Adding (Surgical) Insult to (Myocardial) Injury After Hip Fracture

For what seems like time eternal we have been taught, and I continue to teach, that a low-energy “fragility fracture” of the hip is a bellwether of progressive physiologic decline in elderly patients, a belief that is evidenced by the roughly 30% 1-year mortality rate in this patient cohort. Moreover, we know that the compelling case for surgical management is primarily based on reducing the occurrence of medical complications related to inactivity and recumbency that are poorly tolerated by these same patients. Specifically, the 2 most often cited complications of nonsurgical management are venous thromboembolism and pneumonia, and early mobilization of the patient is designed to mitigate the risk of such events. Primary cardiovascular disease and related events, specifically myocardial infarction, are also know to occur at higher rates in these individuals1–3. However, these events have to date received much less attention in the orthopaedic community other than recommendations to manage them according to standard treatment protocols in order to avoid adding (a surgical) insult to (myocardial) injury that may increase morbidity and mortality in these frail patients. “Clearance for surgery” is indeed embedded into contemporary care pathways for low-energy hip fracture in many hospitals, which often include admission to the medical service until clearance is provided to proceed with the hip fracture surgery. In this issue of JBJS we are put on notice that our priorities, based on good intention and medical conservatism, may have been misguided. Borges and colleagues report on a substudy4 consisting of 322 patients from the HIP fracture Accelerated surgical TreaTment And Care tracK (HIP ATTACK) trial5 who presented, upon admission for a low-energy hip fracture, with an elevated serum troponin level, which was the study definition of a concurrent myocardial injury. Their data suggest that accelerated surgery, at a median of 6 hours from the hip fracture diagnosis, in this high-risk group with known myocardial injury reduced all-cause mortality as well as related major cardiovascular events such as stroke and congestive heart failure by more than half compared with standard-care surgery performed at a median of 29 hours after diagnosis. The HIP ATTACK trial was a randomized controlled study, conducted over 5 years between 2014 and 2019 at 69 hospitals in 17 countries, in which 2,970 of 7,780 eligible patients received either accelerated or standard-care-timing hip fracture surgery (repair or prosthetic replacement)5. In that study, accelerated surgery did not significantly lower the risk of mortality or of a composite of major perioperative vascular complications compared with standard-care surgery. Indeed, the results in the 2 groups were nearly identical, with 90-day all-cause mortality of 9% in the accelerated surgery and 10% in the standard-care group, and a major vascular complication rate of 22% in both groups. However, troponin levels were measured at the discretion of each institution and were not standardized by the study protocol, so variation in the indications for such measurements is to be expected. Of the 2,970 patients in the HIP ATTACK trial, 1,392 (47%) had measurement of troponin levels and 322 (23%) of the 1,392 had an elevated level upon hospital admission. This prevalence of documented myocardial injury is consistent with prior reports1–3, but it should be emphasized that it is unknown whether troponin levels were measured according to local institutional protocol or due to clinical suspicion. In the latter scenario, one might expect that the observed prevalence of myocardial injury in the HIP ATTACK trial may overstate that which might occur in the overall hip fracture population. Despite the neutral findings of the HIP ATTACK trial, which only suggested that accelerated surgery for hip fracture may be safe in many instances, Borges et al. evaluated more specific outcomes in the highest-risk patients4. Notwithstanding the resulting small sample size (322), which likely represents some selection bias, the results are noteworthy because they challenge conventional wisdom. The reduction in both all-cause mortality and related major vascular complications was evident in the very patients presumed to be at highest risk from, and in whom we are currently most cautious in proceeding with, hip fracture surgery—i.e., those with myocardial injury upon admission as evidenced by an elevated troponin level. Unlike the parent study, the study by Borges et al. showed that, among patients with an elevated troponin level upon admission, all-cause mortality was 10% after accelerated surgery compared with 23% in the standard-care cohort and the rates of major perioperative vascular complications were 14% and 30%, respectively. Furthermore, if we accept that a higher troponin elevation is indicative of more extensive myocardial ischemia and greater injury, it is even more noteworthy that patients with the highest troponin elevations (>2.1 times the upper limit of normal) experienced an even greater survival benefit from accelerated surgery, with an all-cause mortality rate of 6% compared with 30% with standard care. For obvious reasons, particularly the need for a larger and adequately powered sample and one that is not biased by clinical suspicion in its selection, these provocative results must be confirmed in trials specifically designed for that purpose. In the meantime, we should ponder the possibility that adding (surgical) insult to (myocardial) injury in low-energy hip fracture care may be in the best interests of our patients. Ironically, those whom we view to be at greatest risk and in whom we are currently most cautious and hesitant to proceed with accelerated surgery for their hip fracture may stand the most to gain.