- Email: [email protected]
Post-traumatic compression fracture
Clinical Chiropractic (2003) 6, 67—72
CASE REPORT
Post-traumatic compression fracture D. Woodhouse* 6 Drayton Green Road, West Ealing, London W13 8RY, UK Received 28 June 2002; accepted 27 February 2003
KEYWORDS Chiropractic manipulation; Human, male, adult; Spinal fractures; Spontaneous fractures; Manipulation/ complications; Manipulation/
Abstract This case report details the case of a 56-year-old builder experiencing low back pain following a fall of three-and-a-half metres, resulting in a compression fracture of the L2 vertebra. The radiological findings of compression fractures are listed and explained; as are the clinical implications to the chiropractor in regards to the differentiation and management of stable and unstable fractures; the risk of further fracture in osteoporotic compression fractures and the possible causative link between spinal manipulation and compression fractures. ß 2003 the College of Chiropractors. Published by Elsevier Science Ltd. All rights reserved.
orthopedic; Manipulation/spinal; Osteoporosis; Radiography; Radiology
Introduction Compression fractures (one of the more innocuous fractures) are a relatively common problem. They are also one of the few categories of fracture for which there exist potential chiropractic treatment protocols. Normally a fracture in the elderly, compression fractures can also be seen in the young after traumatic incidents. This paper will attempt to explain and clarify the current understanding of compression fractures, presenting the possible causes; common diagnostic and radiological findings; chiropractic approach and treatment for people with these fractures, as well as shedding light on the reported cases of manipulation causing vertebral compression fractures.
Case report Mr. S., a 56-year-old builder, first presented to a chiropractic clinic in 1992, complaining of low
Tel.: þ44-208-5663757; fax: þ44-208-5663757. E-mail address: [email protected] (D. Woodhouse).
back pain and a marked decrease in lumbar range of motion. After a full case history and physical examination, lumbopelvic radiological examination (lateral, posterior—anterior (PA) and a lumbosacral spot view) was performed. These revealed degenerative joint disease throughout the lumbar spine and lumbosacral junction, but were otherwise unremarkable. A diagnosis of acute post-traumatic lumbosacral sprain/ strain with facet arthralgia, associated right sacroiliac hypomobility and concomitant muscle hypertonicity was made. Treatment (consisting of sacroiliac and lumbar spinal manipulative therapy, soft-tissue work, cryotherapy and home exercises) was commenced. After a total of eight treatments, Mr. S. was reportedly feeling much better and was seen on a maintenance care basis (once every 3 months) during which he experienced only occasional recurrence of the joint pain. In August 2000, Mr. S. re-presented to the clinic with an acute exacerbation of his low back pain. The pain was located, as previously, bilaterally around the sacroiliac joints and lumbosacral area and was described as a sharp localised pain aggravated by movement. Mr. S. was convinced this episode was
1479-2354/03/$30.00 ß 2003 the College of Chiropractors. Published by Elsevier Science Ltd. All rights reserved. doi:10.1016/S1479-2354(03)00020-8
68
D. Woodhouse
exactly the same as the previous episode experienced in 1992. However, upon further questioning, it was discovered that this episode of pain started within hours of a fall of 12 ft (or 3.6 m) from a rooftop onto cement. The patient landed directly on his buttocks and there was nothing below him to break his fall. A full examination was performed. General observation was unremarkable, but range of motion was painful and restricted especially in flexion and extension. Supported Adams’ test increased lumbar flexion whilst decreasing pain intensity. Kemp’s, Yeoman’s and Gaenslen’s tests also reproduced right sacroiliac joint pain, but other orthopaedic testing (including Valsava’s, Bragaard’s, Sicard’s, Bonnet’s, Bowstring’s, Faber’s and Laguerre’s) were negative. Gillet testing and prone sacroiliac springing revealed a tender fixation of the right upper sacroiliac joint into flexion. Despite the examination findings strongly suggesting biomechanical low back pain of sacroiliac origin, it was decided that radiographic examination of the lumbopelvic region (lateral and PA views) were required to rule out fractures resulting from the fall.
Fig. 2
Radiological findings Alignment is normal throughout the lumbar spine. Bone quality reveals coarsened trabeculae and generalised osteopenia. All cortices are intact except for the superior endplate of the second lumbar vertebra, which is indented irregularly inferiorly and a band of sclerosis is noted adjacent to this. Osteophytes are noted anteriorly to the L5/S1 disc space. Zygoapophyseal joint spaces appear good except for narrowing in the lower lumbar spine. Soft tissues indicate calcification of the aorta anteriorly to the L2/3 intervertebral disc (Figs. 1 and 2). From the findings in the history, examination and radiology, diagnoses were made. These included: a recent infraction of the superior endplate of L2 (small recent compression fracture); with senile osteoporosis; marked degenerative joint disease at the lumbosacral junction and aortic arteriosclerosis.
Discussion Fig. 1
Compression fractures are the most common fractures of the lumbar spine, with a fourfold increase in
Post-traumatic compression fracture incidence during the past 30 years.1 A subtype of impaction fractures, compression fractures occur when a portion of bone is forced into its opposing segments, driving the endplates toward each other.2 These fractures occur especially at the thoracolumbar junction2 as a result of compression and flexion forces, although a rotational element may also be present.3 A wide variety of traumatic causes have been listed, including falls (causing compression and, in a spine with normal curvature, flexion); blows across the shoulders (jack-knifing the thoracolumbar junction) and road-traffic accidents.2,3 In the middle aged and elderly, compression fractures may arise from relatively banal actions, such as lifting. The spinal column is a common site for pathological fracture and, in such circumstances, it is important to investigate the presence of osteoporosis, osteomalacia and, more importantly, malignancy.3 As many as 35% of all compression fractures occur in females over 45 years of age. Although this is mostly due to early menopause, some 30% of cases are secondary most commonly through osteopenia following corticosteroid use (15%); hyperthyroidism (8%) and malignancy (2%).2 Low bone mineral density (BMD) and micro-structural deterioration of bone tissue (such as cortical thinning and destruction of the trabecular lattice) result in weakened bone and an increased fracture risk.4 Age is the major determinant of vertebral bone strength, mass and architecture1 to the extent that, along with femoral and spine BMD, age can be used to predict the risk of future vertebral fractures.5 Despite the obvious importance of an early identification of osteoporosis, radiological determination is not the diagnostic method of choice. Approximately 35—40% of the bone salts must be lost before osteopenia can be identified on plain film radiographs.6 Recent developments in bone densitometry, which is now becoming increasingly used, allows for early detection of bone loss and provides good results.7 The principal difficulty with clinical diagnosis of vertebral compression fractures is that half of all cases are asymptomatic8 or the signs and symptoms are so mild that they are overlooked by the patient, as in the case of Mr. S. who thought he was suffering recurrence of his previous problem. The patient will often reveal a history of low back pain following trauma (that may be only slight in the elderly) and may experience local tenderness or radiation of pain into the abdomen or chest.9 Upon examination, a local angular kyphosis or a prominent spinous process maybe seen and palpation may reveal spinal tenderness or pain on percussion. Often, spinal movement will be restricted and, as was the case
69 for Mr. S., painful in flexion or extension.3,9 In cases where there is a suspicion of spinal fracture, radiographs should be taken.
Radiographic signs of vertebral compression fractures Common findings associated with lumbar vertebral compression fractures include a step defect, wedge deformity, disrupted endplate, linear zone of condensation, paraspinal swelling and abdominal ileus,2 all of which are best visualised on lateral radiographs of the lumbar spine. Step defect This is a sharp marginal shearing fracture of the anterior superior body margin as a result of buckling of the anterior cortex. It is commonly the only radiographic finding in recent compression fractures and results from compression into flexion of the superior endplate, causing great stress of the anterior aspect of the vertebra.2,9 This finding is not apparent in the case of Mr. S. This may be due to the fact that Mr. S. fell straight onto his buttocks, and the lack of spinal flexion meant that the forces were centralised. Wedge deformity This is the triangular wedge shape of the affected vertebral body with regular or irregular crushing of the anterior portion and unchanged posterior height.9 Although this is not seen in the case of Mr. S., it is reported that the anterior wedging must be over 30% before it becomes readily apparent.2 This is made even more difficult by the fact that a normal 10—15% anterior wedging occurs at the levels of T11-L2. Wedging of a single vertebra in the thoracic spine will lead to a localised kinking (possibly visible on physical examination). A smoother kyphosis will be formed if multiple contiguous fractures occur, however, flattening of the normal lordosis can be expected when this occurs in the lumbar spine.9 The importance of describing this wedge deformity is to determine stability of the fracture and to differentiate from pathological compression fractures. A loss of posterior body height would show evidence of greater force (raising the likelihood of the presence of a burst fracture and neurological instability) or can indicate the presence of pathology. Disruption in the vertebral endplate This is seen as an sharp, obvious, jagged and irregular inferior displacement of the superior endplate2 and is the most obvious sign seen in the case of Mr. S., occurring centrally at the superior
70
endplate of L2. In this case, however, the term infraction (used to describe a moderately severe impaction fracture causing a minor localised break in the endplate2) may be more appropriate. Linear band of condensation (zone of impaction) Occasionally present, a radiopaque line can be seen adjacent to the site of the disrupted endplate.2 This represents the site of impaction where the bones are driven together and is well visualised in the case of Mr. S. Paraspinal edema and abdominal ileus These are only seen immediately after extensive trauma and provide a warning that spinal fracture is likely. They are most commonly seen on the PA view of the thoracic spine as asymmetrical bulges lateral to the spine accompanied by excess bowel gas in the small or large intestine.2
Clinical importance of vertebral compression fractures The clinical importance of compression fractures is their association with increased morbidity and mortality but also the increased risk they present in the occurence of further fractures.8 Recent evidence has not only suggested that there is an increased risk of developing subsequent fractures in compression fracture patients, but it is now used as a method to predict the probability of future fractures. Ten years after an initial moderate to severe traumatic compression fracture, the incidence of a further fracture is in the order of 70% (especially in the axial skeleton where there is a 12.6-fold increase).10 Within the year following fracture, there is an increased risk of further fracture by factor of 2.810 and a five-fold increase risk for additional vertebral11 or hip fractures.12 In the management of spinal injuries, although it is important to determine which spinal structures are involved and the extent of damage they have suffered, the main concern is damage to the closely related neurological elements. In the cases where neurological elements are unaffected, it is vital to determine the risks of a later involvement and, therefore, the general stability of the area of trauma.9 Post-fracture stability is based on the classification of Denis,13 who divides the spine into three columns. The anterior column (from the anterior longitudinal ligament (ALL) to the middle of the vertebral body) is comprised of the ALL and the anterior parts of the annular ligament and vertebral body. The middle column (from the mid-vertebral body to the posterior longitudinal ligament (PLL)) is
D. Woodhouse
formed by the PLL and posterior parts of annular ligament and vertebral body. Finally, the posterior column (from PLL to supraspinous ligament), which also includes the neural arch, pedicles, spinous process and posterior ligamentous complex. Instability is said to arise when damage occurs to more than one of these columns and, in such cases, the likeliness of neurological injury is high.2,9 Stability can be confirmed on radiographs if anterior wedging is of less than 158 or under 33% of the posterior body height.9 However, it has also been reported that determination of wedging below 30% is difficult on plain film radiographs.2 Therefore, it is important to note any additional radiological signs of instability, including a reduced posterior vertebral body height; vertebral body displacement; wide separation or avulsion of the tip of the spinous processes and facet or pedicle fractures. In cases where instability is considered, a ‘boggy’ softness upon pressure between the spinous processes over the site of injury will indicate posterior ligamentous injury and rapid medical attention is paramount.9 Based on the instability classification, Denis classifies four categories of compression injury:13 1. Simple compression fractures, stable injuries involving the anterior column only. 2. Burst fractures, failure of the anterior and middle columns due to axial loading, may cause neurological instability. 3. Seatbelt-type injuries, posterior and middle column failure often as a result of laptype seatbelts being worn in road-traffic accidents. Rapid deceleration causes the spine to jack-knife around the seatbelt, and the resultant tension causes this unstable fracture. 4. Fracture dislocation, failure of all three columns so that dislocation ensues.9
Treatment for vertebral compression fractures Treatment for compression fractures is controversial. However, it is generally agreed that for non-malignant, stable fractures the conservative approach, including passive therapy and exercise, is the most apt.14 Loading of bone affects mass, micro-architecture and size, thereby maintaining the trabecular lattice. Exercise throughout life can play an important role in the prevention of osteoporotic fractures.1 The wedging that is associated with stable compression fractures allows for virtually normal func-
Post-traumatic compression fracture
tion and, therefore, surgical correction is not essential.3 For unstable fractures or in the presence of malignancy, the consequences of further deterioration must be taken into consideration and these, therefore, should be managed by a medical specialist.3 Management of stable fractures is generally divided into three stages. During the acute phase (the first week after trauma), analgesic modalities or medication along with bed rest in the recumbent position are beneficial.3,9,15 This should be continued until the pain subsides,3 or until the patient is able to turn easily from side to side,15 but should continue no longer than one week.9 At this point, active extension exercises (for the erector spinae muscles) can be commenced and the intensity gradually increased.3,9 During this time, a back support, worn for brief intervals, may provide some stability and help maintain posture.15 Thereafter, rehabilitation is continued both to strengthen spinal musculature and restore mobility.3 Along with the rehabilitation programme, the patient should follow the Intermittent Horizontal Rest Regimen (IHRR) with the patient lying for 20 min every 2 h.15 From a chiropractic perspective, although the treatment protocols are well within the scope of practitioners, the importance lies in the diagnosis and determination of potential pathological causes of the fracture. As patients’ ages increase, the associated risks of pathology must be taken into consideration and managed accordingly. Osteoporosis and metastases are the most important diagnostic considerations, not only so that correct treatment can be commenced immediately, but also so that the possibility of adverse side effects associated with inappropriate manipulation can be avoided. Chiropractic adjustments apply external forces to the spine that, in the presence of bone weakening disease, is quite susceptible to damage from these forces.16 Osteoporosis is commonly regarded as a relative or absolute contraindication to adjustment,17 the application of the external force believed to be potentially responsible for vertebral collapse. A number of such cases have been reported in the literature. In one case, an insurance company claimed spinal manipulation to be the cause of a compression fracture in an osteoporotic L3 vertebra, resulting in parapesis. However, the outcome of the case was not discussed.18 Another report stated that, in two cases, manipulation caused compression fractures. In both cases, spinal malignancies were found to be the cause and a physiotherapist and a lay person were responsible for the manipulations.19 Four further cases stated that ‘‘since no conclusive evidence could be found,
71
care must be taken in drawing conclusions of causal relationships between chiropractic adjustment and compression fractures’’. However, it was stated that manipulation in areas of compression fractures might cause increased symptomatology.6
Conclusion Compression fractures are common fractures affecting the young after considerable trauma but mainly the elderly, especially in the presence of osteoporosis but also secondarily to malignancy and secondary osteopenia. Although clinical diagnosis is difficult due to the relatively mild nature of signs and symptoms, radiological diagnosis is clear and well documented. Signs to look for include step defect, wedge deformities, endplate disruption, band of impaction and abdominal ileus or paraspinal swelling. Whilst looking at the radiographs, it is important to note signs of instability, including loss of posterior vertebral height, disruption of the middle or posterior columns and vertebral body displacement. Clinical priority from a chiropractic standpoint is diagnosing the cause of fracture and verifying that it is of a stable nature before setting up a treatment protocol. It is also important that chiropractors are aware of the increased risk of further fractures in these patients and the potential link between spinal manipulation and compression fractures so that care can be taken in order to prevent iatrogenic complications.
References 1. Mosekilde L. Age-related changes in bone mass, structure, and strength-effects of loading. Z Rheumatol 2000; 59(Suppl 1):1—9. 2. Yochum TR, Rowe LJ. Trauma, fractures and dislocations of the lumbar spine. In: Essentials of skeletal radiology, 2nd ed. Maryland, USA: Williams and Wilkins; 1996. p. 695—9 [chapter 9]. 3. Adams JC, Hamblen DL. Spine and thorax. In: Outline of fractures, 10th ed. New York, USA: Churchill Livingstone; 1992. p. 90—101 [chapter 8]. 4. Oleksik A, Ott SM, Vedi S, Bravenboer N, Comptson J, Lips P. Bone structure in patients with low bone mineral density with or without vertebral fractures. J Bone Miner Res 2000;15(7):1368—75. 5. Legrand E, Chappard D, Pascaretti C, Duquenne M, Rondeau C, Simon Y, et al. Bone mineral density and vertebral fractures in men. Osteoporos Int 1999;10(4):265—70. 6. Michel BA, Lane NE, Jones HH, Fries JF, Bloch DA. Plain radiographs can be useful in estimating lumbar bone density. J Rheumatol 1990;17:528—31. 7. Hope RA, Longmore JM, Hodgetts TJ, Ramrakha PS. Biochemistry. In: Oxford handbook of clinical medicine, 3rd ed. Oxford, UK: Oxford University Press; 1994. p. 622—56 [chapter 14].
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8. Orstavik R, Haugeberg G, Kvien TK, Lilleas F. Vertebral fractures in osteoporosis-silent fractures of clinical importance. Tidsskr Nor Laegeforen 2000;120(24):2891—4. 9. McRae R. The spine. In: Practical fracture management, 3rd ed. London: Churchill Livingstone; 1999. p. 209—38 [chapter 10]. 10. Melton III LJ, Atkinson EJ, Cooper C, O’Fallon WM, Riggs BL. Vertebral fractures predict subsequent fractures. Osteoporos Int 1999;10(3):214—21. 11. Lindsay R, Silverman SL, Cooper C, Hanley DA, Barton I, Broy SB, et al. Risk of new vertebral fracture in the year following a fracture. JAMA 2001;285(3):320—3. 12. Naves DM, Diaz LJB, Gomez AC, Altadill AA, Rodriguez RA, Cannata AJB. Study of incidence of osteoporotic fractures in a cohort of individuals older than 50 years from Asturias, Spain, after a 6 year follow-up period. Med Clin (Barc) 2000; 115(17):650—3. 13. Denis F. Spinal stability as defined by the three column concept in acute spinal trauma. Clin Orthop 1984;189:65.
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14. Kreitz BG, Cote P, Cassidy JD. L5 vertebral compression fracture: a series of five cases. J Manipulative Physiol Ther 1995;18(2):91—7. 15. Frost HM. Personal experience in managing acute compression fractures, their aftermath, and the bone pain syndrome, in osteoporosis. Osteoporos Int 1998;8(1):13— 5. 16. Haldeman S, Rubinstein SM. Compression fractures in patients undergoing spinal manipulative therapy. J Manipulative Physiol Ther 1992;15(7):450—4. 17. Gatterman MI. Complications of and contraindications to spinal manipulative therapy. In: Chiropractic management of spine related disorders. Baltimore, USA: Williams and Wilkins; 1990. p. 55—69 [chapter 4]. 18. Rydell N, Raf L. Spinal manipulation–—treatment associated with a high risk of complications. Lakartidningen 1999; 96(34):3536—40. 19. Austin RT. Pathological vertebral fractures after spinal manipulation. BMJ 1985;291:1114—5.
CASE REPORT
Post-traumatic compression fracture D. Woodhouse* 6 Drayton Green Road, West Ealing, London W13 8RY, UK Received 28 June 2002; accepted 27 February 2003
KEYWORDS Chiropractic manipulation; Human, male, adult; Spinal fractures; Spontaneous fractures; Manipulation/ complications; Manipulation/
Abstract This case report details the case of a 56-year-old builder experiencing low back pain following a fall of three-and-a-half metres, resulting in a compression fracture of the L2 vertebra. The radiological findings of compression fractures are listed and explained; as are the clinical implications to the chiropractor in regards to the differentiation and management of stable and unstable fractures; the risk of further fracture in osteoporotic compression fractures and the possible causative link between spinal manipulation and compression fractures. ß 2003 the College of Chiropractors. Published by Elsevier Science Ltd. All rights reserved.
orthopedic; Manipulation/spinal; Osteoporosis; Radiography; Radiology
Introduction Compression fractures (one of the more innocuous fractures) are a relatively common problem. They are also one of the few categories of fracture for which there exist potential chiropractic treatment protocols. Normally a fracture in the elderly, compression fractures can also be seen in the young after traumatic incidents. This paper will attempt to explain and clarify the current understanding of compression fractures, presenting the possible causes; common diagnostic and radiological findings; chiropractic approach and treatment for people with these fractures, as well as shedding light on the reported cases of manipulation causing vertebral compression fractures.
Case report Mr. S., a 56-year-old builder, first presented to a chiropractic clinic in 1992, complaining of low
Tel.: þ44-208-5663757; fax: þ44-208-5663757. E-mail address: [email protected] (D. Woodhouse).
back pain and a marked decrease in lumbar range of motion. After a full case history and physical examination, lumbopelvic radiological examination (lateral, posterior—anterior (PA) and a lumbosacral spot view) was performed. These revealed degenerative joint disease throughout the lumbar spine and lumbosacral junction, but were otherwise unremarkable. A diagnosis of acute post-traumatic lumbosacral sprain/ strain with facet arthralgia, associated right sacroiliac hypomobility and concomitant muscle hypertonicity was made. Treatment (consisting of sacroiliac and lumbar spinal manipulative therapy, soft-tissue work, cryotherapy and home exercises) was commenced. After a total of eight treatments, Mr. S. was reportedly feeling much better and was seen on a maintenance care basis (once every 3 months) during which he experienced only occasional recurrence of the joint pain. In August 2000, Mr. S. re-presented to the clinic with an acute exacerbation of his low back pain. The pain was located, as previously, bilaterally around the sacroiliac joints and lumbosacral area and was described as a sharp localised pain aggravated by movement. Mr. S. was convinced this episode was
1479-2354/03/$30.00 ß 2003 the College of Chiropractors. Published by Elsevier Science Ltd. All rights reserved. doi:10.1016/S1479-2354(03)00020-8
68
D. Woodhouse
exactly the same as the previous episode experienced in 1992. However, upon further questioning, it was discovered that this episode of pain started within hours of a fall of 12 ft (or 3.6 m) from a rooftop onto cement. The patient landed directly on his buttocks and there was nothing below him to break his fall. A full examination was performed. General observation was unremarkable, but range of motion was painful and restricted especially in flexion and extension. Supported Adams’ test increased lumbar flexion whilst decreasing pain intensity. Kemp’s, Yeoman’s and Gaenslen’s tests also reproduced right sacroiliac joint pain, but other orthopaedic testing (including Valsava’s, Bragaard’s, Sicard’s, Bonnet’s, Bowstring’s, Faber’s and Laguerre’s) were negative. Gillet testing and prone sacroiliac springing revealed a tender fixation of the right upper sacroiliac joint into flexion. Despite the examination findings strongly suggesting biomechanical low back pain of sacroiliac origin, it was decided that radiographic examination of the lumbopelvic region (lateral and PA views) were required to rule out fractures resulting from the fall.
Fig. 2
Radiological findings Alignment is normal throughout the lumbar spine. Bone quality reveals coarsened trabeculae and generalised osteopenia. All cortices are intact except for the superior endplate of the second lumbar vertebra, which is indented irregularly inferiorly and a band of sclerosis is noted adjacent to this. Osteophytes are noted anteriorly to the L5/S1 disc space. Zygoapophyseal joint spaces appear good except for narrowing in the lower lumbar spine. Soft tissues indicate calcification of the aorta anteriorly to the L2/3 intervertebral disc (Figs. 1 and 2). From the findings in the history, examination and radiology, diagnoses were made. These included: a recent infraction of the superior endplate of L2 (small recent compression fracture); with senile osteoporosis; marked degenerative joint disease at the lumbosacral junction and aortic arteriosclerosis.
Discussion Fig. 1
Compression fractures are the most common fractures of the lumbar spine, with a fourfold increase in
Post-traumatic compression fracture incidence during the past 30 years.1 A subtype of impaction fractures, compression fractures occur when a portion of bone is forced into its opposing segments, driving the endplates toward each other.2 These fractures occur especially at the thoracolumbar junction2 as a result of compression and flexion forces, although a rotational element may also be present.3 A wide variety of traumatic causes have been listed, including falls (causing compression and, in a spine with normal curvature, flexion); blows across the shoulders (jack-knifing the thoracolumbar junction) and road-traffic accidents.2,3 In the middle aged and elderly, compression fractures may arise from relatively banal actions, such as lifting. The spinal column is a common site for pathological fracture and, in such circumstances, it is important to investigate the presence of osteoporosis, osteomalacia and, more importantly, malignancy.3 As many as 35% of all compression fractures occur in females over 45 years of age. Although this is mostly due to early menopause, some 30% of cases are secondary most commonly through osteopenia following corticosteroid use (15%); hyperthyroidism (8%) and malignancy (2%).2 Low bone mineral density (BMD) and micro-structural deterioration of bone tissue (such as cortical thinning and destruction of the trabecular lattice) result in weakened bone and an increased fracture risk.4 Age is the major determinant of vertebral bone strength, mass and architecture1 to the extent that, along with femoral and spine BMD, age can be used to predict the risk of future vertebral fractures.5 Despite the obvious importance of an early identification of osteoporosis, radiological determination is not the diagnostic method of choice. Approximately 35—40% of the bone salts must be lost before osteopenia can be identified on plain film radiographs.6 Recent developments in bone densitometry, which is now becoming increasingly used, allows for early detection of bone loss and provides good results.7 The principal difficulty with clinical diagnosis of vertebral compression fractures is that half of all cases are asymptomatic8 or the signs and symptoms are so mild that they are overlooked by the patient, as in the case of Mr. S. who thought he was suffering recurrence of his previous problem. The patient will often reveal a history of low back pain following trauma (that may be only slight in the elderly) and may experience local tenderness or radiation of pain into the abdomen or chest.9 Upon examination, a local angular kyphosis or a prominent spinous process maybe seen and palpation may reveal spinal tenderness or pain on percussion. Often, spinal movement will be restricted and, as was the case
69 for Mr. S., painful in flexion or extension.3,9 In cases where there is a suspicion of spinal fracture, radiographs should be taken.
Radiographic signs of vertebral compression fractures Common findings associated with lumbar vertebral compression fractures include a step defect, wedge deformity, disrupted endplate, linear zone of condensation, paraspinal swelling and abdominal ileus,2 all of which are best visualised on lateral radiographs of the lumbar spine. Step defect This is a sharp marginal shearing fracture of the anterior superior body margin as a result of buckling of the anterior cortex. It is commonly the only radiographic finding in recent compression fractures and results from compression into flexion of the superior endplate, causing great stress of the anterior aspect of the vertebra.2,9 This finding is not apparent in the case of Mr. S. This may be due to the fact that Mr. S. fell straight onto his buttocks, and the lack of spinal flexion meant that the forces were centralised. Wedge deformity This is the triangular wedge shape of the affected vertebral body with regular or irregular crushing of the anterior portion and unchanged posterior height.9 Although this is not seen in the case of Mr. S., it is reported that the anterior wedging must be over 30% before it becomes readily apparent.2 This is made even more difficult by the fact that a normal 10—15% anterior wedging occurs at the levels of T11-L2. Wedging of a single vertebra in the thoracic spine will lead to a localised kinking (possibly visible on physical examination). A smoother kyphosis will be formed if multiple contiguous fractures occur, however, flattening of the normal lordosis can be expected when this occurs in the lumbar spine.9 The importance of describing this wedge deformity is to determine stability of the fracture and to differentiate from pathological compression fractures. A loss of posterior body height would show evidence of greater force (raising the likelihood of the presence of a burst fracture and neurological instability) or can indicate the presence of pathology. Disruption in the vertebral endplate This is seen as an sharp, obvious, jagged and irregular inferior displacement of the superior endplate2 and is the most obvious sign seen in the case of Mr. S., occurring centrally at the superior
70
endplate of L2. In this case, however, the term infraction (used to describe a moderately severe impaction fracture causing a minor localised break in the endplate2) may be more appropriate. Linear band of condensation (zone of impaction) Occasionally present, a radiopaque line can be seen adjacent to the site of the disrupted endplate.2 This represents the site of impaction where the bones are driven together and is well visualised in the case of Mr. S. Paraspinal edema and abdominal ileus These are only seen immediately after extensive trauma and provide a warning that spinal fracture is likely. They are most commonly seen on the PA view of the thoracic spine as asymmetrical bulges lateral to the spine accompanied by excess bowel gas in the small or large intestine.2
Clinical importance of vertebral compression fractures The clinical importance of compression fractures is their association with increased morbidity and mortality but also the increased risk they present in the occurence of further fractures.8 Recent evidence has not only suggested that there is an increased risk of developing subsequent fractures in compression fracture patients, but it is now used as a method to predict the probability of future fractures. Ten years after an initial moderate to severe traumatic compression fracture, the incidence of a further fracture is in the order of 70% (especially in the axial skeleton where there is a 12.6-fold increase).10 Within the year following fracture, there is an increased risk of further fracture by factor of 2.810 and a five-fold increase risk for additional vertebral11 or hip fractures.12 In the management of spinal injuries, although it is important to determine which spinal structures are involved and the extent of damage they have suffered, the main concern is damage to the closely related neurological elements. In the cases where neurological elements are unaffected, it is vital to determine the risks of a later involvement and, therefore, the general stability of the area of trauma.9 Post-fracture stability is based on the classification of Denis,13 who divides the spine into three columns. The anterior column (from the anterior longitudinal ligament (ALL) to the middle of the vertebral body) is comprised of the ALL and the anterior parts of the annular ligament and vertebral body. The middle column (from the mid-vertebral body to the posterior longitudinal ligament (PLL)) is
D. Woodhouse
formed by the PLL and posterior parts of annular ligament and vertebral body. Finally, the posterior column (from PLL to supraspinous ligament), which also includes the neural arch, pedicles, spinous process and posterior ligamentous complex. Instability is said to arise when damage occurs to more than one of these columns and, in such cases, the likeliness of neurological injury is high.2,9 Stability can be confirmed on radiographs if anterior wedging is of less than 158 or under 33% of the posterior body height.9 However, it has also been reported that determination of wedging below 30% is difficult on plain film radiographs.2 Therefore, it is important to note any additional radiological signs of instability, including a reduced posterior vertebral body height; vertebral body displacement; wide separation or avulsion of the tip of the spinous processes and facet or pedicle fractures. In cases where instability is considered, a ‘boggy’ softness upon pressure between the spinous processes over the site of injury will indicate posterior ligamentous injury and rapid medical attention is paramount.9 Based on the instability classification, Denis classifies four categories of compression injury:13 1. Simple compression fractures, stable injuries involving the anterior column only. 2. Burst fractures, failure of the anterior and middle columns due to axial loading, may cause neurological instability. 3. Seatbelt-type injuries, posterior and middle column failure often as a result of laptype seatbelts being worn in road-traffic accidents. Rapid deceleration causes the spine to jack-knife around the seatbelt, and the resultant tension causes this unstable fracture. 4. Fracture dislocation, failure of all three columns so that dislocation ensues.9
Treatment for vertebral compression fractures Treatment for compression fractures is controversial. However, it is generally agreed that for non-malignant, stable fractures the conservative approach, including passive therapy and exercise, is the most apt.14 Loading of bone affects mass, micro-architecture and size, thereby maintaining the trabecular lattice. Exercise throughout life can play an important role in the prevention of osteoporotic fractures.1 The wedging that is associated with stable compression fractures allows for virtually normal func-
Post-traumatic compression fracture
tion and, therefore, surgical correction is not essential.3 For unstable fractures or in the presence of malignancy, the consequences of further deterioration must be taken into consideration and these, therefore, should be managed by a medical specialist.3 Management of stable fractures is generally divided into three stages. During the acute phase (the first week after trauma), analgesic modalities or medication along with bed rest in the recumbent position are beneficial.3,9,15 This should be continued until the pain subsides,3 or until the patient is able to turn easily from side to side,15 but should continue no longer than one week.9 At this point, active extension exercises (for the erector spinae muscles) can be commenced and the intensity gradually increased.3,9 During this time, a back support, worn for brief intervals, may provide some stability and help maintain posture.15 Thereafter, rehabilitation is continued both to strengthen spinal musculature and restore mobility.3 Along with the rehabilitation programme, the patient should follow the Intermittent Horizontal Rest Regimen (IHRR) with the patient lying for 20 min every 2 h.15 From a chiropractic perspective, although the treatment protocols are well within the scope of practitioners, the importance lies in the diagnosis and determination of potential pathological causes of the fracture. As patients’ ages increase, the associated risks of pathology must be taken into consideration and managed accordingly. Osteoporosis and metastases are the most important diagnostic considerations, not only so that correct treatment can be commenced immediately, but also so that the possibility of adverse side effects associated with inappropriate manipulation can be avoided. Chiropractic adjustments apply external forces to the spine that, in the presence of bone weakening disease, is quite susceptible to damage from these forces.16 Osteoporosis is commonly regarded as a relative or absolute contraindication to adjustment,17 the application of the external force believed to be potentially responsible for vertebral collapse. A number of such cases have been reported in the literature. In one case, an insurance company claimed spinal manipulation to be the cause of a compression fracture in an osteoporotic L3 vertebra, resulting in parapesis. However, the outcome of the case was not discussed.18 Another report stated that, in two cases, manipulation caused compression fractures. In both cases, spinal malignancies were found to be the cause and a physiotherapist and a lay person were responsible for the manipulations.19 Four further cases stated that ‘‘since no conclusive evidence could be found,
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care must be taken in drawing conclusions of causal relationships between chiropractic adjustment and compression fractures’’. However, it was stated that manipulation in areas of compression fractures might cause increased symptomatology.6
Conclusion Compression fractures are common fractures affecting the young after considerable trauma but mainly the elderly, especially in the presence of osteoporosis but also secondarily to malignancy and secondary osteopenia. Although clinical diagnosis is difficult due to the relatively mild nature of signs and symptoms, radiological diagnosis is clear and well documented. Signs to look for include step defect, wedge deformities, endplate disruption, band of impaction and abdominal ileus or paraspinal swelling. Whilst looking at the radiographs, it is important to note signs of instability, including loss of posterior vertebral height, disruption of the middle or posterior columns and vertebral body displacement. Clinical priority from a chiropractic standpoint is diagnosing the cause of fracture and verifying that it is of a stable nature before setting up a treatment protocol. It is also important that chiropractors are aware of the increased risk of further fractures in these patients and the potential link between spinal manipulation and compression fractures so that care can be taken in order to prevent iatrogenic complications.
References 1. Mosekilde L. Age-related changes in bone mass, structure, and strength-effects of loading. Z Rheumatol 2000; 59(Suppl 1):1—9. 2. Yochum TR, Rowe LJ. Trauma, fractures and dislocations of the lumbar spine. In: Essentials of skeletal radiology, 2nd ed. Maryland, USA: Williams and Wilkins; 1996. p. 695—9 [chapter 9]. 3. Adams JC, Hamblen DL. Spine and thorax. In: Outline of fractures, 10th ed. New York, USA: Churchill Livingstone; 1992. p. 90—101 [chapter 8]. 4. Oleksik A, Ott SM, Vedi S, Bravenboer N, Comptson J, Lips P. Bone structure in patients with low bone mineral density with or without vertebral fractures. J Bone Miner Res 2000;15(7):1368—75. 5. Legrand E, Chappard D, Pascaretti C, Duquenne M, Rondeau C, Simon Y, et al. Bone mineral density and vertebral fractures in men. Osteoporos Int 1999;10(4):265—70. 6. Michel BA, Lane NE, Jones HH, Fries JF, Bloch DA. Plain radiographs can be useful in estimating lumbar bone density. J Rheumatol 1990;17:528—31. 7. Hope RA, Longmore JM, Hodgetts TJ, Ramrakha PS. Biochemistry. In: Oxford handbook of clinical medicine, 3rd ed. Oxford, UK: Oxford University Press; 1994. p. 622—56 [chapter 14].
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8. Orstavik R, Haugeberg G, Kvien TK, Lilleas F. Vertebral fractures in osteoporosis-silent fractures of clinical importance. Tidsskr Nor Laegeforen 2000;120(24):2891—4. 9. McRae R. The spine. In: Practical fracture management, 3rd ed. London: Churchill Livingstone; 1999. p. 209—38 [chapter 10]. 10. Melton III LJ, Atkinson EJ, Cooper C, O’Fallon WM, Riggs BL. Vertebral fractures predict subsequent fractures. Osteoporos Int 1999;10(3):214—21. 11. Lindsay R, Silverman SL, Cooper C, Hanley DA, Barton I, Broy SB, et al. Risk of new vertebral fracture in the year following a fracture. JAMA 2001;285(3):320—3. 12. Naves DM, Diaz LJB, Gomez AC, Altadill AA, Rodriguez RA, Cannata AJB. Study of incidence of osteoporotic fractures in a cohort of individuals older than 50 years from Asturias, Spain, after a 6 year follow-up period. Med Clin (Barc) 2000; 115(17):650—3. 13. Denis F. Spinal stability as defined by the three column concept in acute spinal trauma. Clin Orthop 1984;189:65.
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14. Kreitz BG, Cote P, Cassidy JD. L5 vertebral compression fracture: a series of five cases. J Manipulative Physiol Ther 1995;18(2):91—7. 15. Frost HM. Personal experience in managing acute compression fractures, their aftermath, and the bone pain syndrome, in osteoporosis. Osteoporos Int 1998;8(1):13— 5. 16. Haldeman S, Rubinstein SM. Compression fractures in patients undergoing spinal manipulative therapy. J Manipulative Physiol Ther 1992;15(7):450—4. 17. Gatterman MI. Complications of and contraindications to spinal manipulative therapy. In: Chiropractic management of spine related disorders. Baltimore, USA: Williams and Wilkins; 1990. p. 55—69 [chapter 4]. 18. Rydell N, Raf L. Spinal manipulation–—treatment associated with a high risk of complications. Lakartidningen 1999; 96(34):3536—40. 19. Austin RT. Pathological vertebral fractures after spinal manipulation. BMJ 1985;291:1114—5.