data regarding specific adverse events, discontinuations, or serious adverse events were not reported in the input evidence. Consequently, no specific safety profile can be derived from this narrative review alone. The review highlights the substantial healthcare burden and the complex interplay of motor impairments and bone density loss in this population. These factors contribute to the elevated mortality and reduced functional recovery observed.

Key limitations of this evidence include the narrative review format, which precludes the calculation of precise statistical confidence intervals or p-values. The sample size was not reported, and the specific setting was not detailed. As a narrative review, the evidence does not establish causality but rather describes associations. Clinicians should interpret these findings as indicative of a high-risk profile requiring vigilant monitoring, rather than as proof of a specific causal mechanism. Practice relevance is limited by the lack of randomized controlled trial data to guide specific intervention protocols.