Spinal fusion for chronic low back pain: A ‘magic bullet’ or wishful thinking?
Dr KS Dhillon FRCS
Abstract
Chronic low back pain represents a common disabling and costly health problem but unfortunately in 80% to 95% of the patients a pathoanatomical diagnosis cannot be made despite the existence of modern imaging techniques. Specific spinal pathology that fits into a classic disease model which can be accurately diagnosed and appropriately treated is seen in only about 5% to 7% of the patients. This small group of patients with specific diagnosis can be successfully treated with good outcome. The back pain in majority of the patients where no specific pathology exists has been unscientifically labeled as non-specific low back pain. To date there is no imaging technique or diagnostic test which can localize the source of pain in patients with non-specific back pain. Imaging findings such as degenerated disc, facet arthritis, spondylosis, spondylolysis and spondylolisthesis has no causal relationship to the pain in these patients. The outcome of spinal fusion in these patients is no better than nonsurgical treatment, and spinal fusion is associated with significant morbidity and occasional mortality. Yet there is rapid rise in the rates of spinal fusion. There is a growing tension between ethics and conflicts of interest for surgeons. The spine unfortunately has been labeled as profit center and there are allegations of conflicts of interest in the relationships of doctors with the multi-billion dollar spinal devices industry. The devices industry has a significant influence on not only research publications in peer review journals but also on decisions made by doctors which can have a detrimental effect on the welfare of the patient.
Key Words
Chronic low back pain, spinal fusion, conflicts of interest.
Introduction
Low back pain represents a common disabling and costly health problem. Unfortunately the cause of back pain can be accurately diagnosed and treated in only a small proportion of the patients, where specific spinal pathology such as tumours, infection, fractures and nerve root pain caused by prolapsed disc or spinal stenosis, is present. In vast majority of the patients the cause of the pain is not known and such pain has been unscientifically labeled as non-specific back pain. A pathoanatomical diagnosis cannot be made in these patients, even with modern diagnostic imaging techniques such as magnetic imaging of the spine, and this makes the treatment of nonspecific back pain difficult. Surgeons are treating the symptom (back pain) and not a disease, with surgery, when they offer spinal fusion as a modality of treatment to such patients. The rates of spinal fusion are rapidly increasing in most countries. Is there justification for spinal fusion in the treatment of patients with nonspecific low back pain or are there some conflicts of interest?
Definition and classification of chronic low back pain
Uniformity of definitions is essential to study prevalence and management outcome of low back pain. There is a lack of uniform definitions of chronic low back pain in the literature. The most widely used definition of chronic low back pain is persistent low back pain that is present for at least 12 weeks. Acute back pain lasts for less than 6 weeks and subacute back pain lasts between 6 and 12 weeks. There will be patients with a history of back pain for many years who have repeated bouts of acute or subacute back pain but will not be classified as having chronic low back pain unless the episode of pain lasts at least 12 weeks. A recurrence of an episode of low back pain is defined as a return of low back pain lasting at least 24 hours and recurrent low back pain is defined as low back pain which has occurred at least two times over the past year with each episode lasting at least 24 hours1.
There are several classifications of low back pain; the most widely accepted is that proposed by Waddell. Waddell’s diagnostic triage divides low back pain into three categories;
Specific spinal pathology such as tumour, infection, fractures, cauda equina syndrome which occurs in about 1 to 2 % of the patients.
Nerve root pain such as that caused by disc prolapse and spinal stenosis which occurs in about 5% of the patients.
Non-specific low back pain which occurs in about 85 to 95% of the patients2.
The first two categories fit into the classical disease model where the disease can be accurately diagnosed and appropriately treated. However, the third category does not fit into this model, where a proper clinical diagnosis can be made. Such a diagnosis of non-specific low back pain according to Waddell is ‘intellectually and scientifically inadequate and fails to provide any biological basis for real understanding’ which results in treatment remaining ‘empirical or based on unproven hypotheses’ 2. Claims of diagnoses such lumbar strain or degenerative spine disease as a cause of chronic low back pain remain unfounded and leaves room for uncertainty about treatment, prognosis and clinical outcome2.
Pathoanatomical diagnosis of non-specific low back pain
For spinal fusion to be successful in the treatment of chronic or recurrent low back pain there has to be a pathoanatomical diagnosis which accounts for the pain. The role of spinal fusion in progressive or unstable spondylolisthesis, spinal trauma, tumours and spinal infections is well established. However in patients with non-specific chronic low back pain a pathoanatomical diagnosis is often impossible to establish.
The degenerated intervertebral disc is most often implicated as the cause of pain in patients with nonspecific low back pain. Such pain is usually referred to as discogenic back pain. Disc degeneration leading to abnormal shock loading of the disc and micro trauma to annulus and the endplate is believed to cause the pain. This trauma to the annulus and the endplate also allows blood vessel and nerve ingrowth into the normally avascular and aneural disc3. The disc is implicated in about 40% of the patients with nonspecific low back pain4. The facet joints is believed to be the source of low back pain in 15 to 40% of the patients5 while the sacroiliac joint is implicated in about 15% of the patients6. Though we know that these three are the main sources (but not the only source) of chronic low back pain, no conventional clinical test can discriminate the source of pain in patients with disc, facet joint or sacroiliac joint abnormalities4,5,6.
A simple relationship of radiographic structural abnormalities of the lumbar spine and low back pain cannot exist because many individuals with such structural spinal abnormalities are asymptomatic7. Systematic review of published studies show that there is a lack of firm evidence for a causal relationship, between radiographic findings of degeneration of the spine as defined by disc space narrowing, osteophytes and sclerosis, and nonspecific back pain. Neither does a causal relationship exist between radiographic evidence of spondylosis, spondylolysis, spondylolisthesis, spina bifida, transitional vertebra or Scheuermann’s disease and nonspecific back pain8.
Modern imaging techniques can now allow us to accurately depict the anatomical changes that occur with the degeneration of the disc. However, the clinical significance of these changes depicted on magnetic resonance imaging (MRI) remains elusive and often confusing9. In asymptomatic adults, degeneration of the disc can be seen in about 40 to 80% of individuals and it increases with age, while disc protrusion can be seen 40 to 70%, end plate changes in 10 to 30% and annular disruption in 25 to 70% of adults who are asymptomatic10. Jansen et al11 in a study of 98 asymptomatic individuals, found that an MRI examination of the spine revealed a normal disc in only 36% of the individuals.Fifty-twoo percent had a disc bulge at one level, 27% had disc protrusion and 1% had disc extrusion. Nineteen percent had Schmorl’s nodes, 14 % had annular tears and facet arthropathy was present in 8% of the subjects. The findings were the same in males and females. The high prevalence of these findings in asymptomatic individuals and a high prevalence of back pain in general population suggest that the MRI findings of bulges or protrusions in people with low back pain may frequently be coincidental. Hence it makes sense that abnormalities on magnetic resonance images must be strictly correlated with age and any clinical signs and symptoms present before surgery is contemplated.
Since anatomical diagnostic tests such as radiographs and magnetic resonance imaging (the gold standard) are of not much help in elucidating the cause of non-specific low back pain, can other tests help in making a decision as to which of the patients with non-specific low back pain will benefit from surgery? Discography has in the past been advocated (by some proponents) as a useful decision making tool.
Lumbar discography
Discography is used to determine if the low back pain the patient is experiencing is caused by disc pathology. In this procedure dye is injected at pressure of between 15-25 psi, under fluoroscopy, into the suspected disc while the patient is sedated. If the injection reproduces the pain at the same site that the patient has been experiencing before the procedure (concordant pain) then it is believed that the disc is the source of the patient’s low back pain (positive discogram). However there is no universally accepted definition as to what a concordant pain response is and there is a lack of reliability studies on discography12. It is important to know whether discography can accurately define the disc that is generating the patient’s pain for it to be any use in spinal surgery.
We know that imaging of the spine with scans can reveal the degenerated morphology of the disc but the scans cannot tell us that the disc is the source of the pain. This is obvious from the fact that the imaging morphology of the disc does not change over short periods of time but the patient’s symptoms do. Can a discogram which is an invasive procedure with potentially serious complications such as discitis, provide us with the information needed regarding the source of the patient’s pain?
Sackett and Hayes13 have proposed that a critical test of validity of a diagnostic procedure involves measuring it against a gold standard in a clinical setting. The test should be able to distinguish between patients with and those without the target disorder (in this case low back pain) and furthermore patients who undergo the test should fare better compared to those patients who did not have the test (ultimate health outcome). Unfortunately there is no reasonable gold standard against which to test discography. Despite the lack of proven validity against a gold standard, discography has been used to recommend spinal fusion in patients with non-specific low back pain.
Carragee et al14 did a study to test the hypothesis that positive provocative discography will accurately identify patients with low back pain due to a primary discogenic lesion and a clinical cure will be achieved in such patients with a successful spinal fusion. This prospective study was carried out between 1996 and 2000. The first cohort of 32 patients had an episode of low back pain for 6 to 12 months which did not respond to conservative treatment and the discogram was positive at one level with a normal discogram at adjoining levels. The second cohort included 34 patients with an unstable spondylolisthesis who did not respond to conservative treatment. Patients with selection co-morbidities such as compensation claim, abnormal psychometric test, occupational disabilities and prior lumbar surgery were excluded. The patients were followed up for 2 years.
When a high level criterion of successful outcome (highly effective) was adopted, 71.9% of patients in the spondylolisthesis group had a successful outcome after spinal fusion and in the discogenic group only 26.6% had a successful outcome. When a low level criterion of successful outcome (minimal acceptable outcome) was used 91.7% of the spondylolisthesis group had a successful outcome as compared to 43% in the discogenic group. After ‘adjusting for surgical morbidity and drop out failure, by either criteria of success, the best-case positive predictive value of discography was calculated to be 50% to 60%’14. The study showed that provocative discography is not highly predictive in identifying intradiscal lesions as a cause of chronic low back pain. The usefulness of the test hence remains to be proven.
False positive findings on discography are also common. Carragee et al15 did an experimental disc injection in patients who had no past history of low back pain but developed back/buttock pain after posterior iliac graft harvesting for non-thoracolumbar surgical procedures. They studied 8 subjects who had 24 disc injections and 14 disc injections produced some pain response, 35.7% produced non-concordant pain, 50% produced similar pain and 14.3% of the injections produced the ‘exact’ pain. By the usual criteria for positive discography, 50% would have been classified as positive in this group of patients who had no back pain prior to the graft harvest. The response of concordant pain on discography appears to be less meaningful than is often believed.
Systematic review of accuracy of other tests such as orthosis immobilization and temporary external fixation of the spine to identify patients with chronic low back pain for whom spinal fusion is a predictable and effective treatment has not proved to be useful16.
Can spinal fusion be an effective procedure for treatment of chronic non-specific low back pain when there are no accurate diagnostic tests to identify patients who will benefit from such treatment?
Outcome of spinal fusion for non-specific low back pain
None of the imaging studies or other diagnostic test is able to accurately localise the source of pain in patients with non-specific low back pain. How can we then expect lumbar fusion to effectively treat the patient’s pain? Yet there has been a rapid increase in fusion rates (336%) of the lumbar spine from 1996 to 2001in the United States of America17. In England there has been an almost direct relationship between the numbers of operations performed per year and number of orthopaedic and neurosurgeons per head of population18. Do the results of spinal fusion justify the increase in fusion rates or are there some conflicts of interest?
Fairbank et al19, in 2005, published the results of a randomised controlled trial which assessed the clinical effectiveness of spinal stabilization/fusion compared to intensive rehabilitation for patients with chronic low back pain. Their cohort included 349 patients between the ages of 18 to 55 years with at least one year of low back pain who were considered by an experienced surgeon that they were candidates for spinal fusion. The patients were randomised into two groups, 176 to the surgical group and 173 to the rehabilitation group. The cohort was followed up for 2 years.
At 2 years the clinical outcome was assessed using the Oswestry low back pain disability index, which is scored 0% (no disability) to 100% (totally disabled or bed ridden) and is designed to assess the limitation of activities of daily living. Other assessments included the shuttle walking test, short form (SF) general health questionnaire, and psychological distress and risk assessment (DRAM).
The mean Oswestry disability index changed favourably from 46.5 to 34 in the surgical group and from 44.8 to 36.1 in the rehabilitation group. The mean difference between the groups was about -4.1 in favour of the surgical group. There was no difference between the groups in the shuttle walking test and other outcome measures. There were surgical complications in 19 patients. Eleven patients in the surgical group had reoperations. Complications included dural tears, excessive bleeding, implant problems, fractures and vascular injury.
The study showed that there was no clear evidence that primary spinal fusion surgery was any more beneficial than intensive rehabilitation in patients with chronic low back pain. Surgery while not having any superiority over conservative management was associated with potential risk and increased cost.
Brox et al20 did a 4 years follow up of patients to compare surgical versus non-surgical therapy in the treatment of chronic low back pain. In this study of two merged randomised clinical trials the authors compared instrumented transpedicular fusion with cognitive intervention and exercises in 124 patients who had disc degeneration and one year of symptoms. This study included some patients who had previous surgery for disc herniation while others had no previous spinal surgery. Of the 124 patients 66 patients were assigned to the surgical group and 58 to the non-surgical group.
The study showed that lumbar fusion was not superior to cognitive intervention and exercises at reliving back pain, improving function and return to work at 4 years. However there were 14 patients (24%) randomised to the non-surgical group who underwent subsequent surgery (non- adherence to protocol) while 15 patients (23%) in the surgical group had to undergo reoperation.
These studies lack placebo controls. The improvements in the surgical group may be placebo mediated. Hence it is not possible to know whether the marginal positive outcome in these patients reflect the natural course of the disease, placebo effect, patient expectation, or the care provided20. It is a fallacy to believe that new technical solutions in the hands of a skilled surgeon will provide faster and greater improvements in the patient’s symptoms unless the solutions are based on sound knowledge backed by good randomised studies. At the present time there is insufficient evidence to determine the effect of fusion compared to non-surgical treatment. Methodological limitations of the published randomised trials prevent any firm conclusions to be drawn on the effectiveness of spinal fusion for chronic low back pain21.
The Agency for Healthcare Research and Quality (ACHR), U.S. Department of Health and Human Services which conducts the effective health care program as part of its mission to organise knowledge, has conducted an extensive comparative effectiveness review of spinal fusion for treating painful lumbar degenerated discs or joints and has come to the conclusion that there is insufficient evidence to determine the benefits of lumbar fusion compared to more intensive rehabilitation programs22.
In the absences of sufficient evidence of benefits of spinal fusion for chronic non-specific low back pain, is it safe to recommend the procedure to patients?
Complications of spinal fusion
Spinal fusion is a major surgical procedure which involves extensive dissection, decortication of bone, blood loss and longer operating time. Often implants have to be used. More extensive and prolonged procedures are usually associated with more complications. There is a tendency among spinal surgeons to correct all anatomical abnormalities to prevent future symptoms, leading to more complex fusions, although there is no evidence that such ‘prophylactic’ surgery has any benefits. Complex fusions include multi-level surgery involving multiply approaches.
Deyo et al23 did a study to evaluate major complications in Medicare patients undergoing surgery for spinal stenosis in the United States in 2007. Their study of Medicare data avoided the bias which is often associated with studies by surgeons of selected patients from select centres. They were able to obtain nearly complete data on repeat hospitalization and mortality.
They studied 32,152 patients who had surgery for spinal stenosis in the first 11 months of 2007. The patients were 66 years and above. They analysed major medical complications, wound complications and the 30 day mortality. The major medical complications included those that needed cardiopulmonary resuscitation or repeat endotracheal intubation and mechanical ventilation due to cardiorespiratory arrest, acute myocardial infarct, respiratory failure, pulmonary embolism, pneumonia and stroke. The wound complications included haemorrhage, haematoma, seroma, wound break down and post-operative infections. Mortality included all deaths within 30 days of hospital discharge.
In patients who had complex spinal fusion, there was a 5.6% rate of major complication and the 30 day mortality was 0.6%. Complex fusions had an odds ratio of 2.95(95%CI) for life-threatening complications compared to decompression without fusion. The re-hospitalization rate was 13% in patients who had complex fusions. The wound complications were also higher in patients who had complex procedures.
In a study by Fritzell et al24 comparing surgical with non-surgical treatment for low back pain 18% of the patients in the fusion group developed early (within 2 weeks) complications and 6% had late complications. Complications included, bleeding, neural injury, heart failure, major GI bleeding, pulmonary oedema, aspiration sepsis, pulmonary embolism, dural tears, haematomas, pseudoarthrosis and even wrong level surgery. In patients who had complex fusion the complication rate was 31%. The reoperation rate in the surgical group was 6%.
Brox et al25 (2003) in a study comparing instrumented lumbar fusion with conservative treatment for chronic low back reported a 18% complication rate in the surgical group. In the Fairbank19 study the complication rate in the surgical group was 10.7% and the reoperation rate was 0.6%. In the Brox study (2010)20 the reoperation rate in the surgical group was higher at 23%.
There are wide variations in the complication and the reoperation rates in these studies because of insufficient reporting and variations in surgical techniques. This makes it difficult to determine conclusively the complication rates of lumbar fusion in these patients22. Nevertheless, complications associated with spinal fusion are not uncommon and can be life-threatening.
Despite a lack of superiority of spinal fusion over non-operative treatment of patients with chronic non-specific low back pain, there has been a steep rise in the rates of spinal fusion over the last two decades. Spinal fusion is also associated with morbidity and mortality. This begs the question as to why there is such a trend.
‘Spine as a profit centre’
There is growing tension between ethics and conflicts of interest with some surgeons becoming less altruistic and allegations of unethical behaviour among doctors becoming more rampant. The American press is often inundated with reports of unethical behaviour among doctors and these include accusations of exorbitant professional charges, royalties paid to doctors without intellectual property and marketing of medical products and services by doctors for economic gain. Spinal fusion for chronic low back is one such service. Spinal fusion is one of the most lucrative areas of medicine and it generates billions of dollars for the hospitals and the surgeons26.
In the year 2001 in the United States, 122,000 lumbar fusions were carried out for degenerative disease of the spine and this represented a 220% increase from 1990. This increase became more obvious after 1996 when fusion cages for spinal fusion became available. The increase in lumbar fusion from 1996 to 2001 was 113%, while for hip and knee arthroplasty it was only 13% and 15% respectively27. Studies show that a higher proportion of fusion procedures and the introduction of new spinal implants between the years 1993 to 1997 did not reduce re-operation rates. In fact the reoperation rates were higher in the late 1990’s as compared to the early 1990’s27. The authors were of the opinion that introduction and marketing of new surgical devices and the influence of key opinion leaders is the likely reason for invasive procedures in the absences of new indications. Other possible reasons being financial incentives to hospitals and surgeons as well as the desire of surgeons to be innovators.
The influence of key opinion leaders and financial incentives for surgeons has hit the headlines in major U.S. newspapers in recent years. Allegations of kickbacks to spine surgeons to use their products, relationship of surgeons to biomedical firms with financial arrangements involving multibillion dollar medical devices industry have been highlighted28.
One such debacle was that of the use of recombinant human bone morphogenetic protein-2 (rhBMP-2), a bone growth factor for spinal fusion. The Spine Journal, June issue 2011, gained attention from surgeons, researchers, patients, media, and industry when it focused attention on the controversial rhBMP-2 synthetic bone growth factor for use in spinal fusion surgery. It highlighted the limitation of industry sponsored research, bias in research development and reporting as well as weaknesses of peer review publications and inadequate disclosures and ethical shortcomings. The industry sponsored doctors involved in the promotion of rhBMP-2 through publication of studies in peer review journals which showed no complications with the use of rhBMP-2, received millions of dollars in royalties from Medtronic, the manufacturer of the product29. Subsequent non-industry studies showed that the use of rhBMP-2 was associated with many complications30.
Conflicts of interest through consulting ties and other relationship with device manufactures aside, doctors have now started becoming investors in spinal implant manufacture and distribution. As of Oct 2012, there were at least 20 states in U.S. with multiple active physician owned distributorships (PODs) which supply devices to hospital, with California alone having 40 such distributorships31. This has sparked fears that this would provide extra financial incentive for surgeons to recommend spinal fusion.
This prompted the Congress in the U.S. to ask the U.S. Department of Health and Human Services to investigate the prevalence and use of spinal devices supplied by physician-owned distributorships (PODs) 32. In 2011 PODs supplied devices used in one in five spinal surgeries billed to Medicare and contrary to claims by such distributorships the cost were not lower. A third of hospitals surveyed purchased devices from PODs. After hospitals started buying devices from PODs, the rates of spinal fusions grew faster in hospitals that bought devices from PODs compared to fusion rates in hospitals overall. In 2012 surgeons did more spinal surgeries at hospitals that purchased spinal devices from PODs than at hospitals that did not get their devices from PODs.
This new and growing area of partnership between surgeons and the device manufacturers has led some surgeons to express concern about such partnerships, because they believe that it is unethical and it will bias the doctor’s choice of what is best for the patient. Others have described such partnerships as ‘an awfully pernicious conflict of interest’ for doctors26. Some have gone further to described this new business model as ‘low hanging fruits’ waiting to be plucked and not to be deprived of the opportunity Malaysian surgeons have jumped on the bandwagon33.
Conclusions
The definition of chronic low back pain varies in different studies that are published. There is a need for uniformity of definitions to effectively study, the prevalence and outcome of treatment, of chronic low back pain. The most widely used definition is persistent low back pain which last at least 12 weeks.
Chronic back pain is a symptom and not a disease. Specific spinal pathology which fits into a classical disease model, where treatment can be effective, can be found in only about 6% to 7% of the patients. In about 85 to 95% of the patients with back pain no pathoanatomical diagnosis can be made and such pain gets labelled as non-specific back pain.
In the vast majority of patients the degenerated disc is implicated as the cause of chronic low back pain while in others the facet joints and sacroiliac joint is believed to be the cause of the pain. Although MRI scans can accurately depict the anatomical changes seen in the spine as degeneration of the spine sets in, the clinical significance of these changes remain elusive and the scans cannot help in elucidating the cause of the pain. Provocative discography which was in the past touted as a valid diagnostic test, has also failed to stand up to its usefulness.
Despite the inability to make a diagnosis in patients with non-specific low back pain, there has been a sharp increase in the number of patient undergoing spinal fusion for low back pain over the last two decades. Spinal fusion in patients with non-specific back pain is akin to treating a symptom (not a disease) with surgery. Logic dictates that such an approach cannot be very successful.
There is a dearth of level 1 studies in the medical literature comparing spinal fusion to non-surgical treatment of chronic low back pain. There are two relatively good level 1 studies with two to four years follow up comparing surgical to non-surgical treatment published so far, but they do not show superiority of surgical treatment over nonsurgical treatment. Furthermore spinal fusion is associated with significant and sometimes serious medical complications including mortality.
The growth in the number fusions carried out for chronic low back pain despite the lack of evidence of its efficacy has raised concerns about conflicts of interests and unethical behaviour on the part of the surgeons. In recent years, allegations of kickbacks to spine surgeons from the multibillion dollar medical devices industry, to use their products, have made the headlines in major U.S newspapers. To make matters worse surgeons have now become investors in the manufacture and distribution of medical devices used in spinal surgery, raising concerns of pernicious conflicts of interest for the surgeons. The growing partnership between surgeons and the manufacturing and distribution industry has been blamed for an increasing number of spinal fusions and bias in the doctor’s choice of what is in best for the patient.
The frequent allegations of financial conflicts of interest and the absence of scientific evidence of superiority of spinal fusion over non-surgical treatment for chronic low back pain should be reason enough for surgeons to seriously reconsider their indications for spinal fusion, since their decision may have future medico-legal implications and in some countries it may run afoul of existing legislations.
References
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Saturday, 15 October 2016
Fracture dislocations of the talus
Fracture dislocations of the talus
Dr KS Dhillon FRCS
Introduction
The talus is one of the largest bone of the foot. Fractures of the talus are uncommon and constitute less than 1% of all fractures and between 3 to 6% of foot fractures (1). About 60% of the talus is covered by cartilage and its blood supply is precarious. Hence injuries of the talus are associated with a high incidence of avascular necrosis (AVN) of the bone which can approach 100% in comminuted fracture of the body and type IV fractures of the neck. The outcome of treatment of AVN is generally poor with no definite consensus as to the best mode of treatment. To date the quality of evidence about the best method of treatment of AVN of the talus is very low.
Anatomy of the talus
The talus is the largest tarsal bone of the foot after the calcaneus. It is made up of three parts, the body, neck and the head. The head is covered with hyaline cartilage and it articulates inferiorly with the calcaneus (anterior subtalar joint) and anteriorly with the navicular bone (talonavicular joint). The body of the talus has two processes, the lateral and posterior processes. The posterior process forms the medial and lateral tubercle and in the groove between the two, passes the flexor hallucis longus tendon. The lateral process is large and it articulates superiorly with the fibula and inferiorly with the calcaneus to form the posterior subtalar joint. Inferior part of the body has a smaller middle articular facet which forms the middle subtalar joint with the calcaneus. Superiorly the body of the talus articulates with the tibia and fibula to form the tibiotalar joint. The part of the talus which forms the tibiotalar is also known as the dome or the trochlea. About 60% of the talus is covered with articular cartilage. The body of the talus is connected to the head by the neck of the talus which is non-articular and inferiorly it forms the tarsal tunnel (2). The talus has no tendinous or muscular attachments although it has ligamentous attachment.
The vascular supply to the talus is precarious due to the absences of any muscular attachment and the fact that a large portion of talus is covered with articular cartilage. The blood supply reaches the talus through the non-articular surface via the posterior tibial artery, the dorsalis pedis and the peroneal artery (2).
Fractures of the talus
Fractures of the talus may involve the head, neck or the body. Fractures of the body are the most common and constitute about 13 to 61% of talar fractures. Fractures of the neck constitute about 5% and fractures of the head constitute about 5 to 10% of talar fractures (3).
Fractures of the talus can often be associated with talar or peri-talar dislocations. When a talar fracture is suspected an AP, lateral and a mortise view x-ray of the ankle and an AP, lateral and oblique x-ray of the foot has to be done. For an accurate analysis of the talar injury a CT scan is usually needed. Undisplaced fractures can be treated conservatively but displaced fractures would require accurate open reduction and internal fixation (2).
In the past neck fractures were believed to be the most common fractures of the talus but now with clearer differentiation between neck and body fractures, neck fractures are believed to form only 5% of fractures of the talus(3).
Neck fractures were originally classified by Hawkins (4) in 1970 and later modified by Canale and Kelly (5). This classification has prognostic significance (5 and 6).
Type 1 – Nondisplaced fractures of the neck. Incidence of avascular necrosis (AVN) is between 0 to 15%.
Type 11 – Fractures of the neck with talocalcaneal dislocation. Incidence of AVN between 20 to 50%.
Type 111 – Fractures of the neck with talocalcaneal and tibiotalar dislocation. The incidence of AVN is 100%.
Type 1V – Fractures of the neck with disruption of all talar articulations. The incidence of AVN is 100%.
Talar body fractures are divided into 5 types according to a classification by Sneppen (2). The five categories of body fractures as suggested by Sneppen include:
Type A – Compression osteochondral fracture of the dome.
Type B - Coronal shear fractures
Type C – Sagittal shear fractures
Type D – Posterior tubercle fractures
Type E –Lateral process fracture
Type F – Crush comminuted fracture
The fractures are often associated with dislocation of the talocalcaneal, tibiotalar or both the joints. Coronal shear fractures are best seen in the lateral view x-rays and the sagittal shear fractures are best seen in the AP view x-rays. The crush comminuted fractures (type F), which usually result from high impact injuries, have the worse prognosis. They are often open and are associated with bone loss, inaccurate reduction and avascular necrosis (7).
Dislocation of the talus.
Dislocation of the talus can be of two types namely, a subtalar (peritalar) or a pantalar dislocation. Subtalar dislocations can be medial (more common) or lateral (less common). Anterior and posterior dislocation may occur but is very rare. In subtalar dislocation the tibiotalar and the calcaneocuboid joints remain intact while the subtalar and talonavicular joints are disrupted. Lateral dislocations are less common but more serious being associated with higher incidence of AVN and posttraumatic subtalar OA (8).
Pantalar dislocations are very rare. The talus usually dislocates anterolaterally. It may be an open or a close injury and the talus may or may not have soft tissue attachment. Open injuries are often associated with osteomyelitis and AVN. Traditionally pantalar dislocations have been treated by excision of the talus and arthrodesis but there are calls for relocation of the talus whenever possible (9).
Outcome of treatment of talar injuries
Frawley et al (10) studied the long-term outcome of treatment of major talus fractures which excluded isolated fractures of the dome and the posterior tubercle. They studied 26 patients, 15 of whom were treated by open reduction and internal fixation and 11 were treated by nonsurgical means. They found the incidence of AVN to be 15% (4 out of 26 patients) and only in 1 patients the AVN was severe enough to require fusion. Subtalar OA was seen in 61% of the patients. Only 3 patients did not return to work at an average follow-up of 6 years. Forty-two percent of the patients were not able to return to their premorbid activity level.
Ebraheim et al (11)and there were two associated neck fractures. At an average of 26 (18-43) months the AOFAS (American Orthopedic Foot and Ankle Society) scores were excellent in 4, good in 6, fair in 4 and poor in 5 patients. There was AVN in 7, deep infection in 1 and malunion in 1 patient.
Vallier et al (12) in a level IV study reported a 38% incidence of AVN, 65% incidence of tibiotalar OA and 34% incidence of subtalar OA, in 26 talar body fractures at minimal follow-up of 1 year.
Vallier et al (13) in another retrospective review of 100 patients with talar neck fractures who were treated surgically, sixty were available for review at an average of 36 months follow-up. Of these 39 had complete radiographic data. The incidence of AVN was 49%. In 37% of these patients with AVN revascularization occurred with no collapse of the dome. The overall incidence of collapse of the dome was 31%. The incidence of AVN was 39% in the Hawkins II fractures and 64% in Hawkins III fractures. Fifty-four percent of the patients developed post-traumatic OA and it was more common in patients with comminuted and open fractures.
Pajenda et al (14) reviewed the clinical outcome of 50 patients with talar neck fractures. Thirty-two percent were type I, 28% type II, 18% type III and 22% type IV (Hawkins) fractures. Mild ankle OA developed in 28% of patients and severe OA was seen in 20% of the patients. Fifty percent of patients with severe OA needed ankle arthrodesis. Subtalar OA was seen in 8% of the patients and AVN with dome collapse was seen in8% of the patients. Functional scores according to Weber was good to excellent in 95% of patients with type I and II fractures. Good results were seen in 70% of patients with type III and 10% of type IV fractures.
Sneppen et al (15) in a review of 51 patients with fracture of the body of the talus found that the severity of the initial injury determines the long-term outcome. Severe compression fractures of the body are associated with about 50% incidence of OA of the ankle. Shearing pattern fractures are associated with about 41% incidence of ankle and subtalar OA.
Canale and Kelly published the outcome of 71 fractures of the talar neck at an average follow-up of 12.7 years. They reported a 59% good to excellent results in their patients. The incidence of AVN was 52% in their study.They found that ‘triple arthrodesis, tibiocalcaneal fusion, and dorsal beak resection of the talar neck all resulted in a high percentage of satisfactory results, but talectomy did not’ (16).
Post-traumatic avascular necrosis
Seventy-five percent of talar AVN is post-traumatic in origin which results from fracture\dislocations of the talus (17). Non-traumatic causes include steroid use, alcoholism, hyperuricemia, hyperlipidemia, occlusive vascular disease, SLE and sickle cell disease (18).
In type III fractures of the neck the incidence of AVN can approach 83% to 100%. In type IV fractures of the neck and comminuted fractures of the body the incidence of AVN can reach 100% (18). In AVN the amount of bone involved may be small as in osteochondral lesions, partial or complete with total involvement of the body of the talus (19).
The diagnosis of AVN can be made on an AP mortise view of the ankle where the avascular bone will appear dense compared to the surrounding vascular bone. These changes may not be visible till about 3 months or more after the injury to the talus. The earliest sign of revascularization of the talus can be seen as early as 6 to 8 weeks post-trauma and it manifests as the Hawkin’s sign which is a line of subchondral radiolucency due osteoporosis in vascular zone seen in the AP mortise view of the ankle. A partial Hawkin’s line is a sign of partial revascularization most often seen on the medial side where vascularity is better. The presences of Hawkin’s sign is highly predictive of absences of AVN. Though it is highly sensitive (100%), it is not very specific(57.7%) since the absence of the sign does not predict the presences of AVN (19). The posterolateral corner of the body has the poorest blood supply and hence AVN changes are most common at that site. Later as revascularization occurs a partial or complete collapse of subchondral bone will occur. Occasionally fragmentation of the whole talar body can occur (19). An MRI is useful in determining the extent of AVN. The more extensive the AVN the greater the chance of collapse and fragmentation.
The primary goal in the treatment of talus fracture is to achieve an accurate stable reduction and union. Bony union is possible even in the presence of AVN (20). Weight bearing should be avoided till fracture union has occurred. After fracture union in the presence of AVN (absent Hawkin’s sign) the aim of treatment is prevention of late collapse. The process of creeping substitution of the avascular segment can take up to 36 months (21).
From the point of view of treatment it is useful to divide talar AVN into the early and the late stage categories. In the late stage the options for treatment are limited to a talectomy or an arthrodesis (21).
The treatment of early stage AVN is controversial. The question is what to do while revascularization is occurring? Some believe that the patient should be non-weight bearing till revascularization is complete (22-24) while others believe that patients should be partial weight bearing on a patella tendon brace (25-27). There are others who believe that it is not possible to be non-weight bearing or partial weight bearing for long periods of time when we know that revascularization can take up to 36 months. They believe that it is better to deal with the symptoms as and when they arise (28-30). Poor results in patients with AVN of the talus does not apparently correlate with the method of treatment and the time the patient has been non-weight bearing (31).
In patients who have pain due AVN in the pre-collapse stage, core decompression to reduce intraosseous pressure and promote revascularization has been recommended by some surgeons. In patients who continue to have pain after decompression various types of bone grafting has been proposed. This include non-vascularised auto or allografts or vascularized bone grafts (21).
In the late stage when talar collapse and post-traumatic OA has set in the treatment options in symptomatic patients is talectomy or an arthrodesis. Traditionally talectomy has not been associated with good results but Gunal et al (32) has developed a new technique which apparently gives excellent to good results. More often arthrodesis of the ankle, subtalar joints or a triple arthrodesis is carried out depending on the joints affected by post-traumatic OA and the AVN (19).
Although there are many published treatment options for post-traumatic talar AVN, ‘critical outcome studies are still lacking’ (33). Gross et al (34) did a systematic review of treatments for AVN of the talus. They were able to identify 19 suitable studies with 321 ankles at final follow-up. The modalities of treatment included conservative measures such as protective weight bearing, core decompression, bone grafting, vascularized bone grafting, hindfoot fusion and talar replacement. The quality of evidence was ‘very low’ and all the studies were level IV studies. In the early stages protected weight bearing appears to be the treatment of choice and if it fails core decompression may be an option. Arthrodesis would be the salvage operation of choice when all else have failed.
Conclusion
Injuries to the talus are fortunately uncommon.The major part of the talus is covered with cartilage and there is no muscle attachment to the talus.Hence the blood supply to the talus is precarious and it makes it vulnerable to avascular necrosis, the incidence of which can reach 100% in some types of fractures and dislocation of the talus. The outcome of treatment of AVN is generally poor and there is no consensus as to best method of treatment of patients with AVN. The quality of evidence to support any particular form of treatment of patient with AVN remains poor.
References
Dr KS Dhillon FRCS
Introduction
The talus is one of the largest bone of the foot. Fractures of the talus are uncommon and constitute less than 1% of all fractures and between 3 to 6% of foot fractures (1). About 60% of the talus is covered by cartilage and its blood supply is precarious. Hence injuries of the talus are associated with a high incidence of avascular necrosis (AVN) of the bone which can approach 100% in comminuted fracture of the body and type IV fractures of the neck. The outcome of treatment of AVN is generally poor with no definite consensus as to the best mode of treatment. To date the quality of evidence about the best method of treatment of AVN of the talus is very low.
Anatomy of the talus
The talus is the largest tarsal bone of the foot after the calcaneus. It is made up of three parts, the body, neck and the head. The head is covered with hyaline cartilage and it articulates inferiorly with the calcaneus (anterior subtalar joint) and anteriorly with the navicular bone (talonavicular joint). The body of the talus has two processes, the lateral and posterior processes. The posterior process forms the medial and lateral tubercle and in the groove between the two, passes the flexor hallucis longus tendon. The lateral process is large and it articulates superiorly with the fibula and inferiorly with the calcaneus to form the posterior subtalar joint. Inferior part of the body has a smaller middle articular facet which forms the middle subtalar joint with the calcaneus. Superiorly the body of the talus articulates with the tibia and fibula to form the tibiotalar joint. The part of the talus which forms the tibiotalar is also known as the dome or the trochlea. About 60% of the talus is covered with articular cartilage. The body of the talus is connected to the head by the neck of the talus which is non-articular and inferiorly it forms the tarsal tunnel (2). The talus has no tendinous or muscular attachments although it has ligamentous attachment.
The vascular supply to the talus is precarious due to the absences of any muscular attachment and the fact that a large portion of talus is covered with articular cartilage. The blood supply reaches the talus through the non-articular surface via the posterior tibial artery, the dorsalis pedis and the peroneal artery (2).
Fractures of the talus
Fractures of the talus may involve the head, neck or the body. Fractures of the body are the most common and constitute about 13 to 61% of talar fractures. Fractures of the neck constitute about 5% and fractures of the head constitute about 5 to 10% of talar fractures (3).
Fractures of the talus can often be associated with talar or peri-talar dislocations. When a talar fracture is suspected an AP, lateral and a mortise view x-ray of the ankle and an AP, lateral and oblique x-ray of the foot has to be done. For an accurate analysis of the talar injury a CT scan is usually needed. Undisplaced fractures can be treated conservatively but displaced fractures would require accurate open reduction and internal fixation (2).
In the past neck fractures were believed to be the most common fractures of the talus but now with clearer differentiation between neck and body fractures, neck fractures are believed to form only 5% of fractures of the talus(3).
Neck fractures were originally classified by Hawkins (4) in 1970 and later modified by Canale and Kelly (5). This classification has prognostic significance (5 and 6).
Type 1 – Nondisplaced fractures of the neck. Incidence of avascular necrosis (AVN) is between 0 to 15%.
Type 11 – Fractures of the neck with talocalcaneal dislocation. Incidence of AVN between 20 to 50%.
Type 111 – Fractures of the neck with talocalcaneal and tibiotalar dislocation. The incidence of AVN is 100%.
Type 1V – Fractures of the neck with disruption of all talar articulations. The incidence of AVN is 100%.
Talar body fractures are divided into 5 types according to a classification by Sneppen (2). The five categories of body fractures as suggested by Sneppen include:
Type A – Compression osteochondral fracture of the dome.
Type B - Coronal shear fractures
Type C – Sagittal shear fractures
Type D – Posterior tubercle fractures
Type E –Lateral process fracture
Type F – Crush comminuted fracture
The fractures are often associated with dislocation of the talocalcaneal, tibiotalar or both the joints. Coronal shear fractures are best seen in the lateral view x-rays and the sagittal shear fractures are best seen in the AP view x-rays. The crush comminuted fractures (type F), which usually result from high impact injuries, have the worse prognosis. They are often open and are associated with bone loss, inaccurate reduction and avascular necrosis (7).
Dislocation of the talus.
Dislocation of the talus can be of two types namely, a subtalar (peritalar) or a pantalar dislocation. Subtalar dislocations can be medial (more common) or lateral (less common). Anterior and posterior dislocation may occur but is very rare. In subtalar dislocation the tibiotalar and the calcaneocuboid joints remain intact while the subtalar and talonavicular joints are disrupted. Lateral dislocations are less common but more serious being associated with higher incidence of AVN and posttraumatic subtalar OA (8).
Pantalar dislocations are very rare. The talus usually dislocates anterolaterally. It may be an open or a close injury and the talus may or may not have soft tissue attachment. Open injuries are often associated with osteomyelitis and AVN. Traditionally pantalar dislocations have been treated by excision of the talus and arthrodesis but there are calls for relocation of the talus whenever possible (9).
Outcome of treatment of talar injuries
Frawley et al (10) studied the long-term outcome of treatment of major talus fractures which excluded isolated fractures of the dome and the posterior tubercle. They studied 26 patients, 15 of whom were treated by open reduction and internal fixation and 11 were treated by nonsurgical means. They found the incidence of AVN to be 15% (4 out of 26 patients) and only in 1 patients the AVN was severe enough to require fusion. Subtalar OA was seen in 61% of the patients. Only 3 patients did not return to work at an average follow-up of 6 years. Forty-two percent of the patients were not able to return to their premorbid activity level.
Ebraheim et al (11)and there were two associated neck fractures. At an average of 26 (18-43) months the AOFAS (American Orthopedic Foot and Ankle Society) scores were excellent in 4, good in 6, fair in 4 and poor in 5 patients. There was AVN in 7, deep infection in 1 and malunion in 1 patient.
Vallier et al (12) in a level IV study reported a 38% incidence of AVN, 65% incidence of tibiotalar OA and 34% incidence of subtalar OA, in 26 talar body fractures at minimal follow-up of 1 year.
Vallier et al (13) in another retrospective review of 100 patients with talar neck fractures who were treated surgically, sixty were available for review at an average of 36 months follow-up. Of these 39 had complete radiographic data. The incidence of AVN was 49%. In 37% of these patients with AVN revascularization occurred with no collapse of the dome. The overall incidence of collapse of the dome was 31%. The incidence of AVN was 39% in the Hawkins II fractures and 64% in Hawkins III fractures. Fifty-four percent of the patients developed post-traumatic OA and it was more common in patients with comminuted and open fractures.
Pajenda et al (14) reviewed the clinical outcome of 50 patients with talar neck fractures. Thirty-two percent were type I, 28% type II, 18% type III and 22% type IV (Hawkins) fractures. Mild ankle OA developed in 28% of patients and severe OA was seen in 20% of the patients. Fifty percent of patients with severe OA needed ankle arthrodesis. Subtalar OA was seen in 8% of the patients and AVN with dome collapse was seen in8% of the patients. Functional scores according to Weber was good to excellent in 95% of patients with type I and II fractures. Good results were seen in 70% of patients with type III and 10% of type IV fractures.
Sneppen et al (15) in a review of 51 patients with fracture of the body of the talus found that the severity of the initial injury determines the long-term outcome. Severe compression fractures of the body are associated with about 50% incidence of OA of the ankle. Shearing pattern fractures are associated with about 41% incidence of ankle and subtalar OA.
Canale and Kelly published the outcome of 71 fractures of the talar neck at an average follow-up of 12.7 years. They reported a 59% good to excellent results in their patients. The incidence of AVN was 52% in their study.They found that ‘triple arthrodesis, tibiocalcaneal fusion, and dorsal beak resection of the talar neck all resulted in a high percentage of satisfactory results, but talectomy did not’ (16).
Post-traumatic avascular necrosis
Seventy-five percent of talar AVN is post-traumatic in origin which results from fracture\dislocations of the talus (17). Non-traumatic causes include steroid use, alcoholism, hyperuricemia, hyperlipidemia, occlusive vascular disease, SLE and sickle cell disease (18).
In type III fractures of the neck the incidence of AVN can approach 83% to 100%. In type IV fractures of the neck and comminuted fractures of the body the incidence of AVN can reach 100% (18). In AVN the amount of bone involved may be small as in osteochondral lesions, partial or complete with total involvement of the body of the talus (19).
The diagnosis of AVN can be made on an AP mortise view of the ankle where the avascular bone will appear dense compared to the surrounding vascular bone. These changes may not be visible till about 3 months or more after the injury to the talus. The earliest sign of revascularization of the talus can be seen as early as 6 to 8 weeks post-trauma and it manifests as the Hawkin’s sign which is a line of subchondral radiolucency due osteoporosis in vascular zone seen in the AP mortise view of the ankle. A partial Hawkin’s line is a sign of partial revascularization most often seen on the medial side where vascularity is better. The presences of Hawkin’s sign is highly predictive of absences of AVN. Though it is highly sensitive (100%), it is not very specific(57.7%) since the absence of the sign does not predict the presences of AVN (19). The posterolateral corner of the body has the poorest blood supply and hence AVN changes are most common at that site. Later as revascularization occurs a partial or complete collapse of subchondral bone will occur. Occasionally fragmentation of the whole talar body can occur (19). An MRI is useful in determining the extent of AVN. The more extensive the AVN the greater the chance of collapse and fragmentation.
The primary goal in the treatment of talus fracture is to achieve an accurate stable reduction and union. Bony union is possible even in the presence of AVN (20). Weight bearing should be avoided till fracture union has occurred. After fracture union in the presence of AVN (absent Hawkin’s sign) the aim of treatment is prevention of late collapse. The process of creeping substitution of the avascular segment can take up to 36 months (21).
From the point of view of treatment it is useful to divide talar AVN into the early and the late stage categories. In the late stage the options for treatment are limited to a talectomy or an arthrodesis (21).
The treatment of early stage AVN is controversial. The question is what to do while revascularization is occurring? Some believe that the patient should be non-weight bearing till revascularization is complete (22-24) while others believe that patients should be partial weight bearing on a patella tendon brace (25-27). There are others who believe that it is not possible to be non-weight bearing or partial weight bearing for long periods of time when we know that revascularization can take up to 36 months. They believe that it is better to deal with the symptoms as and when they arise (28-30). Poor results in patients with AVN of the talus does not apparently correlate with the method of treatment and the time the patient has been non-weight bearing (31).
In patients who have pain due AVN in the pre-collapse stage, core decompression to reduce intraosseous pressure and promote revascularization has been recommended by some surgeons. In patients who continue to have pain after decompression various types of bone grafting has been proposed. This include non-vascularised auto or allografts or vascularized bone grafts (21).
In the late stage when talar collapse and post-traumatic OA has set in the treatment options in symptomatic patients is talectomy or an arthrodesis. Traditionally talectomy has not been associated with good results but Gunal et al (32) has developed a new technique which apparently gives excellent to good results. More often arthrodesis of the ankle, subtalar joints or a triple arthrodesis is carried out depending on the joints affected by post-traumatic OA and the AVN (19).
Although there are many published treatment options for post-traumatic talar AVN, ‘critical outcome studies are still lacking’ (33). Gross et al (34) did a systematic review of treatments for AVN of the talus. They were able to identify 19 suitable studies with 321 ankles at final follow-up. The modalities of treatment included conservative measures such as protective weight bearing, core decompression, bone grafting, vascularized bone grafting, hindfoot fusion and talar replacement. The quality of evidence was ‘very low’ and all the studies were level IV studies. In the early stages protected weight bearing appears to be the treatment of choice and if it fails core decompression may be an option. Arthrodesis would be the salvage operation of choice when all else have failed.
Conclusion
Injuries to the talus are fortunately uncommon.The major part of the talus is covered with cartilage and there is no muscle attachment to the talus.Hence the blood supply to the talus is precarious and it makes it vulnerable to avascular necrosis, the incidence of which can reach 100% in some types of fractures and dislocation of the talus. The outcome of treatment of AVN is generally poor and there is no consensus as to best method of treatment of patients with AVN. The quality of evidence to support any particular form of treatment of patient with AVN remains poor.
References
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- Günal I, Atilla S, Araç S, Gürsoy Y, Karagözlu H. A new technique of talectomy for severe fracture-dislocation of the talus. J Bone Joint Surg Br. 1993 Jan;75(1):69-71.
- Adelaar RS, Madrian JR. Avascular necrosis of the talus. Orthop Clin North Am. 2004 Jul;35(3):383-95.
- Gross CE, Haughom B, Chahal J, Holmes GB. Treatments for Avascular Necrosis of the Talus. A Systematic Review. Foot Ankle Spec. 2014 Oct;7(5):387-97.
Friday, 9 September 2016
Injuries and osteoarthritis of Acromioclavicular joint
Injuries and osteoarthritis of Acromioclavicular joint
Dr KS Dhillon FRCS, LLM
Introduction
The true incidence acromioclavicular (AC) injuries is not known because many with such injuries do not seek medical treatment. About 12% of shoulder dislocations involve the AC joint. The treatment of AC joint injury remains controversial although good long term results can be seen in patients treated conservatively. There is an increasing tendency to treat higher grade injuries surgically.
Injuries to the AC joint can predispose the joint to osteoarthritis (OA). OA of the AC joint is a common cause of shoulder pain. Radiological changes of OA in the AC joint do not however correlate with symptoms. Symptomatic OA of the AC joint can be effectively treated with excision of the lateral end of the clavicle.
Anatomy of AC joint
The acromioclavicular (AC) joint is a synovial arthrodial joint with an intra-articular disc, where the oval lateral end of the clavicle articulates with an imperfect incongruent facet of the acromion. Although it is a small joint it supports the shoulder girdle and the upper limb (1).
The joint stability is provided superiorly by reinforcement of the capsule with a strong acromioclavicular ligament and inferiorly the capsule and a weak inferior acromioclavicular ligament. These ligaments provide about 68% of joint stability to superior translation of the clavicle. Additional stability is provided by the coracoacromial and the coracoclavicular (conoid and trapezoid) ligaments (1).
The clavicle rotates about 45 degrees on its own axis. Most of this motion occurs at the sternoclavicular joint and only about 5 to 8 degrees of motion occurs at the sternoclavicular joint (2).
Imaging anatomy of the AC joint
The AC joint is best viewed in an AP projection with a 10-15 degree cephalic angulation (Zanca view). In this view the clavicle is projected off the spine of the scapula (3).
The AC joint space is measured as an average of the cranial and caudal joint space measurements. It is usually less than 5mm. In males the average is about 3.3 plus minus 0.8 and in females the average is about 2.9 plus minus 0.8. In both males and females, the joint space reduces with age and space of less than 0.5 mm can be found. A joint space of more than 7 mm in males and more than 6 mm in females is pathological irrespective of age. There is no significant difference between the left and the right (4).
The coracoclavicular distance is usually less than 11-13mm and the right and left difference is usually less than 5mm (5).
Classification of AC joint injuries
The most commonly used classification for AC joint injuries is the one by Rockwood et al (6):
Type I. Partial tear of acromioclavicular ligaments. X-rays usually normal. Pain, swelling and local tenderness at the AC joint often present. Cross arm test is positive.
Type II. Complete tear of the acromioclavicular ligaments. Plain X-rays usually normal. Some widening of the AC joint space may be present. The inferior border of the clavicle is not elevated beyond the superior border of the acromion. Pain, swelling, tenderness and deformity at the AC joint is usually present.
Type III. Clinically obvious deformity is seen. X-rays show vertical translation with the inferior border of the clavicle elevated beyond the superior border of the acromion.
Type IV. Posterior displacement of the lateral end of the clavicle into or through the trapezius muscle occurs. An axial view will show the posterior displacement of the lateral end of the clavicle.
Type V. Disruption of the deltotrapezius fascia occurs which allows the lateral end of the clavicle to lie under the skin. X-rays show marked displacement of the clavicle beyond the medial end of the acromion.
Type VI. A very rare injury. The lateral end of the clavicle is displaced inferiorly and lies below the acromion and the coracoid (as well as the conjoint tendon).
Treatment of AC joint injuries
The treatment of AC joint injuries remains controversial. Although in recent years more surgeons are opting for surgical treatment of severe AC joint injuries, the outcome of conservative treatment is good on long term follow up. Rawes and Dias (7) reviewed 30 patients, who were treated conservatively for dislocation of the AC joint, at an average of 12.5 years after the injury. They found good outcome in all except one patient. X-rays showed persistent dislocation in 17 patients and in 13 the dislocation improved to a subluxation. Atrophy of lateral end of clavicle (similar to resection of lateral end of clavicle) was seen in completely dislocated joints.
Randomised prospective controlled trials also show good outcome of conservative treatment for dislocation of the AC joint (8 and 9). However, the current trend for the treatment of type I and type II injuries is conservative with symptomatic relief provided by ice, arm sling and analgesics. Heavy lifting and sports are usually avoided for 8 to 12 weeks (10).
The current consensus on the treatment of type III injuries remains that of a conservative approach because the prognosis after conservative treatment is excellent (11, 12 and13). However, patients with type III injuries who continue have symptoms after 3 months may be considered for surgical treatment (10). Some surgeons prefer surgical treatment in patients with type III injury who are heavy labourers and overhead athletes (14).
Type VI injuries are very rare and most of the reported cases are case reports where the patients have been treated surgically (15, 16 and 17). In medically fit patients who have type IV and V injuries the treatment is usually surgical (10).
Many surgical procedures have been described for treatment of AC joint injuries and no one procedure has been shown to be superior to the other. Procedures for acute injuries include reduction and stabilization of the joint with reconstruction of the ligaments. For delayed surgery an excision of lateral end of the clavicle is usually carried out in addition to the reduction, stabilization and ligament reconstruction (10).
Osteoarthritis (OA) of the AC joint
Primary OA of the AC joint is less common than that of the knee or the hip but is more common than OA of the glenohumeral joint. The criteria used to define OA of the AC joint is different in different studies hence the true incidence of primary OA of the AC joint remains unknown (1). Degeneration of the AC joint begins in the second decade of life and progresses with age and by the age of 50 almost all joints will have degenerative changes (18). Radiological reduction of AC joint space occurs with age and by age 60 a joint space of 0.5 mm or less is not abnormal (19). Peterson CJ (20) found age related degenerative changes in the AC joints in cadaveric dissections. After the age of 70, degenerative changes were very common. In one study MR imaging of the shoulder in asymptomatic individuals showed OA of the AC joint in 75% of the individuals (21). Despite the high prevalence of morphological and radiological degenerative changes in the AC joint, the presence of symptomatic OA is relatively rare (22).
The true prevalence of post-traumatic OA of the AC joint is unknown. There appears to be no studies in literature which have traced the natural history of OA of the AC joint. Eight to 42% of patients with type I and type II injuries can be symptomatic on long term follow up (1). Radiological changes are commonly seen in patients with type I and type II injuries but these changes do not correlate with symptoms (23). OA is less likely in higher grade injuries due to separation of bone fragments. However degenerative changes have been observed at surgery in these patient but it is uncertain if the degeneration is the cause of symptoms (10).
Treatment of post-traumatic OA
Conservative treatment for symptomatic OA includes, rest if there is acute exacerbation of symptoms, NSAIDs, activity modification in the form of avoidance of repetitive overhead and cross body activities (24).
Physical therapy in the form of cryotherapy, heat, ultrasound, stretching and mobilisation of the shoulder girdle may also be useful (25).
Significant improvement in pain and function can be seen with steroid injection when other treatments have failed. Short term improvement can be seen in about 93% of the patients (26). The effectiveness of steroid injections reduces with time but long term benefit can be seen up to 5 years (27). These injections can be repeated every 3 to 4 months if all other conservative treatment fails (28).
Conservative treatment is usually tried for at least 6 months before surgical option is considered.
Surgical treatment is usually carried out when all conservative treatment has failed to relieve symptoms which are affecting day to day activities (29). Distal (lateral) clavicle resection is the surgical option for OA of the AC joint and for clavicular osteolysis. This procedure involves the excision of 1 to 2 cm of the distal clavicle by an open or an arthroscopic approach (29). The optimal amount of distal clavicle which should be resected remains unknown (1).
Rabalais and McCarty (30) did a systematic review of the literature for articles on surgical treatment of symptomatic AC joints and they found that most of the reports were level III and level IV evidence. The articles all supported the use of distal clavicle resection for treatment of symptomatic AC joints. They found more ‘good and excellent’ results with arthroscopic surgery but the level of evidence was low. They also found that a ‘simple distal clavicle resection may have worse outcomes when performed after preceding trauma’. This probably reflects the uncertainty of the cause of pain in many of these patients. The presence of OA changes on x-rays may be present in asymptomatic patients. Instability of the AC joint has to be excluded and a definitive diagnosis must be established before surgery is contemplated (31).
Pensak et al (32) in another systematic review of literature comparing arthroscopic versus open resection of the distal clavicle for AC joint pathology found that patients undergoing arthroscopic resection returned to activities faster with similar long term results as the open technic. They also found a poor outcome in patients who had post-traumatic AC instability and in Workman Compensation patients.
AC joint surgery can be associated with complications some of which include, inadequate resection of the clavicle, diagnostic error, joint instability, weakness of the shoulder and infection (29). Inadequate resection of the clavicle can cause persistent pain and this is seen more often with the arthroscopic technique and less with the open technique. Diagnostic errors can be reduced by obtaining a complete resolution of symptoms with intra-articular lignocaine injection. Joint instability is usually caused by injury to the superior acromioclavicular ligament and over resection of the clavicle (29). Other complications such as heterotopic ossification, fracture and suprascapular nerve injury have been described.
Conclusion
The AC joint is a small imperfectly congruent arthrodial which supports the shoulder girdle and the upper limb. Though very little movements occur at the joint, injuries to the joint are not uncommon and the joint is not an uncommon cause of shoulder pain.
The long term outcome of conservative treatment of AC joint injuries is good. Despite a good outcome there is an increasing trend toward surgical treatment of these injuries especially for higher grade injuries.
OA of the AC joint though common is often asymptomatic. The radiological changes in the joint do not correlate with symptoms. Most patients with OA of the AC joint can be treated conservatively. Conservative treatment should be tried for at least 6 months. In the event of failure of conservative treatment and when a definite relationship can be established between the radiological changes in the AC joint and the patient’s symptoms, then excision of the distal end of the clavicle will produce a good outcome. The excision can be done arthroscopically or by an open technique with equally good long term outcome, though with the arthroscopic resection patient can return to activities earlier.
References
1. Shaffer B S. Painful conditions of the Acromioclavicular joint. J Am Acad Orthop Surg. 1999; 7: 176-188.
2. Rockwood CA Jr, Williams GR, Young DC: Injuries to the acromioclavicular joint, in Rockwood CA Jr, Bucholz RW, Green DP, Heckman JD (eds): Fractures in Adults, 4th ed. Philadelphia: Lippincott-Raven, 1996, vol 2, pp 1341-1413.
3. Ursula Nemec, Gerhard Oberleitner, Stefan F. Nemec, Michael Gruber, Michael Weber, Christian Czerny and Christian R. Krestan. MRI Versus Radiography of Acromioclavicular Joint Dislocation. American Journal of Roentgenology. 2011; 197:968-973.
4. Peter CJ and Redlund-John I. Radiographic joint space in normal Acromioclavicular joints. Acta orthop. scand. 54, 431-433, 1983.
5. Alyas F, Curtis M, Speed C, Saifuddin A, Connell D. MR imaging appearances of acromioclavicular joint dislocation. RadioGraphics 2008; 28:463–479.
6. Rockwood CA, Williams G, Young D. Disorders of the acromioclavicular joint. In: Rockwood CA, Matsen FA, eds. The shoulder. Second ed. Vol. 1. Philadelphia: WB Saunders, 1998:483-553.
7. Rawes ML, Dias JJ. Long-term results of conservative treatment for acromioclavicular dislocation. J Bone Joint Surg Br. 1996 May;78(3):410-2.
8. Galpin RD, Hawkins RJ, Grainger RW. A comparative analysis of operation versus nonoperative treatment of grade III acromioclavicular separations. Clin Orthop 1985:193;150-5.
9. Larsen E, Bjerg-Nielsen A, Christensen P. Conservative or surgical treatment of acromioclavicular dislocation: a prospective, controlled, randomized study. J Bone Joint Surg [Am] 1986:68-A;552-5.
10. Fraser-Moodie JA, Shortt NL, Robinson CM. Injuries to the acromioclavicular joint. J Bone Joint Surg [Br] 2008;90-B:697-707.
11. Bjerneld H, Hovelius L, Thorling J. Acromio-clavicular separations treated conservatively: a 5-year follow-up study. Acta Orthop Scand 1983;54:743-5.
12. Schlegel TF, Burks RT, Marcus RL, Dunn HK. A prospective evaluation of untreated acute grade III acromioclavicular separations. Am J Sports Med 2001;29:699-703.
13. Spencer EE Jr. Treatment of grade III acromioclavicular joint injuries: a systematic review. Clin Orthop 2007;455:38-44.
14. Epstein D, Day M, Rokito A. Current concepts in the surgical management of acromioclavicular joint injuries. Bull NYU Hosp Jt Dis. 2012;70(1):11-24.
15. Gerber C, Rockwood CA Jr. Subcoracoid dislocation of the lateral end of the clavicle: a report of three cases. J Bone Joint Surg [Am] 1987;69-A:924-7.
16. McPhee IB. Inferior dislocation of the outer end of the clavicle. J Trauma 1980;20:709-10.
17. Torrens C, Mestre C, Pérez P, Marin M. Subcoracoid dislocation of the distal end of the clavicle. A case report. Clin Orthop Relat Res 1998;(348):121-3.
18. DePalma, A.F. Degenerative changes in the sternoclavicular and acromioclavicular joints in various decades. in: Ann Lecture Series 309. 2nd ed. CC Thomas, Springfield, IL; 1957.
19. Petersson CJ, Redlund-Johnell I. Radiographic joint space in normal acromioclavicular joints. Acta Orthop Scand. 1983 Jun;54(3):431-3.
20. Petersson CJ. Degeneration of the Acromioclavicular Joint: A Morphological Study. Acta Orthop Scand. 1983; 54(3): 434-438.
21. Needell SD, Zlatkin MB, Sher JS, Murphy BJ, Uribe JW: MR imaging of the rotator cuff: Peritendinous and bone abnormalities in an asymptomatic population. AJR Am J Roentgenol 1996;166:863-867.
22. Gartsman GM. Arthroscopic resection of the acromioclavicular joint. Am J Sports Med. 1993;21:71-73.
23. Cox JS. The fate of the acromioclavicular joint in athletic injuries. Am J Sports Med. 1981 Jan-Feb;9(1):50-3.
24. Mazzocca AD, Arciero RA, Bicos J. Evaluation and treatment of acromioclavicular joint injuries. Am J Sports Med 2007;35:316–329.
25. Mall NA, Foley E, Chalmers PN, et al. Degenerative joint disease of the acromioclavicular joint: a review. Am J Sports Med 2013;41:2684–2692.
26. Jacob AK, Sallay PI. Therapeutic efficacy of corticosteroid injections in the acromioclavicular joint. Biomed Sci Instrum 1997;34:380–385.
27. Hossain S, Jacobs LG, Hashmi R. The long-term effectiveness of steroid injections in primary acromioclavicular joint arthritis: a five-year prospective study. J Shoulder Elbow Surg 2008;17:535–538.
28. Lemos MJ, Tolo ET. Complications of the treatment of the acromioclavicular and sternoclavicular joint injuries, including instability. Clin Sports Med 2003;22:371–385.
29. Salvatore Docimo Jr.,, Dellene Kornitsky, Bennett Futterman, David E. Elkowitz. Surgical treatment for acromioclavicular joint osteoarthritis: patient selection, surgical options, complications, and outcome. Curr Rev Musculoskelet Med. 2008 Jun; 1(2): 154–160.
30. Rabalais RD, McCarty E. Surgical treatment of symptomatic acromioclavicular joint problems: a systematic review. Clin Orthop Relat Res. 2007 Feb;455:30-7.
31. Mall NA, Foley E, Chalmers PN, Cole BJ, Romeo AA, Bach BR Jr. Degenerative joint disease of the acromioclavicular joint: a review. Am J Sports Med. 2013 Nov;41(11):2684-92
32. Pensak M, Grumet RC, Slabaugh MA, Bach BR Jr. Open versus arthroscopic distal clavicle resection. Arthroscopy. 2010 May;26(5):697-704.
Dr KS Dhillon FRCS, LLM
Introduction
The true incidence acromioclavicular (AC) injuries is not known because many with such injuries do not seek medical treatment. About 12% of shoulder dislocations involve the AC joint. The treatment of AC joint injury remains controversial although good long term results can be seen in patients treated conservatively. There is an increasing tendency to treat higher grade injuries surgically.
Injuries to the AC joint can predispose the joint to osteoarthritis (OA). OA of the AC joint is a common cause of shoulder pain. Radiological changes of OA in the AC joint do not however correlate with symptoms. Symptomatic OA of the AC joint can be effectively treated with excision of the lateral end of the clavicle.
Anatomy of AC joint
The acromioclavicular (AC) joint is a synovial arthrodial joint with an intra-articular disc, where the oval lateral end of the clavicle articulates with an imperfect incongruent facet of the acromion. Although it is a small joint it supports the shoulder girdle and the upper limb (1).
The joint stability is provided superiorly by reinforcement of the capsule with a strong acromioclavicular ligament and inferiorly the capsule and a weak inferior acromioclavicular ligament. These ligaments provide about 68% of joint stability to superior translation of the clavicle. Additional stability is provided by the coracoacromial and the coracoclavicular (conoid and trapezoid) ligaments (1).
The clavicle rotates about 45 degrees on its own axis. Most of this motion occurs at the sternoclavicular joint and only about 5 to 8 degrees of motion occurs at the sternoclavicular joint (2).
Imaging anatomy of the AC joint
The AC joint is best viewed in an AP projection with a 10-15 degree cephalic angulation (Zanca view). In this view the clavicle is projected off the spine of the scapula (3).
The AC joint space is measured as an average of the cranial and caudal joint space measurements. It is usually less than 5mm. In males the average is about 3.3 plus minus 0.8 and in females the average is about 2.9 plus minus 0.8. In both males and females, the joint space reduces with age and space of less than 0.5 mm can be found. A joint space of more than 7 mm in males and more than 6 mm in females is pathological irrespective of age. There is no significant difference between the left and the right (4).
The coracoclavicular distance is usually less than 11-13mm and the right and left difference is usually less than 5mm (5).
Classification of AC joint injuries
The most commonly used classification for AC joint injuries is the one by Rockwood et al (6):
Type I. Partial tear of acromioclavicular ligaments. X-rays usually normal. Pain, swelling and local tenderness at the AC joint often present. Cross arm test is positive.
Type II. Complete tear of the acromioclavicular ligaments. Plain X-rays usually normal. Some widening of the AC joint space may be present. The inferior border of the clavicle is not elevated beyond the superior border of the acromion. Pain, swelling, tenderness and deformity at the AC joint is usually present.
Type III. Clinically obvious deformity is seen. X-rays show vertical translation with the inferior border of the clavicle elevated beyond the superior border of the acromion.
Type IV. Posterior displacement of the lateral end of the clavicle into or through the trapezius muscle occurs. An axial view will show the posterior displacement of the lateral end of the clavicle.
Type V. Disruption of the deltotrapezius fascia occurs which allows the lateral end of the clavicle to lie under the skin. X-rays show marked displacement of the clavicle beyond the medial end of the acromion.
Type VI. A very rare injury. The lateral end of the clavicle is displaced inferiorly and lies below the acromion and the coracoid (as well as the conjoint tendon).
Treatment of AC joint injuries
The treatment of AC joint injuries remains controversial. Although in recent years more surgeons are opting for surgical treatment of severe AC joint injuries, the outcome of conservative treatment is good on long term follow up. Rawes and Dias (7) reviewed 30 patients, who were treated conservatively for dislocation of the AC joint, at an average of 12.5 years after the injury. They found good outcome in all except one patient. X-rays showed persistent dislocation in 17 patients and in 13 the dislocation improved to a subluxation. Atrophy of lateral end of clavicle (similar to resection of lateral end of clavicle) was seen in completely dislocated joints.
Randomised prospective controlled trials also show good outcome of conservative treatment for dislocation of the AC joint (8 and 9). However, the current trend for the treatment of type I and type II injuries is conservative with symptomatic relief provided by ice, arm sling and analgesics. Heavy lifting and sports are usually avoided for 8 to 12 weeks (10).
The current consensus on the treatment of type III injuries remains that of a conservative approach because the prognosis after conservative treatment is excellent (11, 12 and13). However, patients with type III injuries who continue have symptoms after 3 months may be considered for surgical treatment (10). Some surgeons prefer surgical treatment in patients with type III injury who are heavy labourers and overhead athletes (14).
Type VI injuries are very rare and most of the reported cases are case reports where the patients have been treated surgically (15, 16 and 17). In medically fit patients who have type IV and V injuries the treatment is usually surgical (10).
Many surgical procedures have been described for treatment of AC joint injuries and no one procedure has been shown to be superior to the other. Procedures for acute injuries include reduction and stabilization of the joint with reconstruction of the ligaments. For delayed surgery an excision of lateral end of the clavicle is usually carried out in addition to the reduction, stabilization and ligament reconstruction (10).
Osteoarthritis (OA) of the AC joint
Primary OA of the AC joint is less common than that of the knee or the hip but is more common than OA of the glenohumeral joint. The criteria used to define OA of the AC joint is different in different studies hence the true incidence of primary OA of the AC joint remains unknown (1). Degeneration of the AC joint begins in the second decade of life and progresses with age and by the age of 50 almost all joints will have degenerative changes (18). Radiological reduction of AC joint space occurs with age and by age 60 a joint space of 0.5 mm or less is not abnormal (19). Peterson CJ (20) found age related degenerative changes in the AC joints in cadaveric dissections. After the age of 70, degenerative changes were very common. In one study MR imaging of the shoulder in asymptomatic individuals showed OA of the AC joint in 75% of the individuals (21). Despite the high prevalence of morphological and radiological degenerative changes in the AC joint, the presence of symptomatic OA is relatively rare (22).
The true prevalence of post-traumatic OA of the AC joint is unknown. There appears to be no studies in literature which have traced the natural history of OA of the AC joint. Eight to 42% of patients with type I and type II injuries can be symptomatic on long term follow up (1). Radiological changes are commonly seen in patients with type I and type II injuries but these changes do not correlate with symptoms (23). OA is less likely in higher grade injuries due to separation of bone fragments. However degenerative changes have been observed at surgery in these patient but it is uncertain if the degeneration is the cause of symptoms (10).
Treatment of post-traumatic OA
Conservative treatment for symptomatic OA includes, rest if there is acute exacerbation of symptoms, NSAIDs, activity modification in the form of avoidance of repetitive overhead and cross body activities (24).
Physical therapy in the form of cryotherapy, heat, ultrasound, stretching and mobilisation of the shoulder girdle may also be useful (25).
Significant improvement in pain and function can be seen with steroid injection when other treatments have failed. Short term improvement can be seen in about 93% of the patients (26). The effectiveness of steroid injections reduces with time but long term benefit can be seen up to 5 years (27). These injections can be repeated every 3 to 4 months if all other conservative treatment fails (28).
Conservative treatment is usually tried for at least 6 months before surgical option is considered.
Surgical treatment is usually carried out when all conservative treatment has failed to relieve symptoms which are affecting day to day activities (29). Distal (lateral) clavicle resection is the surgical option for OA of the AC joint and for clavicular osteolysis. This procedure involves the excision of 1 to 2 cm of the distal clavicle by an open or an arthroscopic approach (29). The optimal amount of distal clavicle which should be resected remains unknown (1).
Rabalais and McCarty (30) did a systematic review of the literature for articles on surgical treatment of symptomatic AC joints and they found that most of the reports were level III and level IV evidence. The articles all supported the use of distal clavicle resection for treatment of symptomatic AC joints. They found more ‘good and excellent’ results with arthroscopic surgery but the level of evidence was low. They also found that a ‘simple distal clavicle resection may have worse outcomes when performed after preceding trauma’. This probably reflects the uncertainty of the cause of pain in many of these patients. The presence of OA changes on x-rays may be present in asymptomatic patients. Instability of the AC joint has to be excluded and a definitive diagnosis must be established before surgery is contemplated (31).
Pensak et al (32) in another systematic review of literature comparing arthroscopic versus open resection of the distal clavicle for AC joint pathology found that patients undergoing arthroscopic resection returned to activities faster with similar long term results as the open technic. They also found a poor outcome in patients who had post-traumatic AC instability and in Workman Compensation patients.
AC joint surgery can be associated with complications some of which include, inadequate resection of the clavicle, diagnostic error, joint instability, weakness of the shoulder and infection (29). Inadequate resection of the clavicle can cause persistent pain and this is seen more often with the arthroscopic technique and less with the open technique. Diagnostic errors can be reduced by obtaining a complete resolution of symptoms with intra-articular lignocaine injection. Joint instability is usually caused by injury to the superior acromioclavicular ligament and over resection of the clavicle (29). Other complications such as heterotopic ossification, fracture and suprascapular nerve injury have been described.
Conclusion
The AC joint is a small imperfectly congruent arthrodial which supports the shoulder girdle and the upper limb. Though very little movements occur at the joint, injuries to the joint are not uncommon and the joint is not an uncommon cause of shoulder pain.
The long term outcome of conservative treatment of AC joint injuries is good. Despite a good outcome there is an increasing trend toward surgical treatment of these injuries especially for higher grade injuries.
OA of the AC joint though common is often asymptomatic. The radiological changes in the joint do not correlate with symptoms. Most patients with OA of the AC joint can be treated conservatively. Conservative treatment should be tried for at least 6 months. In the event of failure of conservative treatment and when a definite relationship can be established between the radiological changes in the AC joint and the patient’s symptoms, then excision of the distal end of the clavicle will produce a good outcome. The excision can be done arthroscopically or by an open technique with equally good long term outcome, though with the arthroscopic resection patient can return to activities earlier.
References
1. Shaffer B S. Painful conditions of the Acromioclavicular joint. J Am Acad Orthop Surg. 1999; 7: 176-188.
2. Rockwood CA Jr, Williams GR, Young DC: Injuries to the acromioclavicular joint, in Rockwood CA Jr, Bucholz RW, Green DP, Heckman JD (eds): Fractures in Adults, 4th ed. Philadelphia: Lippincott-Raven, 1996, vol 2, pp 1341-1413.
3. Ursula Nemec, Gerhard Oberleitner, Stefan F. Nemec, Michael Gruber, Michael Weber, Christian Czerny and Christian R. Krestan. MRI Versus Radiography of Acromioclavicular Joint Dislocation. American Journal of Roentgenology. 2011; 197:968-973.
4. Peter CJ and Redlund-John I. Radiographic joint space in normal Acromioclavicular joints. Acta orthop. scand. 54, 431-433, 1983.
5. Alyas F, Curtis M, Speed C, Saifuddin A, Connell D. MR imaging appearances of acromioclavicular joint dislocation. RadioGraphics 2008; 28:463–479.
6. Rockwood CA, Williams G, Young D. Disorders of the acromioclavicular joint. In: Rockwood CA, Matsen FA, eds. The shoulder. Second ed. Vol. 1. Philadelphia: WB Saunders, 1998:483-553.
7. Rawes ML, Dias JJ. Long-term results of conservative treatment for acromioclavicular dislocation. J Bone Joint Surg Br. 1996 May;78(3):410-2.
8. Galpin RD, Hawkins RJ, Grainger RW. A comparative analysis of operation versus nonoperative treatment of grade III acromioclavicular separations. Clin Orthop 1985:193;150-5.
9. Larsen E, Bjerg-Nielsen A, Christensen P. Conservative or surgical treatment of acromioclavicular dislocation: a prospective, controlled, randomized study. J Bone Joint Surg [Am] 1986:68-A;552-5.
10. Fraser-Moodie JA, Shortt NL, Robinson CM. Injuries to the acromioclavicular joint. J Bone Joint Surg [Br] 2008;90-B:697-707.
11. Bjerneld H, Hovelius L, Thorling J. Acromio-clavicular separations treated conservatively: a 5-year follow-up study. Acta Orthop Scand 1983;54:743-5.
12. Schlegel TF, Burks RT, Marcus RL, Dunn HK. A prospective evaluation of untreated acute grade III acromioclavicular separations. Am J Sports Med 2001;29:699-703.
13. Spencer EE Jr. Treatment of grade III acromioclavicular joint injuries: a systematic review. Clin Orthop 2007;455:38-44.
14. Epstein D, Day M, Rokito A. Current concepts in the surgical management of acromioclavicular joint injuries. Bull NYU Hosp Jt Dis. 2012;70(1):11-24.
15. Gerber C, Rockwood CA Jr. Subcoracoid dislocation of the lateral end of the clavicle: a report of three cases. J Bone Joint Surg [Am] 1987;69-A:924-7.
16. McPhee IB. Inferior dislocation of the outer end of the clavicle. J Trauma 1980;20:709-10.
17. Torrens C, Mestre C, Pérez P, Marin M. Subcoracoid dislocation of the distal end of the clavicle. A case report. Clin Orthop Relat Res 1998;(348):121-3.
18. DePalma, A.F. Degenerative changes in the sternoclavicular and acromioclavicular joints in various decades. in: Ann Lecture Series 309. 2nd ed. CC Thomas, Springfield, IL; 1957.
19. Petersson CJ, Redlund-Johnell I. Radiographic joint space in normal acromioclavicular joints. Acta Orthop Scand. 1983 Jun;54(3):431-3.
20. Petersson CJ. Degeneration of the Acromioclavicular Joint: A Morphological Study. Acta Orthop Scand. 1983; 54(3): 434-438.
21. Needell SD, Zlatkin MB, Sher JS, Murphy BJ, Uribe JW: MR imaging of the rotator cuff: Peritendinous and bone abnormalities in an asymptomatic population. AJR Am J Roentgenol 1996;166:863-867.
22. Gartsman GM. Arthroscopic resection of the acromioclavicular joint. Am J Sports Med. 1993;21:71-73.
23. Cox JS. The fate of the acromioclavicular joint in athletic injuries. Am J Sports Med. 1981 Jan-Feb;9(1):50-3.
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