Our analysis of data from multiple cohort studies showed that older adults have a 5- to 8-fold increased risk for all-cause mortality during the first 3 months after hip fracture. Relative hazards for mortality decreased thereafter but did not return to rates seen in age- and sex-matched control groups without fracture. Moreover, an excess annual mortality for adults with hip fracture persisted over time in both women and men. At any given age, the excess annual mortality after hip fracture was higher in men than in women.
Several factors may contribute to the marked increase in short-term relative mortality risk after hip fracture. These include postoperative events associated with hip surgery, such as pulmonary embolism (68
), infectious complications (69
), heart failure (69
), or cardiovascular or pulmonary complications (64
). Multiple comorbid conditions predisposing to fracture, such as dementia, chronic obstructive pulmonary disease, psychiatric conditions, cardiovascular disease, kidney disease, and neurologic diseases could also increase short-term mortality risks (5
). Whether some of these factors could help explain why excess mortality after hip fracture is consistently higher in men than in women merits further study. For example, 1 study suggested that the higher excess mortality in men might be related to an increased risk for postoperative complications, including infections (70
). Another study showed that men with fracture have a greater burden of comorbid diseases at the time of fracture than women (71
), although comorbid conditions do not fully explain the mortality difference between the sexes (58
We do not know whether the long-term excess mortality in patients with hip fracture is driven by differences in frailty that existed before hip fracture, were precipitated by hip fracture, or both. Patients with hip fracture are, on average, more functionally impaired and have more comorbid conditions than similar-aged patients without hip fracture. Prospective studies of functional outcomes after fracture also indicate that older adults who have a hip fracture have substantial new functional impairments and loss in quality of life that frequently persist at 1 year (71
). Many of the components of the frailty syndrome that commonly occur after hip fracture are known risk factors for mortality, including poor mobility, balance, reduced muscle strength, impaired cognition, poor nutritional status, low levels of physical activity, and increased risk for falls (37
). However, 1 study comparing survival in women older than age 70 who had hip fracture with control participants matched by age, sex, comorbid conditions, and functional status found that although short-term mortality (up to 2 years) was more pronounced in women with comorbid disease and functional limitations at the time of fracture, excess mortality more than 2 years after the fracture was restricted to those who had fewer baseline comorbid conditions and functional limitations. This intriguing preliminary finding suggests that hip fracture, perhaps through an inflammatory or immunologic effect, may trigger or accelerate frailty in patients with few comorbid conditions at baseline, leading to longer-term effects on survival (78
Several limitations affect the certainty and interpretation of our findings. First, some data derived from individual studies could have been biased. Most studies that we analyzed either pooled nursing home residents with community-dwelling participants or did not specify and differentiate nursing home residents from community-dwelling participants. Data from studies that pooled patients with varying underlying risks could potentially over-estimate the survival of nursing home residents with hip fracture and underestimate the survival of community-dwelling participants with hip fracture. Most studies assembled cohorts from hospital admissions or lists. These studies missed persons with hip fracture who were never admitted and probably had very high early mortality rates.
Second, we included only studies that displayed results with survival curves, and statistical testing suggested the possibility of publication bias. Third, studies varied, sometimes markedly, in size, duration of observation, selection of control populations, ascertainment of death, and adjustment for comorbid conditions. We had limited ability to explore how the accuracy or precision of RH estimates for short- and long-term mortality were affected by between-study heterogeneity.
Fourth, our analyses do not quantify how much of the observed excess mortality is directly attributable to hip fracture and its sequelae. We could not assess or take into account the potentially confounding effects of comorbid conditions and treatments received. Fifth, mortality rates in the hip fracture and control populations may vary over time and could bias the RH estimates. Life-table method–based analyses, as used in our study, assume no secular trends in relative risk for death, which may be unrealistic. Indeed, some evidence suggests that mortality risk after hip fracture has increased over time, even with adjustment for demographic shifts in the hip fracture population (47
Sixth, although we pooled data from studies conducted in several geographic regions, the generalizability of our estimates of age-specific excess mortality is limited, because we modeled excess mortality only for a white U.S. population. Finally, our modeling of excess mortality was hypothetical and not an actual prospective study.
Regardless of limitations, we believe ours is the first systematic review to provide quantitative estimates of both relative and absolute survival in patients with hip fracture. Meta-analyses of survival data require specific techniques because of data censoring; ignoring censoring may bias the overall estimates. Potentially useful information about timing of events (deaths) and the shape of the published survival curves was not discarded in the current analysis, because we computed an RH and its standard error for each contributing cohort study and then increased the power of our analyses by pooling data. An advantage of this method is that we could estimate the RH of death at several intervals after the injury. The cohorts used in this analysis varied in size, and the designs of the studies were heterogeneous in many respects, but no single study was so large that it dominated the overall results regarding RH for all-cause mortality. From a public health perspective, calculations of absolute risk and estimates of excess mortality, such as those presented here, not only allow estimates of the consequences of various diseases and complications but may ultimately contribute to a more appropriate allocation of resources for competing causes of mortality.
Patients with hip fracture have a 5- to almost 8-fold increased hazard of all-cause mortality during the first 3 months after the fracture. This excess mortality decreases substantially during the first 2 years after fracture, but does not return to the mortality rate seen in age- and sex-matched control participants even after 10 years of follow-up. Over time, this excess mortality RH translates into statistically significant differences in the absolute risk for death. The absolute risk for death and the excess all-cause mortality in patients with hip fracture are largely dependent on age. At any given age, excess mortality after hip fracture is higher in men than in women. These findings may be helpful when performing cost-effectiveness analyses of hip fracture prevention strategies or designing treatment strategies in patients with hip fracture.