Complicated fractures: how should one deal with them?

Duarte Nuno ALEGRE,MD
Head of Orthopaedics and Traumatology Unit
Hospital Escola da Universidade
Fernando Pessoa

Complicated fractures: how should one deal with them?

by D. N. Alegre, Portugal

Complicated fractures have always occurred and been a feature in orthopedic trauma centers around the world, but in the very last few decades, they have occurred with increasing incidence and with a complexity never seen before. High-energy trauma is in part responsible for this, but the main cause is osteoporotic fragility fractures in elderly patients. The reason for the latter is the increased longevity of the world’s population; a very good event for humanity, but bad news for the body’s support system, the osteoarticular system, which is generally not prepared for having to bear us every day for an increasing number of decades. The purpose of this article is not only to alert the reader to this new reality, but also to provide information on how to react to the phenomenon, giving numbers and facts. We’ll begin with a real clinical case of an osteoporotic fracture patient, moving on to the incredibly dynamic and alive physiology of bone, followed by a review of what we can do in practice to help change one of the worst realities of becoming old today: osteoporotic fractures and their frightening progressive fracture cascade.

Medicographia. 2014;36:225-229 (see French abstract on page 229)

Orthopedic surgeons are having to treat increasingly more complicated fractures in their hospitals every day. The reason? Osteoporosis, which goes hand in hand with the increasingly long lives being experienced by people worldwide. If, some decades ago, osteoporosis was rarely seen, today it is quite common in everyday clinical practice. In past decades, a patient who was over the age of 65 years would receive the attention and treatment reserved for an “old” person; nowadays, we see patients over 90 years of age every day in the emergency trauma unit, often with fractures. Almost 100% of these cases involve osteoporotic fractures.

Actually, with the increasing age of the world’s population, osteoporosis is behaving like a global epidemic, a real public health concern, and this will continue if medical care keeps improving and the human lifespan keeps increasing.1

Osteoporotic fracture: a clinical case

Rather than through just reading a description, a more effective way of understanding the manner in which bone tissue deterioration results in increased fracture probability and incidence is to look at the 3D high-resolution computed tomography images of an old and osteoporotic bone shown in Figure 1 (page 226). It is not difficult to imagine how the result of all these fragility points is that the bone has an increased susceptibility to breaking at several points on the skeleton (Figure 1B). The final result of all these fragility points is weaker bone that is ready to break in a major way, even with a minor trauma or spontaneously at some key point such as the hip, wrist, dorsolumbar spine, or shoulder.

Figure 1. Impact of osteoporosis on bone microarchitecture

High-resolution 3D computed tomography images of osteoporotic bone showing
thinning of bone tissue (A) and loss of trabecular continuity (B).

It is everyday practice to treat patients with fractures such as the one shown in Figure 2A (see also Figure 2B). What we do not see every day is a new fracture in the contralateral hip following a minor fall at home 3 years after the fracture in the first hip (Figure 2C), but contralateral hip fractures are appearing more and more frequently in the clinics of orthopedic surgeons. In the patient shown in Figure 2, after a surgical reduction and fixation (Figure 2D), the unexpected happened: a third fracture (Figure 2E).

There is no doubt that there is a technical solution to every surgical fracture that an orthopedic surgeon faces, but the frequency of osteoporotic fractures and the complexity of the traumatology is becoming increasingly challenging, that’s a fact. Who’s the guilty culprit? Osteoporosis, no doubt about it.

In the patient shown in Figure 2, all the surgical steps were undertaken in the correct manner, and even if this patient is afflicted with more fractures, we will always be able to solve the problem with more surgery (see Figure 2F). However, by operating on the patient, we are simply fixing the acute problem rather than the basis of the problem. Actually, what we should do is transform the patient’s bone tissue into a stronger structure; that would be the gold standard treatment. Of course, fractures have to be treated when they come along, but a new fracture around a periarthroplasty in the right hip, or another in the left hip surrounding or distal to the second fixation nail, may unfortunately occur in the future.

Management of osteoporosis

We must realize that, as orthopedic surgeons, we have to treat the acute trauma events, but ideally, as well as undertaking the surgical procedure, we should try to put in place measures to avoid additional future fractures. This is not only because of the well-known increased morbidity and mortality that comes with osteoporotic fractures in elderly patients, but also for economic reasons.

Nowadays, osteoporosis affects 200 million people around the world. It is estimated that a fragility fracture occurs every 3 seconds: around 25 000 fractures every day and approximately 9 million fractures per year.2 The economic impact of this sad reality is estimated to be €39 billion in Europe alone.3

Despite this scenario, osteoporosis continues to be underdiagnosed and undertreated. So maybe we are doing just half of the job—operating on osteoporotic fractures, but doing nothing to diminish the risk of a new fracture in the future. Even if there is no way of achieving this surgically, there is increasingly robust support for the beneficial effects of calcium, vitamin D, and certain antiosteoporotic drugs in reaching our goal of decreasing the incidence of fractures by strengthening bone tissue structure. Certainly, we would not be able to avoid all fractures, but we could reduce their complexity and the recurrence of osteoporotic fractures in other anatomical regions; that’s a fact.4

We need more than just a medical drug intervention after the first fracture. We are dealing with a silent disease, which— most of the time—only reveals itself after the first fracture, but we should try and change the course and destructive acts of the disease before this. It is well established that there is an exponential increase in the probability of a fracture occurring after a first osteoporotic fracture; actually, studies show that there is double the risk of a spine fracture occurring after a wrist fracture,4 and the appearance of a spine fracture increases the probability of a hip fracture by five times.5 Moreover, the literature shows that after major osteoporotic trauma events, the majority of patients do not receive medical treatment after the acute problem has been resolved,6 and the percentage of osteoporotic patients that receive antiosteoporotic medication after suffering a fragility fracture is even lower.

Figure 2
Figure 2. Clinical case: sequential hip fractures in an osteoporotic patient.

(A) The first fracture, a femoral neck fracture of the right hip, occurred after a minor fall. (B) This first fracture was corrected with a hemiarthroplasty. (C) Three years later, a trochanteric femoral fracture occurred on the left side. (D) This second fracture was corrected with intramedullary nail fixation. (E) After another minor fall, a new fracture occurred on the left side, on the femur that had just been operated on 6 weeks earlier. (F) The femur was reoperated on, and a longer intramedullary nail was inserted.<

In addition to the well-accepted effects of calcium and vitamin D on the course of osteoporosis, some drugs are putting up a good performance in the fight against this silent pathology,7,8 and these should be seen as partners in the difficult struggle against this deceptive and dangerous entity.9,10 Not only are these drugs used in the prevention of osteoporotic fractures, but also in strengthening cortical and cancellous bone to aid the orthopedic surgeon in the treatment of fractures11,12: the bone is rebuilt to restore its form and function, which have been compromised by fracture. The purpose of surgery is to provide stable fixation of the fracture as close to its original anatomy as possible, while trying to preserve its biological environment to permit consolidation, an extremely demanding healing process. Improved knowledge of bone biology in recent years has led to the development of new physical therapies and local biological treatment during surgery to enhance fracture healing, which is being used and tested around the world with the aim of achieving a more effective and rapid bone healing process.

Bone physiology and osteoporotic pathophysiology

There is no doubt that systemic drugs are displaying increasingly impressive performances in assisting the recovery of bone physiology, something that will help us more and more in our approach to fracture care.13,14 But let us travel inside bone tissue to try and understand its natural physiological response to aggressive trauma. One can understand bone structure and physiology very well just by paying attention to the healing process of bone tissue.15,16 It is a fascinating living tissue, with a huge potential for self-regeneration and an extraordinary architecture that permits it to resist all of the forces found in everyday life.17 The metabolic capacity of bone is so strong and energetic that 10% of the human body’s bone structure is usually rebuilt each year. So, theoretically, every 10 years we get a new skeleton.

In osteoporotic bone, this metabolic vigor weakens and all of the well-known natural steps in bone metabolism become slower, with the osteoblasts losing their capacity to build and respond to the osteoclasts’ cleaning process. What happens is that the action of the osteoclasts becomes harmful, as it is not met with the fast and effective response of the osteoblasts, so a lack of bone starts to appear everywhere. If not compensated for, it is only a matter of time before osteopenia gives rise to osteoporosis, which will become more and more severe.18,19

If even young and healthy bone can break under tensile, compressive, shear forces, then tired osteoporotic bone will fail much more easily. The reason is not only the decrease in bone mass, but also changes in metabolism20 and trabecular architecture, the thinning of cortices combined with a loss of perception, and the reduced capacity for self-protection among old individuals. With this loss of bone tissue response comes complex and more comminuted fractures, with recurrent fractures, delayed fracture consolidation, or even an absence of consolidation altogether.21

Future directions

Once again, there will always be an orthopedic answer to possible disorders of bone union—whether surgical or not—disorders that are essentially symptomatic nonunions. In association with the classic removal of necrotic bone and fibrous scar tissue from the nonunion focus and the filling of bone defects with autologous bone graft, use of local growth factors during surgery is currently being tested with the aim of stimulating mesenchymal cells, growth and differentiation factors, and ultimately bone formation.

Noninvasive adjuvant physical therapies like low-intensity pulsed ultrasound, extracorporeal shockwave therapy, and electrical stimulation have had some success, but the amount of evidence is small due to the heterogeneity of results and lack of a sufficient number of randomized controlled trials.22-26 The next step seems logical; use of medication per os, probably antiosteoporotic drugs, along with the already well-accepted use of calcium and vitamin D supplementation to help activate the bone’s self-regeneration and healing capacities.27-37


Osteoporosis is a silent worldwide disease that is occurring with increasing incidence. Despite being silent, when osteoporosis decides to reveal itself through a major fracture, its destructive effect is usually accompanied by huge morbidity and mortality, depending on the fracture pattern and anatomical region where it appears. There is always an orthopedic surgical answer to a fracture, but the more complex the fracture, the more demanding the surgical technique required will be and the heavier the associated morbidity and mortality. The best way to solve problems is to avoid them; that is what is currently missing in the lack of attention given to medical prescription of licensed treatments (calcium, vitamin D, antiosteoporotic drugs) around the time of the fracture event or for the pre- and postfracture medical care of osteoporotic patients. To understand bone tissue physiology and the way that certain drugs can help in keeping it healthier, and thus stronger, in everyday life, it is essential to change our approach to this prevalent pathology and to be more interventional— and not only in a surgical manner. ■

1. International Osteoporosis Foundation. Available at: http://www.iofbonehealth. com. Accessed November 6, 2013.
2. Capture the Fracture Report 2012. Available at: http://www.iofbonehealth. com/capture-fracture-report-2012. Accessed November 6, 2013.
3. Kanis et al. The economic burden of fractures in the European Union in 2010. Osteoporos Int. 2012. 23(suppl 2):S57-S84.
4. Klotzbuecher CM, Ross PD, Landsman PB, et al. Patients with prior fractures have an increased risk of future fractures: a summary of the literature and statistical synthesis. J Bone Miner Res. 2000;15:721-739.
5. Nguyen ND, Pongchaiyakul C, Center JR, et al. Identification of high risk individuals for hip fracture: a 14-year prospective study. J Bone Miner Res. 2005; 20:1921-1928.
6. Jennings LA, Auerbach AD, Maselli J, et al. Missed opportunities for osteoporosis treatment in patients hospitalized for hip fracture. J Am Geriatr Soc. 2010;58:762-764.
7. Rizzoli R, Chapurlat RD, Laroche JM, et al. Effects of strontium ranelate and alendronate on bone microstructure in women with osteoporosis. Results of a 2-year study. Osteoporos Int. 2012;23:305-315.
8. Meunier PJ, Roux C, Ortolani S, et al. Effects of long-term strontium ranelate treatment on vertebral fracture risk in postmenopausal women with osteoporosis. Osteoporos Int. 2009;20:1663-1673.
9. Meunier PJ, Roux C, Seeman E, et al. The effects of strontium ranelate on the risk of vertebral fracture in women with postmenopausal osteoporosis. N Engl J Med. 2004;350:459-468.
10. Reginster JY, Felsenberg D, Boonen S, et al. Effects of long-term strontium ranelate treatment on the risk of nonvertebral and vertebral fractures in postmenopausal osteoporosis: results of a five-year, randomized, placebo-controlled trial. Arthritis Rheum. 2008;58:1687-1695.
11. Reginster JY, Kaufman JM, Goemaere S, et al. Maintenance of antifracture efficacy over 10 years with strontium ranelate in postmenopausal osteoporosis. Osteoporos Int. 2012;23:1115-1122.
12. Kanis J, Johansson H, Oden A, McCloskey EV. A meta-analysis of the effect of strontium ranelate on the risk of vertebral and non-vertebral fracture in postmenopausal osteoporosis and the interaction with FRAX®. Osteoporos Int. 2011;22:2347-2355.
13. Roux C, Fechtenbaum J, Kolta S, Said-Nahal R, Briot K, Benhamou CL. Prospective assessment of thoracic kyphosis in postmenopausal women with osteoporosis. J Bone Miner Res. 2010;25:362-368.
14. Marquis P, Roux C, de la Loge C, et al. Strontium ranelate prevents quality of life impairment in post-menopausal women with established vertebral osteoporosis. Osteoporos Int. 2008;19:503-510.
15. Aro HT, Chao EY. Bone-healing patterns affected by loading, fracture fragment stability, fracture type, and fracture site compression. Clin Orthop Relat Res. 1993;293:8-17.
16. McKibbin B. The biology of fracture healing in long bones. J Bone Joint Surg Br. 1978;60-B:150-162.
17. Dimitriou R, Tsiridis E, Giannoudis PV. Current concepts of molecular aspects of bone healing. Injury. 2005;36:1392-1404.
18. Marsell R, Einhorn TA. The biology of fracture healing. Injury. 2011;42:551-555.
19. Kolar P, Gaber T, Perka C, Duda GN, Buttgereit F. Human early fracture hematoma is characterized by inflammation and hypoxia. Clin Orthop Relat Res. 2011;469:3118-3126.
20. Gruber R, Koch H, Doll BA, Tegtmeier F, Einhorn TA, Hollinger JO. Fracture healing in the elderly patient. Exp Gerontol. 2006;41:1080-1093.
21. Megas P. Classification of non-union. Injury. 2005;36(suppl 4):S30-S37.
22. Harwood P, Newman J, Michael A. An update on fracture healing and nonunion. Orthop Trauma. 2010;24:9-23.
23. Nelson FR, Brighton CT, Ryaby J, et al. Use of physical forces in bone healing. J Am Acad Orthop Surg. 2003;11:344-354.
24. Rodriguez-Merchan EC, Forriol F. Nonunion: general principles and experimental data. Clin Orthop Relat Res. 2004;419:4-12.
25. Chao EY, Inoue N, Elias JJ, Aro H. Enhancement of fracture healing by mechanical and surgical intervention. Clin Orthop Relat Res. 1998;355(suppl):S163-S178.
26. Einhorn TA, Laurencin CT, Lyons K. An AAOS-NIH symposium. Fracture repair: challenges, opportunities, and directions for future research. J Bone Joint Surg Am. 2008;90:438-442.
27. Axelrad TW, Kakar S, Einhorn TA. New technologies for the enhancement of skeletal repair. Injury. 2007;38(suppl 1):S49-S62.
28. Goldhahn J, Little D, Mitchell P, et al. Evidence for anti-osteoporosis therapy in acute fracture situations–recommendations of a multidisciplinary workshop of the International Society for Fracture Repair. Bone. 2010;46:267-271.
29. Della Rocca GJ, Crist BD, Murtha YM. Parathyroid hormone: is there a role in fracture healing? J Orthop Trauma
. 2010;24(suppl 1):S31-S35.
30. Aspenberg P, Genant HK, Johansson T, et al. Teriparatide for acceleration of fracture repair in humans: a prospective, randomized, double-blind study of 102 postmenopausal women with distal radial fractures. J Bone Miner Res. 2010;25: 404-414.
31. Peichl P, Holzer LA, Maier R, Holzer G. Parathyroid hormone 1-84 accelerates fracture-healing in pubic bones of elderly osteoporotic women. J Bone Joint Surg Am. 2011;93:1583-1587.
32. Yu CT, Wu JK, Chang CC, Chen CL, Wei JC. Early callus formation in human hip fracture treated with internal fixation and teriparatide. J Rheumatol. 2008;35: 2082-2083.
33. Rubery PT, Bukata SV. Teriparatide may accelerate healing in delayed unions of type III odontoid fractures: a report of 3 cases. J Spinal Disord Tech. 2010;23: 151-155.
34. Ozturan KE, Demir B, Yucel I, Cakici H, Yilmaz F, Haberal A. Effect of strontium ranelate on fracture healing in the osteoporotic rat. J Orthop Res. 2011;29: 138-142.
35. Habermann B, Kafchitsas K, Olender G, Augat P, Kurth A. Strontium ranelate enhances callus strength more than PTH 1-34 in an osteoporotic rat model of fracture healing. Calcif Tissue Int. 2010;86:82-89.
36. Alegre DN, Ribeiro C, Sousa C, Correia J, Silva L, de Almeida L. Possible benefits of strontium ranelate in complicated long bone fractures. Rheumatol Int. 2012;32:439-443.
37. Tarantino U, Celi M, Saturnino L, Scialdoni A, Cerocchi I. Strontium ranelate and bone healing: report of two cases. Clin Cases Miner Bone Metab. 2010; 7:65-68.

Keywords: antiosteoporotic drug; bone biology; bone nonunion; bone repair; complicated fracture; fracture healing; osteoporotic fracture; medical management