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inside Achilles tendon rupture Achilles tendinopathy Retrocalcaneal bursitis Sever’s disease Ankle arthritis

The author

DR PETER LAM, specialist orthopaedic foot and ankle surgeon, in private practice at Chatswood, and a consultant at Sydney Olympic Park, Narrabeen, Kensington and Kogarah, Sydney, NSW.

Hindfoot and ankle pain The Achilles tendon THE Achilles tendon is the largest tendon in the body, connecting the calf muscles to the calcaneus. The insertion of the tendon (figure 1) is about 1.5cm distal to the tip of the superior tuberosity of the calcaneus. Interposed between the superior tuberosity anteriorly and the tendon posteriorly is the retrocalcaneal bursa. Posterior to the tendon is a superficial bursa, which lies directly under the skin.

The Achilles is enclosed by a paratenon. The paratenon is not lined with synovial tissue; it contains blood vessels that assist in tendon nourishment. The tendon is narrowest 4cm above the level of insertion into the calcaneus. This narrowing is located in a hypovascular zone that extends from 2-6cm proximal to the tendon’s insertion. This zone is the most common site of tendon pathology, www.australiandoctor.com.au

including tendinosis and rupture. The Achilles tendon transmits forces ranging from 2-3 times body weight in walking to 4-6 times body weight in running and jumping. The Achilles tendon, by virtue of its structure and functional demands, is subject to a spectrum of overuse injuries. Disorders of the Achilles tendon (figure 2) are very common in the cont’d next page 10 September 2010 | Australian Doctor |

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running athlete, with a reported incidence ranging from 6.5% to 18.7%. This spectrum of disorders can be subdivided into: • Acute Achilles tendon rupture. • Non-insertional Achilles tendinopathy. • Insertional Achilles tendinopathy. • Retrocalcaneal bursitis. Non-insertional Achilles tendinopathy tends to occur in younger patients, primarily runners, whereas insertional Achilles tendinopathy tends to occur in middleaged, ‘weekend warrior’ athletes.

Figure 2: Achilles tendon disorders.

Figure 1: Anatomy of the hindfoot. Soleus Peroneus longus Peroneus brevis Lateral malleolus and subcutaneous bursa

Calcaneal (Achilles) tendon

Non-insertional Achilles tendinitis

Common sheath of peroneus longus and brevis tendons Retrocalcaneal bursitis

Subcutaneous calcaneal bursa Subtendinous calcaneal bursa

Insertional Achilles tendinitis

Calcaneus Superior and inferior peroneal retinacula

Abductor digiti minimi

Acute Achilles tendon rupture MOST rupture of the Achilles tendon occurs during sporting activities. It is more common between the ages of 30-40. The mechanism of the rupture is typically indirect loading, such as when pushing off with the foot when the knee is extended as seen in sprinting and jumping sports, or with unexpected dorsiflexion of the ankle with contraction of the calf muscle such as when stepping into a hole.1 Direct impact on the tendon, such as being kicked or hit, leading to rupture is less common and the frequency of this type of injury ranges from 1% to 10%. Other causes include fluoroquinolone treatment and oral or injected corticosteroids. Acute Achilles tendon rupture typically occurs 4-6cm proximal to its insertion into the calcaneus. Proximal rupture at the musculotendinous junction is reported to comprise 10-15% of all Achilles ruptures. Rupture at the insertion site is rare and has a high association with insertional Achilles tendinopathy and prior steroid injection in the area.

Clinical presentation Patients often describe a feeling that they have been hit in the calf, but when they turn around there is no one next to them. Some sense or hear a “pop” at the time of the rupture. There is intense pain but the pain diminishes over the first few days of the injury in most patients. Patients are unable to perform a single-limb heel raise and this causes them to walk with a limp. Examining the extremity with the patient in a prone position usually reveals the non-affected foot to be sitting in a slightly plantarflexed posture, while the affected foot sits with the ankle at 90 degrees, that is, not in plantarflexion (figure 3). There is a palpable gap 2-6cm proximal to the insertion site. However, this can sometimes be difficult to appreciate if there is significant swelling. The palpable defect is pathognomonic of an acute Achilles tendon rupture. A Thompson (calf squeeze) test (figure 4) is done with the patient lying in a prone position. The calf is squeezed at the thickest portion of the gastrocnemius–soleus complex. In the injured leg there is no

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Figure 3: Achilles tendon rupture. Loss of resting tone in the foot with the patient lying prone.

Figure 4: Thompson test — the foot cannot plantarflex when the calf is squeezed, as the Achilles tendon has ruptured.

significant plantarflexion in response to the squeeze test, while in the intact leg there is plantarflexion of the foot. Usually the patient can still plantarflex the ankle when not weight-bearing because of the intact tibialis posterior, long toe flexors and peroneal tendons. Delayed or misdiagnosis of acute Achilles tendon rupture is not uncommon. Inglis and Sculco documented that 23% of acute Achilles tendon ruptures were missed by the first doctor to examine the patient.2 Misdiagnosis may lead to suboptimal treatment.

Investigation Although most Achilles tendon ruptures can be diagnosed clinically, ultrasound and MRI can be helpful in confirming the diagnosis and assessing the size of the gap between the tendon ends. The result of the ultrasound is more reliable if performed by a musculoskeletal ultrasound radiologist.

Management Treatment options depend on patient expectations, performance levels and the presence of systemic illness. When deciding on operative versus non-operative management, the risks and benefits of the various treatment methods need to be carefully discussed with the patient. Closed treatment with prolonged short-leg-cast immobilisation, with www.australiandoctor.com.au

the foot plantarflexed and nonweight-bearing for 6-8 weeks risks loss of strength, decreased motion and increased re-rupture rate. When treated closed, the re-rupture rate is about 20%; with operative intervention, the re-rupture rate is only 2%. The strength of the tendon after non-operative treatment is only 75% of normal strength, but with surgical repair the tendon strength is near normal. The greatest advantage of open repair is restoration of the tendon’s anatomical length and near-normal tendon strength. Surgical repair is recommended for all competitive athletes who plan to return to their previous activity levels. However, surgery, despite its superior results, does

have its own inherent risks, including infection and wound breakdown. The risk of surgical complications can be as high as 5%. Surgical repair is followed by an aggressive physiotherapy regimen. I keep the leg non-weight-bearing in a backslab for two weeks after the surgical repair. After removal of sutures, a walker boot is applied and the patient is then allowed to progress to full weight-bearing. The boot is worn for about six weeks. This is followed by physiotherapy. Controlled early mobilisation results in significant reduction in adhesion formation and a stronger tendon repair. The recovery to maximal strength takes 12 months. cont’d page 30

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Non-insertional Achilles tendinopathy Epidemiology ACHILLES tendinopathy is common in the general population. It tends to be an overuse injury, with a higher incidence in runners. The annual incidence of Achilles tendinopathy has been reported to be 7-9% in elite runners.1 In studies of conditions affecting the Achilles tendon, 66% are non-insertional Achilles tendinopathy.3 This condition is more common in men in whom running is their main sport.

Figure 5: Painful lump in the Achilles tendon 4-6cm proximal to its insertion into the calcaneus.

Clinical presentation The patient presents with a painful lump in the Achilles tendon, located 4-6cm proximal to its insertion into the calcaneus (figure 5). The pain is intermittent. When the pain occurs, it is worse with walking and running activities, especially on inclines, hills and stairs. This is often associated with morning stiffness. There may be a history of fluoroquinolone use.

Figure 6: MRI of non-insertional Achilles tendinopathy.

Investigation Plain radiograph is usually uninformative, but occasionally calcification can be seen in the tendon. Ultrasound by a musculoskeletal radiologist may show the tendon degeneration. However, the focal hypoechoic areas corresponding to the areas of degeneration within the Achilles tendon can sometimes be reported as “partial tears or ruptures” by an inexperienced ultrasound radiologist. MRI is the investigation of

choice because of its ability to quantify the amount of intratendinous degeneration (figure 6).

Management Initial treatment begins with basic non-operative modali-

ties, including: • Modifying activity. • Introducing cross-training methods. • Stretching. • Heel lifts to reduce tension in the tendon. • Massage. • Heat and cold therapy. • Weight reduction (if overweight). • Use of an oral NSAID. However in a randomised, double-blind placebo-controlled trial in 1992, oral piroxicam was found to be no more effective than placebo. 4 Also, a 2007 Cochrane review stated there was at best weak clinical evidence for the use of NSAIDs in the treatment of Achilles tendinopathies.5 Eccentric, heavy-load calfstrengthening training (a 12week program) has produced good results in 90% of patients in multiple studies.6 Eccentric strengthening involves strengthening the calf with the calf muscle–tendon unit in an elongated position. This is achieved by dropping the heel over a step. This eccentric program is supervised by a physiotherapist and forms the mainstay of nonoperative treatment for noninsertional Achilles tendinopathy. Corticosteroid injections for the treatment of Achilles tendinopathy are associated with a risk of tendon rupture. Meta-analysis of the effects of corticosteroid injections has shown little benefit and there is insufficient evidence to accurately predict

the exact rupture rate. Gill reported on fluoroscopically guided low-volume peritendinous corticosteroid injection for Achilles tendinopathy and found the results disappointing, as 53% of patients stated that their condition was unchanged and 7% stated that they were worse off.7 Thus corticosteroid injections into the Achilles tendon should be avoided, as the steroid can predispose the tendon to rupture especially if an intratendinous injection is given. If a corticosteroid injection is to be given, it should be done under ultrasound guidance. Extracorporeal shockwave therapy (ESWT) has been shown to stimulate angiogenesis and inhibit afferent pain-receptor function and may improve soft tissue healing. This lowenergy shock-wave therapy is given in three-weekly sessions. There is some evidence ESWT may be beneficial in the treatment of non-insertional Achilles tendinopathy.8 Polidocanol as a sclerosing agent for treatment of noninsertional Achilles tendinopathy has been reported with promising results although all the reports are from one institution in Sweden. 9 The assumption with sclerosing agent treatment is that the source of pain is the neovascularisation in the damaged tendon. The usual protocol is 2-3 injections given about 6-8

weeks apart. Each injection is followed by a few days of rest, and high-impact activity is restricted for two weeks. Further studies of the treatment are required. Topical glyceryl trinitrate may be beneficial in the treatment of non-insertional Achilles tendinopathy.10 The rationale behind this treatment is that nitric oxide in animal models seems to stimulate collagen synthesis in fibroblasts. There are some conflicting clinical studies and further validation is needed. Platelet-rich plasma injections have gained popularity recently, but few welldesigned studies are available for review. Non-insertional Achilles tendinopathy is a common disorder, but the pathology is still not completely understood. At least 90% of patients find relief with traditional conservative treatments and the eccentric, heavy-load calf-strengthening program. Further prospective studies are needed to demonstrate clinical efficacy of the other non-operative treatment methods. Operative intervention should only be considered after a comprehensive program of non-operative treatment has failed. In most cases, if symptoms have persisted for six months despite non-operative management, surgical treatment is warranted. Most of the literature supports a surgical success rate of 75-100%.

Insertional Achilles tendinopathy THIS is a condition of chronic overuse. It tends to occur in older patients and in overweight sedentary individuals.

Clinical presentation There is posterior heel pain. The pain is initially intermittent. It is exacerbated by walking and running up hills and stairs and on hard surfaces. Early morning stiffness is typical. Posterior heel prominence or swelling is common in chronic cases. On examination, there is tenderness and swelling or prominence at the site of insertion of the Achilles tendon into the calcaneus. There is often tenderness and swelling in the adjacent retrocalcaneal bursa.

Figure 7: Insertional Achilles tendinopathy, showing posterior heel spur.

Figure 8: MRI of insertional Achilles tendinopathy. Degenerate tendon

Calcification

Spur

Investigation Plain radiography (weight-bearing) will usually show the presence of a posterior heel spur on the lateral view (figure 7). This is due to calcification/ossification of the Achilles insertion secondary to the tendon degeneration. Ultrasound can be very useful in identifying the retrocalcaneal bursitis. MRI is the investigation of choice because of its ability to quantify the amount of intratendinous degeneration and identify

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retrocalcaneal bursitis (figure 8).

Management As with the management for noninsertional Achilles tendinopathy, the initial treatment begins with basic non-operative modalities, including: • Activity modification. • Stretching. • Heel lifts to reduce tension in the tendon. www.australiandoctor.com.au

• Massage. • Heat and cold therapy. • Weight reduction (if overweight). • NSAIDs. Shoes with a small heel, or an open-heeled shoe such as a clog, can help by reducing the direct pressure on the Achilles insertion. Cross-training with an emphasis on low-impact exercise such as cycling, swimming or aqua-aerobics is helpful. Corticosteroid injection is controversial because there are insufficient data to determine the comparative benefits and risks. In general, caution should be used when using corticosteroid injections around the Achilles insertion because of the theoretical concern of acute Achilles rupture. An ultrasound-guided corticosteroid injection into the retrocalcaneal bursa can be considered when symptoms of retrocalcaneal bursitis predominate. A randomised controlled trial by Rompe showed patients with insertional Achilles tendinopathy have poor success (28%) with the eccentric heavy-load calf-strengthening program.11 Platelet-rich plasma injection has gained popularity recently, but scientific evidence on the effectiveness

of this treatment is sparse and controversial, especially with regard to the long-term clinical benefits. Thus, unlike non-insertional Achilles tendinopathy, apart from the general treatments mentioned in the first paragraph of this section, there is no effective specific treatment for insertional Achilles tendinopathy. Surgical treatment is considered in patients with chronic insertional Achilles tendinopathy if symptoms persist despite at least six months of the non-operative treatment. The surgery involves removal of the degenerate Achilles tendon (at the insertion), decompression of the mechanical pressure from the adjacent calcaneus, then reattaching the Achilles insertion into the calcaneus. In my practice, the patient generally remains non-weight-bearing for two weeks in a backslab, then progresses to full weight-bearing in a walker boot for a further six weeks. This is followed by physiotherapy. Recovery to maximal strength can take 6-12 months. Recovery in patients who are carrying excess weight tends to be slower. The reported success from this procedure is about 85%.12

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Retrocalcaneal bursitis Retrocalcaneal bursitis

above its insertion into the calcaneus. The pain is aggravated by dorsiflexion of the ankle beyond the neutral position and is relieved by plantarflexion.

Figure 9: Retrocalcaneal bursitis.

THIS is inflammation of the retrocalcaneal bursa. It occurs mainly in young runners but may also occur in patients with rheumatoid arthritis. The overall incidence of retrocalcaneal bursitis with rheumatoid arthritis is reported to be 18%.13 In young runners the retrocalcaneal bursitis is due to the presence of a Haglund deformity, and the Achilles insertion is otherwise normal (ie, these patients do not have insertional Achilles tendinopathy). A Haglund deformity is due to a prominence of the posterosuperior tuberosity of the calcaneus.

Investigation

located just anterior and slightly superior to the Achilles insertion into the calcaneus. The pain is worse with walking and running activities, especially on inclines and stairs. On examination there is tenderness and mild swelling (a bulge) medial and lateral to the Achilles tendon just

Clinical presentation There is posterior heel pain. The pain and swelling is

Summary — Achilles tendon disorders ACHILLES tendon disorders are a spectrum of disorders that can be divided into two main groups: noninsertional and insertional. In the insertional group, they can be subdivided into insertional Achilles tendinopathy and retrocalcaneal bursitis. The clinical features and initial management program in the conditions within each group are similar. It is important to note that in most patients good pain relief can be achieved using simple non-operative measures. Surgery is more often required for treatment of recalcitrant insertional Achilles tendinopathy or retrocalcaneal bursitis.

A weight-bearing radiograph of the foot and ankle will often show a prominent posterosuperior tuberosity of the calcaneus (figure 9). When difficulty in diagnosis arises, an MRI and bone scan may be helpful. MRI will show an enlarged, inflamed bursa (figure 9). A bone scan will show increased uptake along the superior tuberosity of the calcaneus.

Management Shoes with a small heel or open-heeled shoe, such as a

clog, can help by reducing the direct pressure on the retrocalcaneal bursa. In the acute situation, activity modification is needed, with avoidance of hills, inclines and running, and use of heel lifts to reduce tension on the retrocalcaneal bursa. Injection of corticosteroid into the retrocalcaneal bursa has been advocated. This can be an effective shortterm treatment but the bursitis tends to recur, as it does not remove the Haglund deformity. There is always a concern, even though the injection is into the bursa and not into the Achilles tendon, that the steroid solution may come into contact with the Achilles tendon. Thus repeated steroid injections into the retrocalcaneal

bursa are not recommended. If debilitating symptoms persist despite at least six months of non-operative treatment, surgery is indicated. This involves resection of the prominent posterosuperior tuberosity of the calcaneus and the retrocalcaneal bursa. This may be done either endoscopically or by open surgery. The advantages of the endoscopic technique are less postoperative pain, more rapid rehabilitation and an earlier return to sports. When treating a running athlete with recalcitrant retrocalcaneal bursitis, always exclude the possibility of a systemic inflammatory disease. This is especially important if the process is bilateral.

Sever’s disease OSTEOCHONDROSIS of the posterior calcaneal apophysis was first described by Sever in 1912. This condition is considered to be a traction apophysitis. The patients are often aged about 10.

child may walk on the toes and is often unwilling to participate in physical activities. On examination the Achilles insertion into the posterior calcaneus is tender to palpation and there is soft tissue swelling.

Clinical presentation The child presents with posterior heel pain that is exacerbated by activity such as running and jumping. The

Investigation The radiographic findings are nonspecific. There is increased space

between the apophysis and the body of the calcaneus. The apophysis appears irregular and sclerotic. This appearance can be seen in asymptomatic individuals.

Management The diagnosis of Sever’s disease is made clinically. Treatment consists of rest and calf-stretching exercises. The child should avoid running and

jumping activities until the symptoms settle. Low-impact exercise such as cycling and swimming may be tolerated. A heel lift or an orthotic to lift the heel may be of benefit. A short leg-walking cast or a walker boot is seldom required. Sever’s disease is a self-limiting condition and normal activities can be resumed after the pain has subsided.

Ankle arthritis THE pathogenesis of ankle osteoarthritis is a complex event to which anatomical, biomechanical and metabolic factors may all contribute. The incidence of osteoarthritis in the joints of the lower limbs is quite variable despite these joints being subject to similar loads during weight-bearing. The ankle appears to be more resistant to primary osteoarthritis but more susceptible to post-traumatic degeneration. The true incidence of osteoarthritis in the ankle joint is difficult to determine mainly because of the variation between degenerative change and clinical correlation. Cadaveric, radiographical and clinical studies all indicate that arthritis at the ankle is less common than at the knee or hip. Although symptomatic osteoarthritis does present at the ankle, it is rare even in the elderly. In clinical practice, patients who have symptomatic arthritis of the knee are seen about 8-9 times more commonly than those who have symptomatic arthritis of the ankle.14 It is estimated that knee replacement is performed about 25 times more frequently than either arthrodesis or arthroplasty of the ankle. Painful ankle arthritis is more commonly due to post-traumatic degeneration. This may follow an ankle fracture or dislocation. Recurrent ankle instability may lead to either medial or lateral ankle arthritis (figure 10). In this group of patients, the ankle will

Figure 10: Medial ankle arthritis as a result of recurrent ankle sprains.

often still have a relatively good range of motion. This compares with the patient with generalised ankle arthritis, who will typically have significant ankle stiffness.

Clinical presentation The ankle pain is worse with walking activities, especially on stairs, inclines and hills, and uneven ground. There is often night pain or pain at the end of the day. The pain may be worse when the weather changes, such when it becomes colder or when it is about to rain. Examination may reveal ankle swelling due to ankle effusion (from synovitis), and anterior ankle jointline tenderness. There may be calf atrophy from disuse. There may be mal-alignment, either varus or valgus, if there is predominant medial or lateral ankle arthritis, respectively. There will be loss of ankle motion, especially in the dorsiflexion range, due to the presence of anterior ankle impingement spurs that frequently accompany the development of ankle arthritis. There is pain on movement of the ankle joint.

Investigation A weight-bearing radiograph of the ankle will show the severity of the ankle arthritis and any associated ankle deformity. CT can be helpful to assess for the presence of associated subtalar joint arthritis.

Management Initial treatment begins with basic non-operative modalities including www.australiandoctor.com.au

activity modification with emphasis on low-impact exercise, such as cycling, swimming and aqua-aerobics, weight reduction (if overweight) and oral NSAIDs. Corticosteroid injection into the ankle joint may provide short-term relief. Data regarding dietary supplementation and viscosupplementation and their effects in the ankle joint are still evolving. Glucosamine and chondroitin sulfate are the most well-marketed dietary supplements. The presumption of their benefit in the ankle is based largely on promising results from their use in knee osteoarthritis. Visco-supplementation has proved to be efficacious in the management of knee osteoarthritis. Preliminary studies suggest a benefit for visco-supplementation use in ankle osteoarthritis. Further research is needed to determine the onset and duration of efficacy for dietary supplementation and viscosupplementation. Operative treatment is considered only after all conservative measures have failed. The current gold standard surgical treatment for ankle arthritis is ankle fusion. This may be done arthroscopically (when there is minimal or no deformity or bone loss) or open. The main advantages or arthroscopic fusion (figure 11) are that it is associated with: • Lower morbidity (significantly less postsurgical pain). • Shorter hospital stay. • More rapid mobilisation. cont’d next page 10 September 2010 | Australian Doctor |

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HOW TO TREAT Hindfoot and ankle pain

Figure 11: Arthroscopic ankle fusion.

Figure 12: Total ankle replacement.

arthritic joints and may cause them to become symptomatic. Ankle replacement (figure 12) is an alternative surgical option for patients with painful ankle arthritis. It maintains ankle motion and does not increase the risk of subtalar and talonavicular arthritis. However, the longevity of the ankle replacement is a concern. The longest follow-up study is from

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• Reduced risk of wound complication. After ankle arthrodesis the ankle arthritis pain goes and the gait is relatively normal, with a shortened stride length. Ankle fusion is relatively contraindicated if there is associated subtalar or talonavicular joint arthritis, as ankle fusion will place more stress on these adjacent

Conclusion THE spectrum of Achilles tendon disorders can be divided into acute Achilles tendon rupture, noninsertional Achilles tendinopathy, insertional Achilles tendinopathy and retrocalcaneal bursitis. Good pain relief can be achieved using nonoperative measures in most patients. These include activity modification concentrating on low-impact activities such as cycling, swimming and aqua-aerobics, use of heel lifts or wearing shoes with a small heel or open-heeled shoes, and oral anti-inflammatory medication. Corticosteroid injections into the Achilles tendon should be avoided, as the steroid will predispose to Achilles tendon rupture. If symptoms persist despite at least six months of non-operative treatment, surgery may be required.

Fiona FIONA, 57, presents with 10month history of increasing posterior heel pain. The pain was initially intermittent and worse with walking especially, on inclines and stairs. Fiona’s weight has increased by 10kg over the past six months, as the posterior heel pain has restricted her walking activities. She had been a keen walker. She is unable to wear a closed shoe due to the pressure of the heel counter-pressing against her posterior heel. She finds sandals or clogs with a small heel more comfortable. She has tried meloxicam, with some minor relief. Examination revealed tenderness and swelling of the distal Achilles tendon at its insertion into the calcaneus. There was swelling and tenderness in the adjacent retrocalcaneal bursa. The more proximal Achilles tendon was not tender. Fiona weighed 80kg. Weight-bearing radiographs show the presence of a posterior heel spur at the site of the Achilles tendon insertion into the calcaneus.

Fiona has painful insertional Achilles tendinopathy. I encouraged her to try low-impact exercise such as cycling, swimming and aqua-aerobics. Ultimately she required surgical reconstruction of the Achilles insertion. She was non-weight-bearing in a backslab for two weeks after the surgery. This was followed by weight-bearing in a walker boot for a further six weeks. She started physiotherapy eight weeks after surgery, when she was able to be weaned off use of the walker boot. She was comfortable going on a long walk four months after surgery. The recovery to maximal strength took 12 months. | Australian Doctor | 10 September 2010

Sweden. It shows the survival rate of the ankle replacement is 77% over 15 years. 15 Thus 23% of ankle replacements will require revision within 15 years of the procedure. If the ankle replacement fails, it may need to be converted to an ankle fusion, depending on the degree of bone loss that has occurred as a result of the loose ankle replacement.

Author’s case studies

Comment

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References

Matt

Comment

Matt is a 26-year-old runner. He would run more than 50km a week. He presents with a fourmonth history of left posterior heel pain. The pain has been worse over the past month and is worse with running, especially up hills and inclines. He has not been able to run over the last few weeks because of the pain, and experiences increasing pain when walking up hills and inclines. He has discomfort in his posterior heel when he wears his dress shoes. He has tried orthotics without significant improvement. He is keen to resume running. Examination reveals mild swelling in the posterior heel. The swelling and tenderness is located at the retrocalcaneal bursa, on either side of the Achilles tendon at its insertion. There is no tenderness at the Achilles insertion into the posterior calcaneus. A lateral weight-bearing radiograph showed a Haglund deformity. MRI confirmed the retrocalcaneal bursitis, with no evidence of significant insertional Achilles tendinopathy.

Matt has painful retrocalcaneal bursitis with a Haglund deformity. Ultimately he will require surgical treatment, as he is keen to return to running. This is because the other treatment modalities are unlikely to allow him to return to the level of running he desires. The non-surgical treatment options for Matt include: • Heel lift to reduce the pressure of the Haglund deformity on the retrocalcaneal bursa. • Activity modification concentrating on cycling and swimming and avoiding hills, inclines and stairs. • A trial of ultrasound-guided corticosteroid injection into the retrocalcaneal bursa. From the surgery point of view, I would recommend endoscopic debridement of the retrocalcaneal bursa and Haglund deformity. This is a day surgery ‘keyhole’ procedure. Matt may weight-bear fully eight weeks postoperatively. He will start physiotherapy two weeks after surgery. He may start light jogging 2-3 months after surgery, depending on his comfort and progress with physiotherapy.

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1. Lysholm J, Wiklander J. Injuries in runners. American Journal of Sports Medicine 1987; 15:168-71. 2. Inglis AE, Sculco TP. Surgical repair of ruptures of the tendo Achilles. Clinical Orthopaedics and Related Research 1981; 156:160-69. 3. Kvist M. Achilles tendon injuries in athletes. Sports Medicine 1994; 18:173-201. 4. Astrom M, Westlin N. No effect of piroxicam on Achilles tendinopathy: a randomized study of 70 patients. Acta Orthopaedica Scandinavica 1992; 63:63134. 5. McLaughlin GJ, Handoll HHG. Interventions for treating acute and chronic Achilles tendonitis. Cochrane Database of Systematic Reviews 2007;2:CD000232. 6. Alfredson H, et al. Heavy load eccentric calf muscle training fort the treatment of chronic Achilles tendinosis. American Journal of Sports Medicine 1998; 26:360-66. 7. Gill SS, et al. Fluoroscopically guided low volume peritendinous corticosteroid injection for Achilles tendinopathy. A safety study. Journal of Bone and Joint Surgery (America) 2004; 86:802-06. 8. Rompe JD, et al. Eccentric loading, shock wave treatment, or a wait and see policy for tendinopathy of the main body of the tendon Achilles. American Journal of Sports Medicine 2007; 35:374-83. 9. Alfredson H, Ohberg L. Sclerosing injections to areas of neo-vascularization reduce pain in chronic Achilles tendinopathy: a double blind randomized controlled trial. Knee Surgery, Sports Traumatology, Arthroscopy 2005; 13:338-44. 10. Paoloni JA, Murrell GAC. Three-year followup study of topical glyceryl trinitrate treatment of chronic noninsertional Achilles tendinopathy. Foot and Ankle International 2007;28:106468. 11. Rompe JD, et al. Eccentric loading compared with shock wave treatment for chronic insertional Achilles tendinopathy. A randomized.controlled trial. Journal of Bone and Joint Surgery (America) 2008; 90:52-61. 12. McGarvey WC, et al. Insertional Achilles tendinosis: surgical treatment through a central tendon splitting approach. Foot and Ankle International 2002; 23:19-25. 13. Falsetti P, et al. Sonographic study of calcaneal entheses in erosive osteoarthritis, nodal osteoarthritis, rheumatoid arthritis and psoriatic arthritis. Scandinavian Journal of Rheumatology 2003; 32:229-34. 14. Cushnaghan J, Dieppe P. Study of 500 patients with limb joint osteoarthritis. I. Analysis by age, sex, and distribution of symptomatic joint sites. Annals of the Rheumatic Diseases 1991; 50:8-13. 15. Henricson A, et al. The Swedish Ankle Arthroplasty Register: an analysis of 531 arthroplasties between 1993 and 2005. Acta Orthopaedica 2007; 78:56974.

Online resource American Orthopaedic Foot and Ankle Society: www.aofas.org cont’d page 34

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GP’s contribution

DR DAVID SENA Dee Why, NSW

A case of unusual Achilles tendinitis MRS M, 58, presented with a 6-8-week history of pain in the back of her heels. She had been well in the previous 12 months apart from a persistent UTI. She had no regular exercise pattern, and joggers were her preferred footwear. The pain had come on gradually, initially worse in the morning and easing when she began weight-bearing, but her pain had dramatically worsened for two weeks despite rest and topical diclofenac gel. On examination she was overweight and had difficulty walking. Both Achilles tendons were swollen and

extremely tender. She was unable to stand on her toes and there was crepitus in the tendons on passive movement. Clinically, Achilles tendinitis was suspected. She was referred to a local physiotherapist, who taught her how to strap, stretch and ice her ankle. She was also given celecoxib for 10 days. However, two weeks later her pain was no better and she returned for review. She had further investigations, including: • X-ray. • Ultrasound. • FBE, ESR and CRP. • Rheumatoid factor, antinuclear antibody and extractable nuclear antibodies. • Uric acid. Mrs M phoned for her results. The blood tests were unremarkable apart from a CRP of 19 (normal range