- Email: [email protected]
Soft tissue disorders of the foot and ankle: The Achilles tendon and plantar fascia
i n d i a n j o u r n a l o f r h e u m a t o l o g y 9 ( 2 0 1 4 ) S 3 7 eS 4 1
ScienceDirect Available online at www.indianjrheumatol.com and www.sciencedirect.com
Review Article
Soft tissue disorders of the foot and ankle: The Achilles tendon and plantar fascia Cathy A. Speed Cambridge Centre for Health & Performance, Conqueror House, Vision Park, Cambridge CB24 9ZR, UK
abstract Keywords:
Disorders of the foot and ankle are common in the rheumatology clinic and are frequently
Soft tissue
soft tissue in origin. In this context, pain can arise from tendon, ligament, nerve, bursa and
Foot
muscle. Pain and disability are common consequences and hence the rheumatologist must
Ankle
have a comprehensive understanding of the diagnosis and management of such
Tendinopathy
complaints.
Plantar fasciitis
1.
Copyright © 2014, Indian Rheumatology Association. All rights reserved.
Introduction
Disorders of the foot and ankle are common in the rheumatology clinic and are frequently soft tissue in origin. In this context, pain can arise from tendon, ligament, nerve, bursa and muscle. Pain and disability are common consequences and hence the rheumatologist must have a comprehensive understanding of the diagnosis and management of such complaints. The most common soft tissue disorders in this region are tendinopathies affecting the Achilles tendon, and plantar fasciitis. These complaints will form the subject of this article.
2.
Principles of evaluation
Evaluation of all soft tissue complaints starts with taking a comprehensive history, followed by a careful clinical examination. Imaging modalities are often useful, and indeed diagnostic ultrasound should be considered as an extension of the clinical examination.
The cardinal symptom of a soft tissue injury is one of pain. Other symptoms include stiffness, clicking, instability, and neurological symptoms, all of which can lead to loss of function. A description of the mechanism of onset should be obtained and a pain history recorded, including the site, nature, and radiation and relieving and exacerbating factors identified. If the presentation is acute, the degree of swelling often corresponds to the severity of the injury. Always seek to identify the cause of the complaint. Intrinsic and extrinsic factors that should be considered are given in Table 1. Clarify what measures have already been taken in the form of analgesia and other treatments. Examination includes evaluation of lower limb biomechanics, functional core control and proprioception. Evaluate for lower limb musculotendinous stiffness, especially the calves and hamstrings. In the acute phase, assess for swelling, bruising (in the case of Achilles or plantar fascial rupture). Assess range of motion of lower limb joints, and palpate the affected areas for tenderness, swelling and in the case of an Achilles rupture, a palpable gap which is not always apparent. Patients with a severe Achilles injury will be unable to perform a single heel raise. Note that Achilles ruptures are often missed at initial presentation due to a lack of full assessment.
E-mail address: [email protected]. http://dx.doi.org/10.1016/j.injr.2014.09.012 0973-3698/Copyright © 2014, Indian Rheumatology Association. All rights reserved.
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i n d i a n j o u r n a l o f r h e u m a t o l o g y 9 ( 2 0 1 4 ) S 3 7 eS 4 1
Table 1 e Factors predisposing soft tissue disorders of the foot and ankle. Intrinsic factors: Biomechanical malalignments including gait abnormalities (usually hyperpronation) Stiff gastrocnemiusesoleus complex, tight hamstrings Leg length discrepancy Muscle imbalance Hyper/hypomobile hindfoot Haglund's deformity Spondyloarthritides (enthesopathies) Medical conditions Extrinsic factors: Overtraining Training type (e.g. too much heavy weight training) Poor footwear (too old, poor cushioning, high heel tab, wrong size) Poor technique Inappropriate surface Environment (too hot/too cold) Iatrogenic: fluoroquinolones, corticosteroid injections Anabolic steroid abuse
3.
Relevant anatomy and pathophysiology
The Achilles tendon forms as a broad tendinous sheet from the gastrocnemius muscle in the mid leg. The soleus muscle is deep and adherent to the Achilles and allows a blood supply to the Achilles. The soleus fibres blend with, and become part of, the Achilles tendon. When complete, the inferior fibres of the Achilles tendon twist obliquely in their descent to their insertion onto the posterior aspect of the mid-third of the calcaneus. The Achilles tendon is invested by a paratenon, consisting of loose elastic connective tissue, invest the Achilles and when healthy stretches with movement of the tendon, allowing the tendon to glide freely. The paratenon supplies much of the blood supply of the Achilles. Vascularity in the area 2e5 cm above the insertion, where much pathology occurs, is poor.1 Two bursae are associated with the Achilles tendon - the superficial retroachilles bursa, and the deeper retrocalcaneal bursa, lying between the upper third of the posterior surface of the calcaneus and the Achilles tendon. The retrocalcaneal bursa has a synovial lining in the proximal portion, where it abuts against the Achilles fat pad. The anterior bursal wall is composed of fibrocartilage laid over the calcaneus, while the posterior wall is indistinguishable from the epitenon of the Achilles tendon. It is important to note that communication between the Achilles insertion and retrocalcaneal bursa is common; hence injection of steroid to the bursa may have deleterious consequences on the Achilles. The Achilles is continuous with the plantar fascia, the short, long and spring plantar ligaments that provide stability to the foot during gait. Tightness in the soft tissue structures of the calf will therefore contribute to the onset of proximal plantar fasciitis. The insertion of soft tissues (typically tendon or ligaments) to bone are called entheses. Examples of these are the Achilles insertion and plantar ligament attachments at the calcaneum. Benjamin & McGonagle chose to describe the enthesis as the
“entheseal organ”, to include the tendon, its insertion, fibrocartilage interface, the local bursa, fat pad and local synovium.2 The entheseal organ serves to dissipate stress concentration at the hard soft tissue interface. The crural and plantar fascia help to dissipate that stress further. The fat pad is thought to facilitate the movement of tendon relative to bone, prevent tendonebone adhesion, aid in the spread of bursal fluid and act as a space filler and immune organ.3,4 Enthesopathies may be associated with a broad range of medical conditions, as listed in Table 2. The concept of the entheseal organ is helpful to a rheumatologist, as these tissues are variably affected in an enthesopathy, and specific features can help to distinguish an inflammatory enthesitis from a mechanical injury. All structures should therefore be evaluated closely, as will be described below.
4.
Achilles tendinopathies
4.1.
Classification and principles
Disorders of the Achilles tendon can be classified according to whether they affect the tendon sheath (paratendinitis), mid portion of the tendon (tendinosis), or insertion (enthesopathy). Para tendinitis typically occurs after mechanical overload such as a sudden increase in running. Patients will experience acute pain and crepitus, and stiffness on getting out of bed in the morning. Tendinosis is typically an overuse injury due to intrinsic and/or extrinsic factors, but can be related to other medical conditions (Table 2). The sudden onset of bilateral Achilles tendon pain suggests an underlying medical cause or drug induced injury. Insertional tendinopathies (enthesopathies) have a number of different causes. Mechanical factors as described in Table 1 often play a role. However, underlying rheumatological diseases should be considered in all cases (Table 3). When a tendon is injured, the attempt to heal involves an inflammatory phase (days), a proliferative phase (weeks) and remodeling phase (months). If this process is disrupted or stalls then disrepair and chronicity occur, leading to tendon angiogenesis, dystrophic calcification, tenocyte apoptosis, fibre disarray, and reduced structural integrity.5 The priority in the management of tendon injury is early, progressive, con-trolled loading. Ensuring the loading is appropriate requires expertise by a supervising clinician, since too much load is pro-inflammatory and damaging, and too little load is catabolic. Controlled loading of tendons, however, can provide stimulation of tenocytes, activation of cellular pathways and tendon remodeling6 and therefore plays a major role in management of these conditions. This applies to both core tendon injuries and those of the enthesis, although the characteristics of the loading differ according to the pathology involved.
4.2.
Clinical presentation
Patients with mid portion and insertional tendinopathy report localized pain, and stiffness on putting their foot to the floor in
i n d i a n j o u r n a l o f r h e u m a t o l o g y 9 ( 2 0 1 4 ) S 3 7 eS 4 1
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Table 2 e Medical disorders manifesting with tendinosis and/or enthesopathy. Site
Rheumatic disorders
Medical disorders
Drug induced
Core tendon
RA Other inflammatory arthritides including gout CPPD
Fluorquinolones Glococorticosteroids Statins Retinoids Fluoride
Entheseal organ
Spondyloarthropathies RA (bursitis) CPPD Osteoarthritis DISH SAPHO
Hyperlipidaemia Diabetes mellitus Hyperuricaemia Chronic renal failure Thyroid disease Haemochromatosis Parathyroid disease Chronic renal failure Hyperuricaemia Haemochromatosis Parathyroid disease X-linked hypophosphataemia Acromegaly Ochronosis
the morning. The affected area is often swollen. There may be a history of overuse or other alteration in equipment or activity patterns (Table 1). Clinical examination is performed as described above, to evaluate for signs of the pathology, additional features as described in Table 1 and searching for stigmata of other conditions (Table 2). The degree of functional impairment should be evaluated. Diagnostic ultrasound with Power or Colour Doppler should be performed if possible as part of the clinical assessment. Where the Achilles insertion is affected, there may be swelling and hypoechogenicity of the tendon, an enthesophyte, neovascularization, and calcification. A bursitis with increased blood flow may be present. There may be evidence of cortical erosion and fat pad inflammatory change. Note that patients with associated diseases such as psoriasis may have subclinical disease, with changes on ultrasound but no symptoms.
Distinguishing between mechanical and inflammatory enthesitis on the basis of clinical, ultrasound and/or MRI findings can be difficult. Significant Doppler flow and cortical erosion are indicative of underlying inflammatory disease. MRI can detect bone oedema and soft tissue oedema in the area around an enthesitis. It can also detect a Haglund's deformity, a posterior-superior process of the calcaneum. This may be present in an enthesopathy, and when a bursitis is also present this is called ‘Haglund's syndrome’. This is considered a mechanical cause of an enthesitis but can be misleading. Bursitis and cortical erosion may also be seen and the latter indicates an inflammatory condition. MRI demonstrates tendinosis in mid-portion tendinopathy but does not have the sensitivity to ultrastructural change that ultrasound has.
4.3. Table 3 e Important features to note in the Achilles tendon in the assessment of Achilles tendinopathies. Clinical: Site of symptoms Swelling Paratenon crepitus Retrocalcaneal bursal tenderness Inflammatory signs at insertion (?seronegative enthesopathy) Heel deformity VAS and VISA Score Ultrasound Site of core tendon involved (insertional vs midtendon) Degree of swelling Percentage of cross sectional area of tendon that is hypoechogenic Is there partial tear/split? Presence of neovascularization Paratenon involvement Retrocalcaenal bursitis X-Ray: Bony/Haglunds deformity Insertional changes MRI Tendon swelling, signal change, Tearing, Calcaneal deformity, Erosions at enthesis, Bursitis
Fluorquinolones Glococorticosteroids Retinoids Fluoride
Management
Management of an acute paratendinitis is straightforward: ice, NSAIDs, rest and then a review for biomechanical abnormalities that may have caused the condition. Controlled loading of a mid-portion or insertional Achilles tendinopathy is a vital component of management of these conditions. The correct level of controlled loading will vary according to the tendon involved, the extent of pathology, the chronicity and individual patient characteristics. Progressive loading should begin with light concentric exercise, progressing to eccentric exercise as tolerated. Research has shown that eccentric Achilles tendon loading reduces pain and returns patients to activity more rapidly than concentric loading. For example one controlled study of patients with mid portion Achilles tendinosis found that a 12week programme of eccentric calf-muscle exercises with dorsiflexion performed on a step led to a faster return to preinjury activity levels than surgery.7 Improvements with such a programme are shown even after 5 years.8 Good results have been demonstrated with insertional Achilles tendinopathy, using eccentric calf-muscle training without dorsiflexion on a flat surface with additional weight loading, as appropriate, to ensure the exercises were associated with some pain. Hence, when introducing controlled loading for Achilles injuries, it is best to use lower loads and
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i n d i a n j o u r n a l o f r h e u m a t o l o g y 9 ( 2 0 1 4 ) S 3 7 eS 4 1
restricted range for insertional tendinopathies, while midportion tendinopathies may require more aggressive loading.7e10 Pain management is important to allow rehabilitation to proceed. Approaches include topical ice after rehabilitation exercises, topical NSAID gel or in severe cases oral NSAIDs with gastroprotection over the short term, basic paracetamol (acetaminophen). Steroid injections are contraindicated. Corticosteroids may also have a negative impact on tendon healing and there is no good evidence to support the use of local corticosteroid injections in chronic tendon lesions.5 In tendinosis, treatments that may potentially stimulate a healing response in the tendon should be sought. Approaches in chronic tendinopathies can include topical glyceryl trinitrate (GTN), focused extracorporeal shock wave therapy and platelet rich plasma (PRP) injection. More research is needed on all of these approaches. Nitric oxide is generated after tendon injury. Reduced production of nitric oxide has been shown to result in reduced tendon healing and the addition of nitric oxide has been shown to enhance tendon healing and enhanced collagen synthesis. . Furthermore, in cultured human cells, the addition of nitric oxide results in enhanced collagen synthesis. A randomized, double-blind controlled trial of a GTN patch to deliver nitric oxide demonstrated a significant positive beneficial effect on clinical symptoms in patients with Achilles tendinopathy.11 A three-year prospective follow-up study also demonstrated significant long-term efficacy of GTN patches in treating non-insertional Achilles tendinopathy.12 Extracorporeal shock wave treatment is used as a nonsurgical treatment for various enthesopathies. The mechanism of action is not certain, but may involve direct stimulation of the healing process, production of microcavitations, neovascularization, destruction of calcium and neural effects.13 Investigations in cultured tenocytes have found that extracorporeal shock wave therapy demonstrates downregulation of inflammatory and other adverse MMP mediators.13 Focused extracorporeal shock wave therapy (F-ESWT) has been shown to be effective in the treatment of plantar fasciitis, Achilles tendinopathy calcific tendinitis. This appears to be dose dependent, with greater success seen with higher dose regimes. There is low level evidence for lack of benefit of low dose F-ESWT in noncalcific rotator cuff disease and mixed evidence in lateral epicondylitis.14
5.
Plantar fasciits
There are many causes of plantar heel pain, as described in Table 4. Repetitive traction at the insertion of the plantar fascia, can lead to inflammation then degeneration and tears of the plantar ligaments at the calcaneum. The patient presents with plantar heel pain, with start-up pain after rest and pain aggravated by walking and standing. Radiation of the pain and/or neuralgia is unusual and, when present, the clinician should consider other causes. Examination reveals point tenderness at the medial calcaneal tuberosity, with less marked tenderness 1e2 cm distally. Swelling is absent. There may be gastroc-soleus
Table 4 e Causes of plantar heel pain. Proximal plantar fasciitis Plantar fascial rupture Heel bruise syndrome Heel pad atrophy Plantar fibromatosis Nerve lesion: Tarsal tunnel syndrome Disorder of lateral plantar nerve or its 1st branch Entrapment/irritation/neuroma Postoperative neuroma of medial calcaneal sensory nerves Calcaneal stress fracture Tumour Medial calcaneal nerve entrapment
tightness. It is important to consider associations such as seronegative arthritis and other causes of plantar heel pain. Typical findings on ultrasonography may include swelling of the fascia, with increased thickness, hypoechogenicity and insertional irregularity of the plantar fascia.15 Ultrasound in expert hands can also identify causes of nerve compression or neuromata that may cause heel pain. MRI will show thickening and signal alterations at the plantar fascial origin16 and in some cases bone oedema in the os calcis at the site of fascial insertion. The cause must be addressed; and weight loss and modification of activity levels are usually necessary. The patient should wear supportive, cushioned footwear, heel inserts and in some cases orthoses. Dorsiflexion night splints can help to prevent excessive tightening of the plantar fascia overnight. Anti-inflammatory approaches including NSAIDs and regular ice massage are recommended but of variable benefit. Stretching of the plantar fascia and calf muscles and a programme of strengthening for the intrinsic muscles of the foot should be commenced early. Extracorporeal shock wave therapy (ESWT) may help to reduce symptoms. A randomised controlled trial (RCT) of 293 patients treated by ESWT or sham ESWT reported that 47% (67/144) and 30% (42/141) of patients, respectively, had 'successful' outcomes at 3-month follow-up (defined as at least 50% reduction in pressure-induced pain and pain during walking, at least a 1-point reduction in pain score on a 5-point visual analogue scale [VAS] [higher scores indicate greater pain] and no requirement for pain medication 10e12 weeks after treatment) (p ¼ 0.008).17 In an RCT of 172 patients treated by ESWT or sham ESWT, the mean reduction in pain score (assessed by a 5-point VAS) from baseline to 3-month follow-up was 3.4 in the ESWT group (n ¼ 112) compared with 1.8 in the sham ESWT group (n ¼ 56) (p < 0.001).18 In chronic resistant cases where the above measures 12 weeks have not been effective then an ultrasound-guided corticosteroid injection may be indicated. Injudicious placement of injection, use of long acting preparations and multiple injections can all lead to fat pad atrophy and plantar fascial rupture. In a study of 82 patients, McMillan et al found that a single ultrasound guided dexamethasone injection is a safe and effective short term treatment for plantar fasciitis. It provides greater pain relief than placebo at four weeks and reduces abnormal swelling of the plantar fascia for up to three
i n d i a n j o u r n a l o f r h e u m a t o l o g y 9 ( 2 0 1 4 ) S 3 7 eS 4 1
months. However, the authors emphasized that clinicians offering this treatment should also note that significant pain relief did not continue beyond four weeks.19 In a small study of 36 patients, injection with Botox-A [BTX-A] was compared with steroid injection in patients with plantar fasciitis. A combination of BTX-A and plantar fascia stretching exercises yielded better results for the treatment of plantar fasciitis than intralesional steroids.20 The benefit of platelet rich plasma (PRP) injections for plantar fasciitis has yet to be adequately proven with robust trials but there are reports of benefit from limited trials.21 A small number of patients will continue to have significant symptoms beyond 18 months, and in these cases surgical intervention may be considered. Many surgical procedures are described, and range from percutaneous release, to endoscopic release to open procedures. However patient satisfaction is limited.22
6.
Conclusions
Soft tissue disorders of the foot and ankle are common in the rheumatology clinic. Achilles tendon and plantar fascia pathologies are the most common of these. Having a thorough understanding of the anatomy, pathologies and differential diagnosis is essential in making a clear diagnosis and defining best management for individual cases.
Conflicts of interest The author has none to declare.
references
1. Carr AJ, Norris SH. The blood supply of the calcaneal tendon. J Bone Jt Surg Br. 1989 Jan;71:100e101. 2. Benjamin M, McGonagle D. The anatomical basis for disease localisation in seronegative spondyloarthropathy at enthuses and related sites. J Anat. 2001;199:503e526. 3. Shaw HM, Santer RM, Watson AH, Benjamin M. Adipose tissue at entheses: the innervation and cell composition of the retromalleolar fat pad associated with the rat Achilles tendon. J Anat. 2007;211:436e443. 4. Theobald P, Bydder G, Dent C, Nokes L, Pugh N, Benjamin M. The functional anatomy of Kager's fat pad in relation to retrocal-caneal problems and other hindfoot disorders. J Anat. 2006;208:91e97. 5. Rees JD, Wilson AM, Wolman RL. Current concepts in the management of tendon disorders. Rheumatology. 2006;45:508e521. 6. Killian ML, Cavinatto L, Galatz LM, et al. The role of mechanobiology in tendon healing. J Shoulder Elbow Surg. 2012;21:228e237.
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7. Alfredson H, Pietila T, Jonsson P, et al. Heavy-load eccentric calf muscle training for the treatment of chronic Achilles tendinosis. Am J Sports Med. 1998;26:360e366. 8. Van der Plas A, de Jonge S, de Vos RJ, et al. A 5-year follow-up study of Alfredson's heel-drop exercise programme in chronic midportion Achilles tendinopathy. Br J Sports Med. 2012;46:214e218. 9. Jonsson P, Alfredson H, Sunding K, et al. New regimen for eccentric calf- muscle training in patients with chronic insertional Achilles tendinopathy: results of a pilot study. Br J Sports Med. 2008;42:746e749. 10. Young MA, Cook JL, Purdam CR, et al. Eccentric decline squat protocol offers superior results at 12 months compared with traditional eccentric protocol for patellar tendinopathy in volleyball players. Br J Sports Med. 2005;39:102e105. 11. Paoloni JA, Appleyard RC, Nelson J, Murrell GA. Topical glyceryl trinitrate treatment of chronic noninsertional Achilles tendinopathy. A randomised double blind placebo-controlled trial. J Bone Jt Surg Am. 2004;86-A: 916e922. 12. Paoloni JA, Murrell GA. Three year follow up study of topical glyceryl trinitrate treatment of chronic noninsertional Achilles tendinopathy. Foot Ankle Int. 2007;28:1064e1068. 13. Han SH, Lee JW, Guyton GP, et al. Effect of extracorporeal shock wave therapy on cultured tenocytes. Foot Ankle Int. 2009;30:93e98. 14. Furia JP. High-energy extracorporeal shock wave therapy as a treatment for chronic noninsertional Achilles tendinopathy. Am J Sports Med. 2008;36:502e508. 15. Kane D, Greaney T, Shanahan M, et al. The role of ultrasonography in the diagnosis and management of idiopathic plantar fasciitis. Rheumatoogy. 2001;40:1002e1008. 16. Berkowitz JF, Kier R, Rudicel S. Plantar fasciitis: MR imaging. Radiology. 1991;179:665e667. 17. Ogden JA, Alvarez RG, Levitt RI, et al. Electrohydraulic highenergy shock-wave treatment for chronic plantar fasciitis. J Bone Jt Surg. 2004;86:2216e2228. 18. Malay DS, Pressman MM, Assili A, et al. Extracorporeal shockwave therapy versus placebo for the treatment of chronic proximal plantar fasciitis: results of a randomized, placebo-controlled, double-blinded, multicenter intervention trial. J Foot Ankle Surg. 2006;45:196e210. 19. McMillan AM, Landorf KB, Gilheany MF, Bird AR, Morrow AD, Menz HB. Ultrasound guided corticosteroid injection for plantar fasciitis: randomised controlled trial. BMJ. 2012 May 22;344. 20. Elizondo-Rodriguez J, Araujo-Lopez Y, Moreno-Gonzalez JA, Cardenas-Estrada E, Mendoza-Lemus O, Acosta-Olivo C. A comparison of botulinum toxin a and intralesional steroids for the treatment of plantar fasciitis: a randomized, doubleblinded study. Foot Ankle Int. 2013 Jan;34:8e14. 21. Shetty VD, Dhillon M, Hegde C, Jagtap P, Shetty S. A study to compare the efficacy of corticosteroid therapy with platelet-rich plasma therapy in recalcitrant plantar fasciitis: a preliminary report. Foot Ankle Surg. 2014 Mar;20:10e13. 22. Davies MS, Weiss GA, Saxby TS. Plantar fasciitis: how successful is surgical intervention? Foot Ankle Int. 1999;20:803e807.
ScienceDirect Available online at www.indianjrheumatol.com and www.sciencedirect.com
Review Article
Soft tissue disorders of the foot and ankle: The Achilles tendon and plantar fascia Cathy A. Speed Cambridge Centre for Health & Performance, Conqueror House, Vision Park, Cambridge CB24 9ZR, UK
abstract Keywords:
Disorders of the foot and ankle are common in the rheumatology clinic and are frequently
Soft tissue
soft tissue in origin. In this context, pain can arise from tendon, ligament, nerve, bursa and
Foot
muscle. Pain and disability are common consequences and hence the rheumatologist must
Ankle
have a comprehensive understanding of the diagnosis and management of such
Tendinopathy
complaints.
Plantar fasciitis
1.
Copyright © 2014, Indian Rheumatology Association. All rights reserved.
Introduction
Disorders of the foot and ankle are common in the rheumatology clinic and are frequently soft tissue in origin. In this context, pain can arise from tendon, ligament, nerve, bursa and muscle. Pain and disability are common consequences and hence the rheumatologist must have a comprehensive understanding of the diagnosis and management of such complaints. The most common soft tissue disorders in this region are tendinopathies affecting the Achilles tendon, and plantar fasciitis. These complaints will form the subject of this article.
2.
Principles of evaluation
Evaluation of all soft tissue complaints starts with taking a comprehensive history, followed by a careful clinical examination. Imaging modalities are often useful, and indeed diagnostic ultrasound should be considered as an extension of the clinical examination.
The cardinal symptom of a soft tissue injury is one of pain. Other symptoms include stiffness, clicking, instability, and neurological symptoms, all of which can lead to loss of function. A description of the mechanism of onset should be obtained and a pain history recorded, including the site, nature, and radiation and relieving and exacerbating factors identified. If the presentation is acute, the degree of swelling often corresponds to the severity of the injury. Always seek to identify the cause of the complaint. Intrinsic and extrinsic factors that should be considered are given in Table 1. Clarify what measures have already been taken in the form of analgesia and other treatments. Examination includes evaluation of lower limb biomechanics, functional core control and proprioception. Evaluate for lower limb musculotendinous stiffness, especially the calves and hamstrings. In the acute phase, assess for swelling, bruising (in the case of Achilles or plantar fascial rupture). Assess range of motion of lower limb joints, and palpate the affected areas for tenderness, swelling and in the case of an Achilles rupture, a palpable gap which is not always apparent. Patients with a severe Achilles injury will be unable to perform a single heel raise. Note that Achilles ruptures are often missed at initial presentation due to a lack of full assessment.
E-mail address: [email protected]. http://dx.doi.org/10.1016/j.injr.2014.09.012 0973-3698/Copyright © 2014, Indian Rheumatology Association. All rights reserved.
S38
i n d i a n j o u r n a l o f r h e u m a t o l o g y 9 ( 2 0 1 4 ) S 3 7 eS 4 1
Table 1 e Factors predisposing soft tissue disorders of the foot and ankle. Intrinsic factors: Biomechanical malalignments including gait abnormalities (usually hyperpronation) Stiff gastrocnemiusesoleus complex, tight hamstrings Leg length discrepancy Muscle imbalance Hyper/hypomobile hindfoot Haglund's deformity Spondyloarthritides (enthesopathies) Medical conditions Extrinsic factors: Overtraining Training type (e.g. too much heavy weight training) Poor footwear (too old, poor cushioning, high heel tab, wrong size) Poor technique Inappropriate surface Environment (too hot/too cold) Iatrogenic: fluoroquinolones, corticosteroid injections Anabolic steroid abuse
3.
Relevant anatomy and pathophysiology
The Achilles tendon forms as a broad tendinous sheet from the gastrocnemius muscle in the mid leg. The soleus muscle is deep and adherent to the Achilles and allows a blood supply to the Achilles. The soleus fibres blend with, and become part of, the Achilles tendon. When complete, the inferior fibres of the Achilles tendon twist obliquely in their descent to their insertion onto the posterior aspect of the mid-third of the calcaneus. The Achilles tendon is invested by a paratenon, consisting of loose elastic connective tissue, invest the Achilles and when healthy stretches with movement of the tendon, allowing the tendon to glide freely. The paratenon supplies much of the blood supply of the Achilles. Vascularity in the area 2e5 cm above the insertion, where much pathology occurs, is poor.1 Two bursae are associated with the Achilles tendon - the superficial retroachilles bursa, and the deeper retrocalcaneal bursa, lying between the upper third of the posterior surface of the calcaneus and the Achilles tendon. The retrocalcaneal bursa has a synovial lining in the proximal portion, where it abuts against the Achilles fat pad. The anterior bursal wall is composed of fibrocartilage laid over the calcaneus, while the posterior wall is indistinguishable from the epitenon of the Achilles tendon. It is important to note that communication between the Achilles insertion and retrocalcaneal bursa is common; hence injection of steroid to the bursa may have deleterious consequences on the Achilles. The Achilles is continuous with the plantar fascia, the short, long and spring plantar ligaments that provide stability to the foot during gait. Tightness in the soft tissue structures of the calf will therefore contribute to the onset of proximal plantar fasciitis. The insertion of soft tissues (typically tendon or ligaments) to bone are called entheses. Examples of these are the Achilles insertion and plantar ligament attachments at the calcaneum. Benjamin & McGonagle chose to describe the enthesis as the
“entheseal organ”, to include the tendon, its insertion, fibrocartilage interface, the local bursa, fat pad and local synovium.2 The entheseal organ serves to dissipate stress concentration at the hard soft tissue interface. The crural and plantar fascia help to dissipate that stress further. The fat pad is thought to facilitate the movement of tendon relative to bone, prevent tendonebone adhesion, aid in the spread of bursal fluid and act as a space filler and immune organ.3,4 Enthesopathies may be associated with a broad range of medical conditions, as listed in Table 2. The concept of the entheseal organ is helpful to a rheumatologist, as these tissues are variably affected in an enthesopathy, and specific features can help to distinguish an inflammatory enthesitis from a mechanical injury. All structures should therefore be evaluated closely, as will be described below.
4.
Achilles tendinopathies
4.1.
Classification and principles
Disorders of the Achilles tendon can be classified according to whether they affect the tendon sheath (paratendinitis), mid portion of the tendon (tendinosis), or insertion (enthesopathy). Para tendinitis typically occurs after mechanical overload such as a sudden increase in running. Patients will experience acute pain and crepitus, and stiffness on getting out of bed in the morning. Tendinosis is typically an overuse injury due to intrinsic and/or extrinsic factors, but can be related to other medical conditions (Table 2). The sudden onset of bilateral Achilles tendon pain suggests an underlying medical cause or drug induced injury. Insertional tendinopathies (enthesopathies) have a number of different causes. Mechanical factors as described in Table 1 often play a role. However, underlying rheumatological diseases should be considered in all cases (Table 3). When a tendon is injured, the attempt to heal involves an inflammatory phase (days), a proliferative phase (weeks) and remodeling phase (months). If this process is disrupted or stalls then disrepair and chronicity occur, leading to tendon angiogenesis, dystrophic calcification, tenocyte apoptosis, fibre disarray, and reduced structural integrity.5 The priority in the management of tendon injury is early, progressive, con-trolled loading. Ensuring the loading is appropriate requires expertise by a supervising clinician, since too much load is pro-inflammatory and damaging, and too little load is catabolic. Controlled loading of tendons, however, can provide stimulation of tenocytes, activation of cellular pathways and tendon remodeling6 and therefore plays a major role in management of these conditions. This applies to both core tendon injuries and those of the enthesis, although the characteristics of the loading differ according to the pathology involved.
4.2.
Clinical presentation
Patients with mid portion and insertional tendinopathy report localized pain, and stiffness on putting their foot to the floor in
i n d i a n j o u r n a l o f r h e u m a t o l o g y 9 ( 2 0 1 4 ) S 3 7 eS 4 1
S39
Table 2 e Medical disorders manifesting with tendinosis and/or enthesopathy. Site
Rheumatic disorders
Medical disorders
Drug induced
Core tendon
RA Other inflammatory arthritides including gout CPPD
Fluorquinolones Glococorticosteroids Statins Retinoids Fluoride
Entheseal organ
Spondyloarthropathies RA (bursitis) CPPD Osteoarthritis DISH SAPHO
Hyperlipidaemia Diabetes mellitus Hyperuricaemia Chronic renal failure Thyroid disease Haemochromatosis Parathyroid disease Chronic renal failure Hyperuricaemia Haemochromatosis Parathyroid disease X-linked hypophosphataemia Acromegaly Ochronosis
the morning. The affected area is often swollen. There may be a history of overuse or other alteration in equipment or activity patterns (Table 1). Clinical examination is performed as described above, to evaluate for signs of the pathology, additional features as described in Table 1 and searching for stigmata of other conditions (Table 2). The degree of functional impairment should be evaluated. Diagnostic ultrasound with Power or Colour Doppler should be performed if possible as part of the clinical assessment. Where the Achilles insertion is affected, there may be swelling and hypoechogenicity of the tendon, an enthesophyte, neovascularization, and calcification. A bursitis with increased blood flow may be present. There may be evidence of cortical erosion and fat pad inflammatory change. Note that patients with associated diseases such as psoriasis may have subclinical disease, with changes on ultrasound but no symptoms.
Distinguishing between mechanical and inflammatory enthesitis on the basis of clinical, ultrasound and/or MRI findings can be difficult. Significant Doppler flow and cortical erosion are indicative of underlying inflammatory disease. MRI can detect bone oedema and soft tissue oedema in the area around an enthesitis. It can also detect a Haglund's deformity, a posterior-superior process of the calcaneum. This may be present in an enthesopathy, and when a bursitis is also present this is called ‘Haglund's syndrome’. This is considered a mechanical cause of an enthesitis but can be misleading. Bursitis and cortical erosion may also be seen and the latter indicates an inflammatory condition. MRI demonstrates tendinosis in mid-portion tendinopathy but does not have the sensitivity to ultrastructural change that ultrasound has.
4.3. Table 3 e Important features to note in the Achilles tendon in the assessment of Achilles tendinopathies. Clinical: Site of symptoms Swelling Paratenon crepitus Retrocalcaneal bursal tenderness Inflammatory signs at insertion (?seronegative enthesopathy) Heel deformity VAS and VISA Score Ultrasound Site of core tendon involved (insertional vs midtendon) Degree of swelling Percentage of cross sectional area of tendon that is hypoechogenic Is there partial tear/split? Presence of neovascularization Paratenon involvement Retrocalcaenal bursitis X-Ray: Bony/Haglunds deformity Insertional changes MRI Tendon swelling, signal change, Tearing, Calcaneal deformity, Erosions at enthesis, Bursitis
Fluorquinolones Glococorticosteroids Retinoids Fluoride
Management
Management of an acute paratendinitis is straightforward: ice, NSAIDs, rest and then a review for biomechanical abnormalities that may have caused the condition. Controlled loading of a mid-portion or insertional Achilles tendinopathy is a vital component of management of these conditions. The correct level of controlled loading will vary according to the tendon involved, the extent of pathology, the chronicity and individual patient characteristics. Progressive loading should begin with light concentric exercise, progressing to eccentric exercise as tolerated. Research has shown that eccentric Achilles tendon loading reduces pain and returns patients to activity more rapidly than concentric loading. For example one controlled study of patients with mid portion Achilles tendinosis found that a 12week programme of eccentric calf-muscle exercises with dorsiflexion performed on a step led to a faster return to preinjury activity levels than surgery.7 Improvements with such a programme are shown even after 5 years.8 Good results have been demonstrated with insertional Achilles tendinopathy, using eccentric calf-muscle training without dorsiflexion on a flat surface with additional weight loading, as appropriate, to ensure the exercises were associated with some pain. Hence, when introducing controlled loading for Achilles injuries, it is best to use lower loads and
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restricted range for insertional tendinopathies, while midportion tendinopathies may require more aggressive loading.7e10 Pain management is important to allow rehabilitation to proceed. Approaches include topical ice after rehabilitation exercises, topical NSAID gel or in severe cases oral NSAIDs with gastroprotection over the short term, basic paracetamol (acetaminophen). Steroid injections are contraindicated. Corticosteroids may also have a negative impact on tendon healing and there is no good evidence to support the use of local corticosteroid injections in chronic tendon lesions.5 In tendinosis, treatments that may potentially stimulate a healing response in the tendon should be sought. Approaches in chronic tendinopathies can include topical glyceryl trinitrate (GTN), focused extracorporeal shock wave therapy and platelet rich plasma (PRP) injection. More research is needed on all of these approaches. Nitric oxide is generated after tendon injury. Reduced production of nitric oxide has been shown to result in reduced tendon healing and the addition of nitric oxide has been shown to enhance tendon healing and enhanced collagen synthesis. . Furthermore, in cultured human cells, the addition of nitric oxide results in enhanced collagen synthesis. A randomized, double-blind controlled trial of a GTN patch to deliver nitric oxide demonstrated a significant positive beneficial effect on clinical symptoms in patients with Achilles tendinopathy.11 A three-year prospective follow-up study also demonstrated significant long-term efficacy of GTN patches in treating non-insertional Achilles tendinopathy.12 Extracorporeal shock wave treatment is used as a nonsurgical treatment for various enthesopathies. The mechanism of action is not certain, but may involve direct stimulation of the healing process, production of microcavitations, neovascularization, destruction of calcium and neural effects.13 Investigations in cultured tenocytes have found that extracorporeal shock wave therapy demonstrates downregulation of inflammatory and other adverse MMP mediators.13 Focused extracorporeal shock wave therapy (F-ESWT) has been shown to be effective in the treatment of plantar fasciitis, Achilles tendinopathy calcific tendinitis. This appears to be dose dependent, with greater success seen with higher dose regimes. There is low level evidence for lack of benefit of low dose F-ESWT in noncalcific rotator cuff disease and mixed evidence in lateral epicondylitis.14
5.
Plantar fasciits
There are many causes of plantar heel pain, as described in Table 4. Repetitive traction at the insertion of the plantar fascia, can lead to inflammation then degeneration and tears of the plantar ligaments at the calcaneum. The patient presents with plantar heel pain, with start-up pain after rest and pain aggravated by walking and standing. Radiation of the pain and/or neuralgia is unusual and, when present, the clinician should consider other causes. Examination reveals point tenderness at the medial calcaneal tuberosity, with less marked tenderness 1e2 cm distally. Swelling is absent. There may be gastroc-soleus
Table 4 e Causes of plantar heel pain. Proximal plantar fasciitis Plantar fascial rupture Heel bruise syndrome Heel pad atrophy Plantar fibromatosis Nerve lesion: Tarsal tunnel syndrome Disorder of lateral plantar nerve or its 1st branch Entrapment/irritation/neuroma Postoperative neuroma of medial calcaneal sensory nerves Calcaneal stress fracture Tumour Medial calcaneal nerve entrapment
tightness. It is important to consider associations such as seronegative arthritis and other causes of plantar heel pain. Typical findings on ultrasonography may include swelling of the fascia, with increased thickness, hypoechogenicity and insertional irregularity of the plantar fascia.15 Ultrasound in expert hands can also identify causes of nerve compression or neuromata that may cause heel pain. MRI will show thickening and signal alterations at the plantar fascial origin16 and in some cases bone oedema in the os calcis at the site of fascial insertion. The cause must be addressed; and weight loss and modification of activity levels are usually necessary. The patient should wear supportive, cushioned footwear, heel inserts and in some cases orthoses. Dorsiflexion night splints can help to prevent excessive tightening of the plantar fascia overnight. Anti-inflammatory approaches including NSAIDs and regular ice massage are recommended but of variable benefit. Stretching of the plantar fascia and calf muscles and a programme of strengthening for the intrinsic muscles of the foot should be commenced early. Extracorporeal shock wave therapy (ESWT) may help to reduce symptoms. A randomised controlled trial (RCT) of 293 patients treated by ESWT or sham ESWT reported that 47% (67/144) and 30% (42/141) of patients, respectively, had 'successful' outcomes at 3-month follow-up (defined as at least 50% reduction in pressure-induced pain and pain during walking, at least a 1-point reduction in pain score on a 5-point visual analogue scale [VAS] [higher scores indicate greater pain] and no requirement for pain medication 10e12 weeks after treatment) (p ¼ 0.008).17 In an RCT of 172 patients treated by ESWT or sham ESWT, the mean reduction in pain score (assessed by a 5-point VAS) from baseline to 3-month follow-up was 3.4 in the ESWT group (n ¼ 112) compared with 1.8 in the sham ESWT group (n ¼ 56) (p < 0.001).18 In chronic resistant cases where the above measures 12 weeks have not been effective then an ultrasound-guided corticosteroid injection may be indicated. Injudicious placement of injection, use of long acting preparations and multiple injections can all lead to fat pad atrophy and plantar fascial rupture. In a study of 82 patients, McMillan et al found that a single ultrasound guided dexamethasone injection is a safe and effective short term treatment for plantar fasciitis. It provides greater pain relief than placebo at four weeks and reduces abnormal swelling of the plantar fascia for up to three
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months. However, the authors emphasized that clinicians offering this treatment should also note that significant pain relief did not continue beyond four weeks.19 In a small study of 36 patients, injection with Botox-A [BTX-A] was compared with steroid injection in patients with plantar fasciitis. A combination of BTX-A and plantar fascia stretching exercises yielded better results for the treatment of plantar fasciitis than intralesional steroids.20 The benefit of platelet rich plasma (PRP) injections for plantar fasciitis has yet to be adequately proven with robust trials but there are reports of benefit from limited trials.21 A small number of patients will continue to have significant symptoms beyond 18 months, and in these cases surgical intervention may be considered. Many surgical procedures are described, and range from percutaneous release, to endoscopic release to open procedures. However patient satisfaction is limited.22
6.
Conclusions
Soft tissue disorders of the foot and ankle are common in the rheumatology clinic. Achilles tendon and plantar fascia pathologies are the most common of these. Having a thorough understanding of the anatomy, pathologies and differential diagnosis is essential in making a clear diagnosis and defining best management for individual cases.
Conflicts of interest The author has none to declare.
references
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7. Alfredson H, Pietila T, Jonsson P, et al. Heavy-load eccentric calf muscle training for the treatment of chronic Achilles tendinosis. Am J Sports Med. 1998;26:360e366. 8. Van der Plas A, de Jonge S, de Vos RJ, et al. A 5-year follow-up study of Alfredson's heel-drop exercise programme in chronic midportion Achilles tendinopathy. Br J Sports Med. 2012;46:214e218. 9. Jonsson P, Alfredson H, Sunding K, et al. New regimen for eccentric calf- muscle training in patients with chronic insertional Achilles tendinopathy: results of a pilot study. Br J Sports Med. 2008;42:746e749. 10. Young MA, Cook JL, Purdam CR, et al. Eccentric decline squat protocol offers superior results at 12 months compared with traditional eccentric protocol for patellar tendinopathy in volleyball players. Br J Sports Med. 2005;39:102e105. 11. Paoloni JA, Appleyard RC, Nelson J, Murrell GA. Topical glyceryl trinitrate treatment of chronic noninsertional Achilles tendinopathy. A randomised double blind placebo-controlled trial. J Bone Jt Surg Am. 2004;86-A: 916e922. 12. Paoloni JA, Murrell GA. Three year follow up study of topical glyceryl trinitrate treatment of chronic noninsertional Achilles tendinopathy. Foot Ankle Int. 2007;28:1064e1068. 13. Han SH, Lee JW, Guyton GP, et al. Effect of extracorporeal shock wave therapy on cultured tenocytes. Foot Ankle Int. 2009;30:93e98. 14. Furia JP. High-energy extracorporeal shock wave therapy as a treatment for chronic noninsertional Achilles tendinopathy. Am J Sports Med. 2008;36:502e508. 15. Kane D, Greaney T, Shanahan M, et al. The role of ultrasonography in the diagnosis and management of idiopathic plantar fasciitis. Rheumatoogy. 2001;40:1002e1008. 16. Berkowitz JF, Kier R, Rudicel S. Plantar fasciitis: MR imaging. Radiology. 1991;179:665e667. 17. Ogden JA, Alvarez RG, Levitt RI, et al. Electrohydraulic highenergy shock-wave treatment for chronic plantar fasciitis. J Bone Jt Surg. 2004;86:2216e2228. 18. Malay DS, Pressman MM, Assili A, et al. Extracorporeal shockwave therapy versus placebo for the treatment of chronic proximal plantar fasciitis: results of a randomized, placebo-controlled, double-blinded, multicenter intervention trial. J Foot Ankle Surg. 2006;45:196e210. 19. McMillan AM, Landorf KB, Gilheany MF, Bird AR, Morrow AD, Menz HB. Ultrasound guided corticosteroid injection for plantar fasciitis: randomised controlled trial. BMJ. 2012 May 22;344. 20. Elizondo-Rodriguez J, Araujo-Lopez Y, Moreno-Gonzalez JA, Cardenas-Estrada E, Mendoza-Lemus O, Acosta-Olivo C. A comparison of botulinum toxin a and intralesional steroids for the treatment of plantar fasciitis: a randomized, doubleblinded study. Foot Ankle Int. 2013 Jan;34:8e14. 21. Shetty VD, Dhillon M, Hegde C, Jagtap P, Shetty S. A study to compare the efficacy of corticosteroid therapy with platelet-rich plasma therapy in recalcitrant plantar fasciitis: a preliminary report. Foot Ankle Surg. 2014 Mar;20:10e13. 22. Davies MS, Weiss GA, Saxby TS. Plantar fasciitis: how successful is surgical intervention? Foot Ankle Int. 1999;20:803e807.