HIP fractures are common, disabling, and sometimes fatal

Transcription

1 Journal of Gerontology: MEDICAL SCIENCES Vol.44. No. 4. MI07-III Copyright 1989 by The Geronlologial Soiety of Ameria A HYPOTHESIS: The Causes of Hip Fratures Steven R. Cummings and Mihael C. Nevitt Division of General Internal Mediine and the Clinial Epidemiology Program, University of California, San Franiso. Neither age-related osteoporosis nor the inreasing inidene of falls with age suffiiently explain the exponential inrease in the inidene of hip frature with aging. We propose that four onditions must be satisfied in orderfor a fall to ause a hip frature: (a) the fatter must be oriented to impat near the hip; (b) protetive responses must fail; () loal soft tissues must absorb less energy than neessary to prevent frature, and (d) the residual energy of the fall applied to the proximal femur must exeed its strength. All of these events beome more likely with aging and lead to an exponential rise in the risk of hip frature with advaning age. This model also suggests that a ombination of measurements of neuromusular funtion and of bone strength may be the most aurate approah to assessing the risk of hip frature. HIP fratures are ommon, disabling, and sometimes fatal events, and their inidene rises exponentially with age (1,2). This dramati inrease is widely believed to result primarily from age-related osteoporosis (2), whih plays an important role in the pathogenesis of hip fratures. However, even elderly women with very low bone mineral density of the proximal femur (< 0.6 g/m 2 ) have only about a 2% annual risk of hip frature (3). Women with hip fratures have only somewhat lower bone mineral density in the proximal femur than do ontrols of similar age, and there is substantial overlap in bone density values between these groups (4). Furthermore, mathematial models have not been able to aount for the exponential inrease in hip fratures with age on the basis of bone density alone (5,6). About 80-90% of hip fratures in elderly people are due to falls (7,8). Fewer than 10% our before the fall, perhaps as a result of severe osteoporosis and sudden transmission of shearing or torque-like fores through the hip from a misstep (9). This hypothesis fouses on hip fratures that our as a result of impat on the hip after a fall. Among white women in the United States, the risk of falling approximately doubles from ages to ages (10). The risk of hip frature inreases almost 100-fold during the same interval (11). Thus, the rise in the inidene of hip fratures an, at best, be only partially aounted for by inreases in the inidene of falling. Furthermore, ommunity-based studies have found that only 1-2% of falls result in hip fratures (12-14). Other fators besides osteoporosis and frequeny of falls must also be important in the pathogenesis of hip fratures (15). When both the deline in bone density of the hip and the inreased inidene of falls with aging were inorporated into a mathematial model of hip fratures, Horsman (6) was unable to fully aount for the exponential rise in the inidene of hip fratures with aging. He onluded that other age-related fators must also play a role in hip fratures, but these fators have not been desribed. The inidene of hip fratures inreases exponentially with age while the inidene of Colles' (distal forearm) fratures reahes a plateau after age 65 (see Figure 1). Some have proposed that the differene in the pattern of these two fratures is due to differenes in the type of osteoporosis and bone loss (16). Aording to this hypothesis, Colles' fratures are a manifestation of Type 1 osteoporosis resulting primarily from aelerated loss of trabeular bone after menopause, while hip fratures are a manifestation of Type 2 osteoporosis, a slower loss of both ortial and trabeular bone with aging. But the differenes in the age-related inidene of these fratures might also be due to hanges in the mehanis of falls with advaning age. To understand the pathogenesis of hip fratures and guide omprehensive researh about the auses and prevention of hip fratures, it is neessary to have a hypothesis that integrates falling, osteoporosis, and other "protetive fators." We propose that, in addition to osteoporosis and falling, hip fratures are the result of several age-related hanges in neuromusular funtion that inrease the likelihood that a fall will lead to a hip frature. Furthermore, the ombination of these age-related fators may aount for the exponential inrease in hip fratures with aging. This hypothesis an be tested by making appropriate measurements in prospetive studies of fratures. A Hypothesis: The Link Between Falls and Hip Fratures Most hip fratures are the immediate onsequene of falling. A simple fall from a standing height has several times the potential energy required to frature even a normal hip (17). (Falling from a lower initial height, suh as falling out of a low bed, will have less potential energy.) In order to transmit this energy to the proximal femur, the primary impat of the fall must our near the hip. Protetive responses, like grabbing an objet, and loal shok absorbers, like fat and musles around the hip, might absorb part of the energy of a fall. If the residual energy of the fall that is transmitted to the proximal femur exeeds a ritial threshold, then the proximal femur will frature. This threshold depends on the strength of the bone in the proximal femur for the partiular diretion and rate of the fore that is applied (18). Thus, we hypothesize that in order for the fall from a standing height to ause a hip frature, a sequene of four onditions must all be satisfied (Figure 2): (a) The fall must M107

2 M108 CUMMINGS AND NEVITT to a: 30 - / HIP FRACTURES Fall Z 0 CO O LU Z LU '/... s I AGE COLLES FRACTURES Figure 1. Age-speifi inidene of hip and Colles' (distal forearm) fratures among white women. Adapted from Riggs & Melton (2). Table 1. Fators That May Contribute to Inreased Risk of Hip Fratures with Falls Step Potential Contributing Fators 1. Orientation of fall Slow gait speed Fall during bed and hair transfers Fall during desent of stairs or urbs 2. Protetive responses Slow reation time in upper and lower extremities (response and movement times) Musular weakness Sedation (alohol, sedative drugs) Synope or impaired onsiousness during fall Disorientation, dementia Sudden onset of fall (slippery surfaes) Delayed reognition of falling (peripheral neuropathy, impaired vestibular funtion) 3. Loal shok absorbers Weakness or atrophy of musles surrounding the hip Redued fat around hip and buttoks Hard impat surfae 4. Bone strength Osteoporosis (redued mineral density) Osteomalaia Qualitative mirosopi abnormalities (mirodamage, rystal size) Arhitetural weakness (loss of major trabeulae, thinned orties, thin bone diameter) be oriented so as to land on or near the hip; (b) Protetive responses must be inadequate to redue the energy of the fall below the ritial threshold; () Loal shok absorbers, suh as fat and musles around the hip, must be inadequate to absorb enough of the energy of the fall to prevent the [Orientation of ] I the Faller J To impat the hip Protetive Responses Loal "Shok Absorbers" Insuffiient Insuffiient [ Bone Strength ] Hip Frature Less than residual energy of the fall Figure 2. Defenses against hip frature that must fail in order for a fall to result in a hip frature. frature; (d) Bone strength in the proximal femur must be insuffiient to resist the residual energy of the fall that is transmitted to the hip. Speifi fators that ould ontribute to eah of these steps are outlined in Table 1. Orientation of the fall. In order for most of the energy of a fall to be transmitted to the proximal femur, the faller must land on or near the hip. If the prinipal impat ours elsewhere, little or no energy will be transmitted to the proximal femur. Falls that arry the pelvis straight down, to the side, or bakwards are the type most likely to ause a diret impat on or near the hip (Figure 3). These types of falls are more likely when the faller has little or no forward momentum, as

3 THE CAUSES OF HIP FRACTURES M109 Figure 3. A fall ourring while standing still, walking slowly, or slowly desending a step has little forward momentum. With little forward momentum, the prinipal point of impat will be near the hip. Figure 4: A fall ourring during rapid walking has enough forward momentum to arry the faller onto her hands or knees instead of her hip. when the faller is standing still, or walking slowly. In ontrast, falls that our at a more rapid gait speed will tend to arry her forward on to hands or knees and are more likely to frature the distal forearm than the hip (Figure 4). Gait speed slows about 25% from age 65 to 85 (19). There may be a threshold for gait speed below whih falls are very likely to land on the hip. If so, then, with advaning age, an inreasing proportion of elderly walk at speeds that inrease their risk of landing on the hip and suffering a hip frature. Falls that our in ertain irumstanes might also be more likely to arry the faller onto her hip. Falls that our during transfers between bed and hair have little or no forward momentum and are more likely to impat near the hip. The inidene of suh falls also inreases with age (20). Protetive responses. The onset of a fall initiates several types of reflexes and postural responses that an prevent a fall, hange the orientation of the faller, or redue the energy of a fall if it ours (21,22). One a fall is inevitable, grabbing nearby objets ould substantially slow the rate of falling. By quikly extending the arms, the faller an absorb the energy of the fall with the arms and hands and minimize the fore of impat on the hip or other parts of the body. Quik stumbling movements of the feet (21) might also derease the downward veloity of the fall and thus derease its potential energy. Beause falls our rapidly, the effetiveness of these responses depends on their speed of exeution. During falls, there is a ritial threshold time for protetive reations; responses delayed beyond that threshold will be too late to redue the energy or hange the diretion of a fall (23). Reation times slow with aging (24); thus, protetive responses may be too late to protet the very elderly faller against hip fratures. Sedatives and alohol also slow reation times (25,26), and this might partly explain the inreased risk of hip fratures assoiated with use of longating sedatives (27) and regular intake of alohol (28). The effetiveness of protetive responses also depends on strength. If musles are too weak to hold the arm in extension, an outstrethed arm may absorb little or no energy of a fall. Thus, the deline in arm strength that ours with aging (29) might inrease the risk of hip fratures after a fall while dereasing the risk of Colles' fratures. Protetive responses are lost during synopal falls. We have found that the risk of suffering a frature of any type is four times greater during a synopal than during a nonsynopal fall (30). The inidene of synopal falls and "drop attaks" also inreases substantially with age (20) and might aount for a small part of the inreased risk of fratures with aging. Loal shok absorbers: Skin, fat, and musles surrounding the hip are apable of absorbing substantial amounts of energy of an impat (9). Therefore, falls may be more likely to ause hip fratures in those who have less soft tissue around the hip. Abdutors of the hip are the largest group of musles attahed to the proximal femur. We have observed that, among women, the isometri strength of hip abdutors delines about 27% from age 65 to age 80 (31). This age-related deline in strength may indiate a similar deline in the apaity of musles around the hip to absorb the energy of impat and may, in turn, aount for some of the inreased inidene of hip fratures with aging. There have been no studies of hanges in skin and fat around the hip with advaning age. Bone strength. If the residual energy of the fall applied to the proximal femur exeeds the strength of the bone, the proximal femur will frature. Hene, bone strength is the "last defense" against hip fratures. In the very small proportion of hip fratures that our "spontaneously" during weight bearing, osteoporosis, fatigue damage, or other loalized disease may be the sole ausal fator (8,32). Bone mineral density is highly orrelated with bone strength (9,33). The density of the proximal femur dereases at a rate of about 1% per year after age 50 (3). Crosssetional studies have found that the risk of hip frature inreases with dereasing mineral density of the proximal femur (5). Besides the bone mineral density, the strength of the proximal femur is also determined by its arhiteture. The ortial shell aounts for 50-70% of the strength of the femoral nek (9). The thikness and strength of the ortial shell may be espeially important in regions suh as the alar femorale, where ompression fores are the greatest. The internal trabeular system is aligned to resist speifi ompressive and tensile fores transmitted through the proximal femur; these bundles of trabeulae thin and disappear

4 MHO CUMMINGS AND NEVITT with aging. These features an be measured on radiographs (34). Women with hip fratures have thinner orties and fewer trabeulae than other women of the same age (35). Deterioration in the quality of bone due to aumulation of mirosopi damage (36) and hanges in the sizes of mineral rystals (37) also play an important role in the loss of bone strength with age. However, these harateristis an only be aurately assessed by bone biopsy. Impliations for Studies of Hip Frature This hypothesis is testable; most of the fators an be measured indiretly. Two reent prospetive studies (13,19) have found that the risk of falling is at least partially preditable by ombinations of simple questions and examinations. If falling plays a large role in the pathogenesis of frature, then these fators should also be preditive of hip frature. If the orientation of the fall is important, then hip fratures should be more likely in those who have the slowest gaits. Conversely, those with faster gaits should have a greater risk of forearm fratures than those who walk slowly. Gait speed is easy to measure and should also be inluded in prospetive studies of hip frature. To test the importane of protetive responses, studies should inlude measurements of reation time and arm strength. There is no method for diretly measuring the energy-absorbing apaity of soft tissues around the hip. However, indiret measurements of the amount of fat or other tissue overlying the greater trohanter by ultrasound or by measurements on radiographs might provide an adequate test of the hypothesis. The bone mineral density of the hip an be aurately assessed by dual-photon absorptiometry (38) or quantitative digital radiography. Gross trabeular struture and ortial thikness in the proximal femur an be assessed by radiographs (34). Transmission ultrasound might provide a noninvasive index of both mineral density and the mirosopi quality of bone (39). Many of these fators may be altered by hip fratures. Thus, the pathogenesis of hip fratures would be most aurately desribed by prospetive studies. Many of the fators involved in the pathogenesis of hip fratures are likely to be assoiated. For example, musle weakness may be assoiated both with dereased bone mineral ontent and dereased effetiveness of protetive responses. Therefore, the independent ontribution of any fator must be determined from arefully onstruted multivariate analyses. This hypothesis also suggests that the probability of a hip frature is the produt of the probability of eah step of the sequene (Figure 2). This suggests that risk fators for eah step in the sequene will interat in a multipliative fashion; the probability of a hip frature would approah zero as the probability of any step in the sequene approahes zero. Impliations for Theories of Osteoporosis This hypothesis suggests that the differenes between the epidemiology of hip and Colles' fratures may be due to hanges in the orientation of falls and protetive responses with advaning age rather than differenes in the type of osteoporosis. As gait speed and protetive responses slow, a smaller proportion of falls impat the hands, and a greater proportion of falls impat the hip. This would explain the inreasing inidene of fratures of the hip (and pelvis) and the blunted rise in the inidene of Colles' fratures with age. Impliations for Prevention of Hip Fratures Estrogen therapy redues bone loss and the risk of hip fratures (1,2). This hypothesis suggests that other types of interventions might also redue the risk of hip fratures. For example, if regular exerise prevents the slowing of gait with age (40), it might derease the risk of hip fratures by altering the orientation of falls. Interventions might fous on improving the speed and strength of protetive responses during falls. The feasibility of enhaning loal shok absorbers with unobtrusive padding around the hip also warrants investigation. It may eventually be possible to inrease the bone mass in the proximal femur. However, it will be muh more diffiult to restore the normal arhiteture of bone. To estimate the value of therapies designed to inrease bone mass, it will be important to understand the relative ontributions of mineral ontent, marosopi arhiteture, and mirosopi qualities of bone to the pathogenesis of hip fratures. This model suggests that the risk of hip frature an be redued substantially by dereasing the probability of any one step in the sequene of events from fall to hip frature. Theoretially, virtually all hip fratures due to falls ould be prevented by maintaining or inreasing bone strength to a level that was always greater than the potential energy of a fall, or by preventing all falls that are oriented to land on the hip. Furthermore, the model suggests that interventions aimed at different steps in the sequene would have synergisti effets in preventing hip fratures. Conlusion We hypothesize that most hip fratures are the result of a sequene of events all of whih beome more likely with advaning age. This hypothesis an be tested by measuring several neuromusular and anthropometri harateristis in addition to measurements of bone mass and struture. The ultimate goal should be identifiation of treatable or preventable auses and pratial interventions that an be widely applied to minimize the growing epidemi of hip fratures. ACKNOWLEDGMENTS This work was supported by grants from the Commonwealth Fund (number 7550), National Institute on Aging (1-R01-AG05407), and the Henry J. Kaiser Family Foundation Faulty Fellowship in General Internal Mediine (to Dr. Cummings). Address orrespondene and reprint requests to Dr. Steven R. Cummings, Division of General Internal Mediine, A-405, University of California Medial Center, 400 Parnassus, San Franiso, CA REFERENCES 1. Cummings SR, Kelsey JL, Nevitt MC, O'Dowd KJ. Epidemiology of osteoporosis and osteoporoti fratures. Epidemiol Rev 1985;7:I Riggs BL, Melton LJ III. Involutional osteoporosis. N Engl J Med 1986;314:I Melton LJ, Wahner HW, Rihelson LS, O'Fallon WM, Riggs BL. Osteoporosis and the risk of hip fratures. Am J Epidemiol 1986; 124:

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