Michael E. Frey, MD; Gopi Kasturi, MD; Robert A. Adler, MD; David X. Cifu, MD;
Abu Qutubuddin, MD; Heidi Prather, DO

Case Presentation
A 76-year-old woman presents to your office with a six-week history of low back pain (LBP) and buttock pain. She has no specific history of LBP other than “the occasional twinge.” She does not report any specific history of trauma but remembers sitting down hard on a wooden chair about two months ago. Her pain has been gradual in onset and mildly progressive to the point that she has pain with walking, rising from a chair and rolling over in bed at night. She lives alone and remains independent for her activities of daily living and is using a cane in the community for short distances. The cane is new since the onset of pain. She has a history of osteopenia and has been taking Fosamax for the past 10 years. Her last bone density test was 10 years previously when she was placed on the medication. The  primary care physician has referred her to you because the X-ray studies, according to the patient, “just show arthritis.” Her main goal in seeing you is to reduce her pain level, get rid of the cane and get back to her walking routine with her girlfriends.

On physical examination, she reports pain in sitting, rising from the chair, standing and ambulation. Her pain further worsens with lumbar flexion. She ambulates with the cane in the left hand and has an antalgic gait on the left. Her neurological exam for muscle strength, sensation and reflexes are normal. You order a bone scan that demonstrates a sacral fracture. What do you recommend for evaluation and treatment? 

Drs. Kasturi, Adler, Cifu and Qutubuddin Respond
Insufficiency fractures are believed to be a form of stress fractures and are caused by normal (physiological) stress applied to bone with deficient elastic resistance.¹ Sacral insufficiency fractures (SIF) occur mostly in women aged >55 years,^2,3 but they have been reported in men as well.⁴ Osteoporosis is the most important cause of SIF, including such secondary causes as oral glucocorticoid therapy.

Presentation
The chief complaint after a SIF is low back and buttock pain exacerbated by movement.² Patients may also have other fractures, most commonly pubic ramus fractures, leading to groin pain. It is believed that initial mechanical failure of the pelvic ring occurs in the sacrum, with subsequent fracture through the pubis.⁵ Other associated fractures include vertebral compression fractures, iliac wing fractures and intertrochanteric hip fractures that are identified on scintigraphy.^6,7 It has been reported that most sacral insufficiency fractures occur in Zone 1 of the sacrum, according to the Denis classification,⁸ usually displaying a vertical pattern extending parallel to the sacroiliac joint and lateral to the sacral foramina, thus making neurological deficits uncommon.⁷ Although several case reports describe neurological complications such as limb paresthesias and cauda equina syndrome with sphincter dysfunction.^9-12

Diagnosis
The most specific finding after a SIF is pain upon palpation over the sacrum. Plain film X-rays have poor sensitivity in diagnosis. A technetium-99 bone scan may be helpful, especially in view of the occurrence of associated fractures. The classic “H” or “Honda” sign seen on bone scan, representing combined bilateral vertical and horizontal sacral fractures, is present inconsistently and may vary from 15–68%.⁶ MRI demonstrating bone marrow edema as low signal intensity on T1 weighted and high signal intensity on T2 weighted images and the T2 weighted short tau inversion recovery (STIR) images are particularly sensitive.¹³ However, CT is regarded as the gold standard in diagnosing occult SIF because it can delineate bony details.⁶ Apart from routine imaging tests, evaluation should include serum 25-hydroxyvitamin D and calcium levels. Further work-up for secondary causes of osteoporosis can be initiated as indicated. The potential for misdiagnosis exists in patients with a history of prior malignancy.¹³ A high index of suspicion would greatly help obviate unnecessary investigations which have included bone biopsies to rule out cancer.⁷ Some studies have recommended that bone biopsy should be avoided because histological findings of the healing bone can mimic malignancy.13

Twenty to 30% of postmenopausal women and more than 50% of men with osteoporosis have a secondary cause.¹⁴ Some experts believe that postmenopausal osteoporosis is a diagnosis of exclusion, and secondary causes of osteoporosis should be considered in all cases.¹⁵ Causes of secondary bone loss include adverse effects of drug therapy, endocrine disorders, eating disorders, immobilization, organ transplantation, bone marrowrelated disorders, renal disease, disorders of the gastrointestinal or biliary tract and cancer.

All patients with osteoporosis should have a complete medical and social history, and a complete physical examination. The laboratory tests should include serum chemistries (calcium, phosphorus, total protein, albumin, globulin, alkaline phosphatase, liver enzymes, creatinine, electrolytes), a blood count (white blood cell, hemoglobin, hematocrit) and urinary calcium. All men should have serum testosterone measurements. If clinically indicated, tests to evaluate thyroid function, ovarian status, parathyroid hormone and Vitamin D metabolites, and multiple myeloma should be ordered.¹⁶

Low bone mineral density (BMD) is a major risk factor for osteoporotic fractures.¹⁷ It is measured using dual X-ray absorptiometry [DXA] and is commonly expressed as a T score and Z score. The T score compares the BMD of an individual with the mean value for a young healthy subject. The Z score compares the BMD of an individual with the mean value for age-matched controls. Special attention to secondary causes of osteoporosis should be paid in patients who have a low Z score.

Spine radiographs should be ordered for patients who have height loss, back pain or spinal deformity. Individuals with
complex secondary causes should be referred to a bone and mineral specialist for a consult.

Management
While bed rest may be needed in the acute phase (up to 72 hours), there is growing evidence that patients with sacral
fractures should be mobilized early.¹⁵ The adverse effects of prolonged bed rest are well recognized.18 Acetaminophen is the analgesic of choice for most elderly people with mild to moderate pain.¹⁹ NSAIDs may be used to address the pain caused by periosteal reaction secondary to the acute vertebral fracture²⁰ but NSAIDs can have major side effects in the elderly including gastrointestinal and cardiac events.^21,22 Several medications used to treat osteoporosis have been shown to relieve pain after acute vertebral fractures. In one study, calcitonin provided pain relief from the second day of treatment onward. Over the following two weeks, the patients were able to sit and stand, and gradually started to walk again.²³ Teriparatide, an anabolic agent, has also been shown to reduce back pain and severe back pain after a vertebral fracture.²⁴ Intravenous bisphosphonates have also been shown to decrease pain from recent vertebral compression fractures.²⁵ Patients on oral alendronate reported fewer days of limited activity because of back pain and bed rest.²⁶ This, along with evidence that bisphosphonates did not show any adverse effects on fracture healing in dogs,²⁷ makes a strong case for starting definitive therapy early after a fracture.

A sound management plan would also include measuring bone density by DXA prior to or soon after discharge to follow response to therapy. FDA-approved medications for osteoporosis currently available include antiresorptive agents, such as bisphosphonates, calcitonin, estrogen or selective estrogen receptor mediators [SERMs] and anabolic agents, such as teriparatide. ²⁸ These agents increase bone mineral density, reduce fracture risk and are generally safe. With the FDA approval of the once yearly intravenous bisphosphonate zolendronic acid,²⁹ it is hoped that treatment of osteoporosis will be convenient for both the patient as well as the physician and thus have enhanced compliance. This drug has been reported to decrease subsequent fracture and mortality in patients who have suffered a hip fracture. Vitamin D deficiency should be corrected to levels above 30ng/ml [80nM]. Evidence is mounting that the currently prescribed levels of daily intake for vitamin D may be inadequate.³⁰ High doses of vitamin D may be required to achieve correction of severe deficiency.³¹ Calcium and vitamin D supplementation are generally continued along with pharmacotherapy.

Sacroplasty,³² an evolving strategy to address painful sacral fracture via percutaneous injection of polymethylmethacrylate [PMMA] may be used if all the strategies mentioned above have failed to manage the pain. However, only a few case series have assessed the safety and efficacy of this procedure, and the long-term effects of sacroplasty on the biomechanics of spine have not been studied further.

Prognosis
Prognosis is significantly better for unilateral sacral insufficiency fractures than bilateral fractures.⁶ While no objective measures of functional ability or psychological assessments have been utilized in the existing research publications, an overview of the prognosis for return to mobility after SIF reveals that gross assessments have demonstrated as low as 38% of patients regaining their pre-injury mobility level in one investigation,⁶ while other studies report more favorable outcomes by six months.⁷

Discussion
Underlying osteoporosis must be recognized in patients with SIF or other low trauma fracture. The compressive strength of trabecular bone is proportional to the square of its density. A decrease in density by a factor of 2 consequently reduces its compressive strength by a factor of 4.6 It would then be safe to consider all low trauma or sacral “insufficiency” fractures to be secondary to osteoporosis until proven otherwise. Only a minority of fracture patients are evaluated for osteoporosis, with some studies reporting rates as low as 5%.33 A review article34 reported that the recommendations for adequate doses of calcium and vitamin D were made in as low as 8% of the cases. It might be worthwhile doing away with terms like “insufficiency” and using diagnostic terms like osteoporotic sacral fracture or pathological fractures where indicated. A previous fracture is a major risk for subsequent fractures.^35-39 Appropriate diagnosis and treatment of osteoporosis after a sacral fracture may prevent subsequent fractures, especially hip fracture with its high mortality rate.⁴⁰ Thus, while the approach to pain relief could vary depending on the unique medical, surgical, social, and psychological status of individual patients, it is imperative that they be worked up and treated for osteoporosis. Quality improvement measures are being established to better diagnose and treat osteoporosis. Several successful methods have included education of patient and caregivers after an acute fracture⁴¹ or the use of an osteoporosis nurse.⁴² Standing discharge orders (eg, for medications, primary care follow-up, bone density testing) have been recommended to improve compliance and prevent subsequent fractures.⁴³

References
1. Pentecost RL, Murray RA, Brindley HH. Fatigue, insufficiency, and pathologic fractures. JAMA. 1964; 187:1001–1004.

2. Grasland A, Pouchot J, Mathieu A, Paycha F, Vinceneux P. Sacral insufficiency fractures: an easily overlooked cause of back pain in elderly women. Arch Intern Med. 1996;156:668–674.

3. Dasgupta B, Shah N, Brown H, Gordon TE, Tanqueray AB, Mellor JA. Sacral insufficiency fractures: an unsuspected cause of low back pain. Br J Rheumatol. 1998;37:789–793.

4. Taguchi H, Inoue T, Kawai S. Midline longitudinal fracture of the sacrum: case report and review of the literature. J Ortho & Trauma. 2004;5(2):5.

5. Schindler OS, Watura R, Cobby M. Sacral insufficiency fractures. J Orthop Surg. 2007;15(3):339-346.

6. Gotis-Graham I, Mcguigan L, Diamond T, et al. Sacral insufficiency fractures in the elderly. J Bone Joint Surg [Br]. 1994;76:882-886.

7. DeSmet AA, Neff JR. Pubic and sacral insufficiency fractures: clinical course and radiologic findings. AJR Am J Roentgenol. 1985;145:601-606.

8. Denis F, Davis S, Comfort T. Sacral fractures: an important problem. Retrospective analysis of 236 cases. Clin Orthop Relat Res. 1988;227:67–81.

9. Martineau PA, Ouellet J, Reindl R, et al. Surgical images: musculoskeletal. Delayed cauda equina syndrome due to a sacral insufficiency fracture missed after a minor trauma. Can J Surg. 2004;47(2):117-118.

10. Jacquot JM, Finiels H, Fardjad S, Belhassen S, Leroux JL, Pelissier J. Neurological complications in insufficiency fractures of the sacrum. Three case-reports. Rev Rhum Engl Ed. 1999;66(2):109-114.

11. Muthukumar T, Butt SH, Cassar-Pullicino VN, McCall IW. Cauda equina syndrome presentation of sacral insufficiency fractures. Skeletal Radiol. 2007;36(4):309-313.

12. Singh H, Rao VS, Mangla R, Laheri VJ. Traumatic transverse fracture of sacrum with cauda equina injury: a case report and review of literature. J Postgrad Med. 1998;44(1):14-15.

13. Blake SP, Connors AM. Pictorial review sacral insufficiency fracture. British J Radiol. 2004;77:891–896.

14. Fitzpatrick LA. Secondary causes of osteoporosis. Mayo Clin Proc. 2002;77:453-468.

15. Babayev M, Lachmann E, Nagler W. The controversy surrounding sacral insufficiency fractures: to ambulate or not to ambulate? Am J Phys Med Rehabil. 2000;79(4):404-409.

16. Watts NB. Diagnosis and evaluation of patients with osteoporosis. South Med J. 2004;97(6)540-541.

17. Ross P. Risk factors for osteoporotic fracture. Endocrinolog Metab Clin North Am. 1998;27(2):289-301.

18. Brown CJ, Friedkin RJ, Inouye SK. Prevalence and outcomes of low mobility in hospitalized older patients. J Am Geriatr Soc. 2004;1263–1270.

19. Beers MH, Berkow R, eds. Merck Manual of Geriatrics. Whitehouse Station, NJ; Merck Research Laboratories; 2000:383-396.

20. Prather H, Watson JO, Gilula LA. Nonoperative management of osteoporotic vertebral compression fractures. Injury. 2007;38S3:S40-48.

21. Heerdink ER, Leufkens HG, Herrings RM, Ottervanger JP, Stricker BH, Bakker A. NSAIDs associated with increased risk of congestive heart failure in elderly patients taking diuretics. Arch Intern Med. 1998;158:1108-1112.

22. Laine L, Connors LG, Reicin A, et al. Serious lower gastrointestinal clinical events with nonselective NSAID or coxib use. Gastroenterology. 2003;124(2):288-292.

23. Lyritis GP, Tsakalakos N, Magiasis B, Karachalios T, Yiatzides A, Tsekoura M. Analgesic effect of salmon calcitonin in osteoporotic vertebral fractures: a double-blind placebo-controlled clinical study. Calcif Tissue Int. 1991;49(6):369-372.

24. Nevitt MC, Chen P, Dore RK. Reduced risk of back pain following teriparatide treatment: a meta-analysis. Osteoporos Int. 2006;17(2):273-280.

25. Armingeat T, Brondino R, Pham T, Legré V, Lafforgue P. Intravenous pamidronate for pain relief in recent osteoporotic vertebral compression fracture: a randomized double-blind controlled study. Osteoporos Int. 2006;17:1659–1665.

26. Nevitt MC, Thompson DE, Black DM, et al for the Fracture Intervention Trial Research Group. Effect of alendronate on limited-activity days and bed-disability days caused by back pain in postmenopausal women with existing vertebral fractures. Arch Intern Med. 2000;160:77-85.

27. Peter CP, Cook WO, Nunamaker DM, Provost MT, Seedor JG, Rodan GA. Effect of alendronate on fracture healing and bone remodeling in dogs. J Orthop Res. 1996;14:74–79.

28. National Osteoporosis Foundation. Physician’s Guide To Prevention And Treatment Of Osteoporosis. Washington, DC;2003.

29. Black DM, Delmas PD, Eastell R, et al. Once-yearly zoledronic acid for treatment of postmenopausal osteoporosis. New Engl J Med. 2007;356:1809-1822.

30. Heaney R. Nutrion and osteopororis. In: Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, 6 th Ed. Favus M, ed. Durham, NC; American Society for Bone and Mineral Research; 2006.

31. Allain TJ. Vitamin D and fracture prevention—treatment still indicated but clarification needed. Age Ageing. 2005;34:542–544.

32. Cifu DX, Bhagia SM, Daitch JS, Frey ME, DePalma MJ. Efficacy and safety of percutaneous sacroplasty for painful osteoporotic sacral insufficiency fractures. Spine. 2007;32(15)1635-1640.

33. Melton LJ III, Thamer M, Ray NF, et al. Fractures attributable to osteoporosis: report for the National Osteoporosis Foundation. J Bone Miner Res.1997;12:16-23.

34. Elliot-Gibson V, Bogoch ER, Jamal SA, Beaton DE. Practice patterns in the diagnosis and treatment of osteoporosis after a fragility fracture: a systematic review. Osteoporos Int. 2004;15:767–778.

35. Van Helden S, Cals J, Kessels F, Brink P, Dinant GJ, Geusens P. Risk of new clinical fractures within 2 years following a fracture. Osteoporosis Int. 2006;17(3):348–354.

36. Haentjens P, Autier P, Collins J, Velkeniers B, Vanderschueren D, Boonen S. Colles fracture, spine fracture, and subsequent risk of hip fracture in men and women. A meta-analysis. J Bone Joint Surg (Am). 2003;85-A(10);1936–1943.

37. Hasserius R, Karlsson MK, Nilsson BE, Redlund-Johnell I, Johnell O. Prevalent vertebral deformities predict increased mortality and increased fracture rate in both men and women: a 10- year population-based study of 598 individuals from the Swedish cohort in the European Vertebral Osteoporosis Study. Osteoporos Int. 2003;14(1):61–68.

38. Kanis JA, Johnell O, De Laet C, et al. A meta-analysis of previous fracture and subsequent fracture risk. Bone. 2004;35(2):375–382.

39. Klotzbuecher CM, Ross PD, Landsman PB, Abbott TA 3rd, Berger, M. 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(4):721–739.

40. Cummings SR, Melton LJ III. Epidemiology and outcomes of osteoporotic fractures. Lancet. 2002;359:1761–1767.

41. Gardner MJ, Brophy RH, Demetrakopoulos D, et al. Interventions to improve osteoporosis treatment following hip fracture: a prospective, randomized trial. J Bone Joint Surg Am. 2005;87:3-7.

42. van Helden S, Cauberg E, Geusens P, et al. The fracture and osteoporosis outpatient clinic: an effective strategy for improving implementation of an osteoporosis guideline. J Eval Clin Pract. 2007;13:801–805.

43. Skedros JG. The orthopaedic surgeon’s role in diagnosing and treating patients with osteoporotic fractures: standing discharge orders may be the solution for timely medical care. Osteoporos Int. 2004;15:
405–410.

Michael E. Frey, MD, Responds
A patient who presents with minimal pain as a result of a sacral or vertebral fracture care should be offered conservative care as an initial appropriate treatment. If a patient fractures a hip or a wrist, stabilization of the fracture is performed for pain relief, preservation of function and to prevent further damage. If a patient is having severe pain with a vertebral or sacral fracture, conservative care is not the best option in improving patient outcome. In the “age of vertebral augmentation,” percutaneous sacroplasty is a more aggressive, but very applicable treatment option in this case presentation.

Osteoporosis, the most common metabolic bone disorder affecting 25 million people in the United States, is the leading cause of compression fractures. In this case report, we have a 76-year-old woman who has been taking Fosamax for 10 years and has not had a recent DXA scan. This patient by definition, even with a diagnosis of osteopenia, is considered osteoporotic regardless of her DXA score because she has fractured without
severe trauma.

A patient with a sacral insufficiency fracture (SIF) can present clinically as low back, buttock and/or lower extremity pain.¹ Although first described in 1982 by Lourie et a^l,2 SIFs may escape detection because of a low clinical suspicion and poor sensitivity of plain radiography.² Patients are often “bounced out” of emergency rooms,^3-6 sent to skilled nursing facilities because of their lack of mobility or sent to physical therapy for a “lumbar strain.”

Conservative treatments such as bed rest, partial weightbearing, early mobilization with a walker or a cane, analgesic medications and lumbosacral orthotics (LSOs) significantly increase the risks of deep venous thromboses, pulmonary emboli, decreased muscle strength, pneumonia, pressure ulcers and depression as a result of pain. All these factors contribute to what I formally call the four Ds in fracture prevention. We want to prevent Disability, Deconditioning, Debilitation and Death. Immobility causes depletion of calcium from bone in 4-5 days and loss of muscle mass in less than two weeks. Recovery from immobility takes an average of three days recovery for every day lost to immobility.

The overall one-year mortality rate associated with pelvic insufficiency fractures is 14.3%, and 50% of affected patients will not return to their prior level of function.⁶ Denying sacroplasty in this case may contribute to a prolonged recovery for the patient⁶ or extreme deconditioning leading to death.

The percutaneous injection of polymethylmethacrylate (PMMA) into fractured vertebral bodies (vertebroplasty/kyphoplasty) has been safely performed to treat painful osteoporotic vertebral compression fractures.^7-9 A logical extension of the vertebroplasty is the percutaneous injection of PMMA into the fractured sacrum (sacroplasty) to treat persistent pain and restore function. First reported in 2001 as treatment of symptomatic sacral metastatic lesions,^10,11 subsequent reports have documented its safe and effective performance.^12-15 However, these studies had several flaws including short follow-up intervals and small study cohorts. With this limited information, one could not conclude the true safety and efficacy of sacroplasty. It was not until 2007 that Frey, De Palma, et al¹⁶ reported the first prospective multicenter trial. This study evaluated the safety and efficacy, incidence of complications, and clinical utility of percutaneous sacroplasty in treating painful osteoporotic SIFs.

This prospective, multicenter, observational cohort study enrolled 37 patients with a mean age of 76.6 years and a failure of conservative care after a mean of 34.4 days (13-82 range). All patients were available at all follow-up intervals. The mean VAS score at baseline was 7.7, dropping to 3.2 within 30 minutes after the procedure. Weekly VAS scores were 2.1 at two weeks, 1.7 at four weeks, 1.3 at 12 weeks, 1.0 at 24 weeks, and 0.7 at 52 weeks.¹⁶ At 30 minutes after the procedure, five patients reported complete pain relief, increasing to 10 pain-free patients at two weeks and 25 pain-free patients at 52 weeks. At two weeks postprocedure, 20 patients reported a VAS score of 1-3, while 11 patients reported a VAS rating between 1 and 3 at the 52-week follow-up.¹⁶ Twenty patients were using narcotic analgesics at baseline and only six patients were using narcotics at 2-8 weeks postprocedure. No catastrophic complications were encountered immediately or during the follow-up intervals. One patient, however, did develop S1 radicular pain during the procedure necessitating termination of injection of the PMMA. Although the primary sacral pain was alleviated, the patient experienced persistent inferior buttock and posterior thigh pain that was completely relieved seven days later by perineural instillation of 2.0 mls of preservative free betamethasone (6mg/ml) and 1.0 ml of 1.0% lidocaine at the S1 nerve root. Potential risks for the procedure are cement leakage to the presacral space, sacral nerve roots, cement emboli, and into the sacroiliac joint. To help prevent cement leakage one must be extremely comfortable with the fluoroscopic anatomy of the sacrum. Betts recently published an article on fluoroscopic anatomy landmarks with open dissection of the sacrum.¹⁷

In February 2008, Frey, De Palma, et al¹⁸ published a subsequent study which included 52 patients. In this study more than 75% of the patients had more than 50% of their VAS score reduced 30 minutes postprocedure. More than 80% of the patients had dramatic pain reduction which was maintained throughout the two-year follow-up period. This study corroborates both the safety and efficacy of sacroplasty.

In the case report of this 76-year-old female patient with a positive bone scan, additional studies are necessary before performing sacroplasty. The most important study is an MRI of the pelvis with fat suppression or short tau inversion recovery (STIR) images (Figure 1, page 12). When performing sacroplasty, especially when using fluoroscopy, an anatomical view of the pelvis is important. This will determine exactly where to place the trochars and subsequent instillation of PMMA. The majority of sacral insufficiency fractures occur at the S1 and S2 segments but can occur only at S3, S4 or isolated to one particular segment. Important MRI findings that may cause concern are (a) the fracture line penetrating the sacral foramen, or (b) a metastatic lesion—which are not picked up by conventional bone scan. If the patient has a pacemaker, then a CT scan and a bone scan are necessary. I traditionally order an MRI of the pelvis and do not order bone scans anymore. Bone scans can be hot for up to two years postinjury.

Another important study in the continued evaluation of this osteoporotic patient is a bone density test. Traditionally, I discuss osteoporotic management on the initial visit as well as the follow-up visit to assist the patient’s risk factures for spine fractures and potential osteoporotic pharmacological treatment options. This patient needs further evaluation of her bone health and may be a candidate for other medications.

Sacroplasty can be performed using CT, CT fluoroscopy, or fluoroscopy guidance alone. The majority of physicians performing this procedure are interventional radiologists and interventional pain physicians who are either anesthesiology– or physiatry–trained. Radiologists have the tendency to perform this procedure under CT guidance whereas the latter perform this procedure under fluoroscopic guidance. The primary reason for this difference is that interventional radiologists have easy access to CT technology while interventional anesthesiologists and physiatrists are accustomed to performing all their pain treatment procedures using fluoroscopy.

At my facility, all sacroplasty procedures are performed under fluoroscopic guidance with light sedation. Every patient receives antibiotics preoperatively and minimal (conscious sedation) sedation using midazolam and fentanyl. The procedure, from initial set up to the patient walking out of the room, takes about an hour. The patient is placed in a prone position and after an aligning the entire sacroiliac joint in an oblique view, two 13-gauge bone trochars are placed between the sacral foramen and sacroiliac joint on the side of the fractured ala at a 45° angle toward the sacroiliac joint. The needles are then inserted approximately to mid point of the sacrum, under lateral fluoroscopic  view, maintaining the 45° angle.¹⁶ After mixing the cement (SpineplexTM) using the precision cement mixing system(Stryker, Kalamazoo, MI) 2-5 cc of PMMA is injected through each trochar under AP fluoroscopy, monitoring the spread of the bone cement to avoid medial extension toward the sacral nerve roots (Figure 2, page 12).¹⁶ This technique is similar to the one described by Betts.¹⁷ Each patient is maintained in the prone position for 30 minutes after the procedure before ambulation. The patient is then asked to stand on the affected leg only to assess their pain improvement. If they have bilateral pain, they stand on each leg individually to assess their pain improvement.

This particular patient has already exhausted conservative care and has been suffering for six weeks. She has decreased ambulation and is currently using a cane. She has three of the four Ds we are trying to prevent: deconditioning, disability and debilitation. The patient’s and her physician’s goals are simple: reduce her pain, remove the need for a cane and improve her walking. In this case, conservative care has failed and the appropriate next step is percutaneous sacroplasty.

References
1.  Lin JT, Lane JM. Sacral stress fractures. J Wom Hlth. 2003;12(9):879-888.

2. Lourie H. Spontaneous osteoporotic fracture of the sacrum. An unrecognized syndrome of the elderly. JAMA. 1982;248:715.

3. Weber M, Hasler P, Gerber H. Insufficiency fractures of the sacrum. Twenty cases and review of the literature. Spine. 1993;16:2507.

4. Gotis-Graham I, McGuiganL, Diamond T, et al. Sacral insufficiency fractures in the elderly. J Bone Joint Surg (Br). 1994;76-B:882.

5. Grasland A, Pouchot J, Mathieu A, et al. Sacral insufficiency fractures, an easily overlooked cause of back pain in elderly women. Arch Intern Med. 1996;156:668.

6. Taillandier J, Langue F, Alemanni M, et al. Mortality and functional outcomes of pelvic insufficiency fractures in older patients. Joint Bone Spine. 2003;70:287.

7. Jensen ME, Evans AJ, Mathis JM, et al. Percutaneous polymethylmethacrylate vertebroplasty in the treatment of osteoporotic vertebral compression fractures: technical aspects. AJNR. 1997;18:1897-1904.

8. Evans AJ, Jensen ME, Kip KE, et al. Vertebral compression fractures: pain reduction and improvement in functional mobility after percutaneous polymethylmethacrylate vertebroplasty. A retrospective report of 245 cases. Radiology. 2003;226(2):366-372.

9. Grados F, Depriester C, Cayrolle G, et al. Long-term observations of vertebral osteoporotic fractures treated by percutaneous vertebroplasty. Rheumatology. 2000;39(12):1410-1414.

10. Dehdashti AR, Martin JB, Jean B, et al. PMMA cementoplasty in symptomatic metastatic lesions of the S1 vertebral body. Cardiovasc Intervent Radiol. 2000;23:235.

11. Marcy PY, Palussiere J, Descamps B, et al. Percutaneous cementoplasty for pelvic bone metastasis. Support Care Cancer. 2000;8:500.

12. Grant M. Sacroplasty: a new treatment for sacral insufficiency fracture. J Vasc Interv Radiol. 2002;13:1265.

13. Pommersheim W, Huang-Hellinger F, Baker M, et al. Sacroplasty: a treatment for sacral insufficiency fractures. Case report. AJNR. 2003;24:1003.

14. Butler CL, Given CA, Michel SJ, et al. Percutaneous sacroplasty for the treatment of sacral insufficiency fractures. AJR. 2005;184:1956.

15. Zaman FM, Frey ME, Slipman CW. Sacral stress fractures. Cur Sports Med Rep. 2006;5:37-43.

16. Frey ME, DePalma MJ, Cifu DX, et al. Efficacy and safety of percutaneous sacroplasty for painful osteoporotic sacral insufficiency fractures: a prospective, mulitcenter trial. Spine. 2007;32:1635- 1640.

17. Betts A. Sacral vertebral augmentation: confirmation of fluoroscopic landmarks by open dissection. Pain Physician. 2008;11:57-65.

18. Frey ME, DePalma MJ, Cifu DX, et al. Percutaneous sacroplasty for painful osteoporotic sacral insufficiency fractures: a prospective, mulitcenter observational pilot study. Spine J. 2008 (in press).

Disclosures

• Frey: c-3, Stryker, Covidien; e-2, Pfizer.
• G Kosturi: nothing to disclose.
• R Adler: c-2, Novaritis, Eli Lilly, Merck; e-2, Novaritis, Proctor & Gamble; k-3, Novaritis, Proctor & Gamble, Eli Lilly, Glaxo Smith Kline.
• D Cifu: nothing to disclose.
• A Qutubuddin: nothing to disclose.