Introduction
Heel pain is widely perceived as a minor ailment that will get better by itself. This is not always true and both plantar fasciitis and tendo Achillis (TA) problems are prevalent, affecting millions of people each year. Most sufferers will improve with a combination of time and proper stretching regimens. Nevertheless a proportion of patients suffer with resistant symptoms that can be difficult to manage and require operative treatment.
Heel pain is classified as either posterior or plantar1. Posterior heel pain is usually from the TA. Tendinopathy of TA is associated with sport and is an increasingly common complaint as people continue to exercise into older age2. Plantar heel pain is most commonly caused by plantar fasciitis. In the United States over 1 million people seek help for this pain every year3. The majority of cases never reach the secondary care sector. This chapter aims to outline the treatment of these two causes of heel pain.
General Management of Heel Pain
Clinical History
Pain, especially with the first steps in the morning or after a period of rest, is the main symptom. Most patients report that the pain improves after an initial period of painful stiffness, but that after prolonged standing (plantar fasciitis) or after exercise (TA) the symptoms return. Inability to walk long distances and reduced exercise and sports participation are also common complaints.
There may be no distinct injury preceding the symptoms, but there is frequently an alteration in activity levels, new sports shoes, increase in body weight, including pregnancy, or alteration in working patterns requiring longer periods of standing. In chronic cases the nature of the pain and its radiation is important. Plantar heel pain radiating to the arch of the foot may indicate disease in the more distal plantar fascia but, especially if associated with tingling or numbness, can indicate a neurological cause.
The duration of symptoms should be noted as so many cases run a self-limiting course and little active intervention is needed for uncomplicated cases of recent onset. Conversely chronic cases, particularly when proper first-line treatments have been tried and failed, need more help. There is increasing awareness of the association between adverse biomechanics, particularly isolated gastrocnemius tightness, and heel pain. Specific enquiry regarding symptoms of other conditions associated with gastrocnemius tightness should be part of the history. Conditions associated with gastrocnemius tightness include posteromedial pain and swelling from the tibialis posterior tendon with an acquired flat foot, previous medial gastrocnemius calf muscle tear (tennis leg), forefoot overload, hallux valgus, difficulty wearing flat shoes, and calf cramps.
Examination
In moderate or severe cases the patient limps into the clinic. In chronic cases in non-athletes there is a strong association with raised body mass index. Planovalgus foot posture is more common than “normal,” reflecting the association of heel pain with calf contracture, but a cavus foot with increased calcaneal pitch may also be associated with plantar fascia pain. Similarly forefoot ground clearance may be reduced and Silfverskiöld’s test should be performed once the patient is seated to confirm and quantify the gastrocnemius contracture. Pulses and sensation are checked. If symptoms suggest an atypical cause for the pain then full lumbar spine and neurological assessment is needed, particularly looking for signs of lumbar radiculopathy. Tarsal tunnel syndrome is very rare, but a Tinel’s test over the tibial nerve, lying just behind the medial malleolus, should still be recorded. The calcaneal squeeze test where the heel is squeezed between the thenar eminences of both hands is often weakly positive in long-standing cases of plantar fasciitis, but if the heel is very tender this may indicate a calcaneal stress fracture.
Local examination of the plantar fascia is conveniently performed with the patient sitting on a high couch with their legs dangling over the side, facing the examiner who is seated in a lower chair. In plantar fasciitis tenderness is usually maximal at the medial calcaneal tuberosity on the plantar aspect of the foot. Posterior tenderness may seem “plantar” when it is in fact from insertional Achilles tendinopathy. Central plantar tenderness may indicate traumatic or iatrogenic fat pad atrophy as a result of steroid injections or, rarely, a bursa. It is important to palpate along the non-insertional plantar fascia as it extends into the medial longitudinal arch, because tenderness or lumps in this part of the plantar fascia may merit different treatment strategies. Plantar fibromata are best managed with relief orthotics because the rate of complications after attempted excision is devastatingly high. Midfoot arthrosis occasionally presents as plantar arch pain.
The TA and its insertion may be examined with the clinician and patient sitting as described above, but it is also convenient to ask the patient to kneel on a chair (as one would to perform Simmonds’ test for an TA rupture). This affords a better view of the heel and allows accurate palpation of the tendon from the musculo-tendinous junction to the insertion.
It is important to distinguish between disease of the main body (non-insertional) and insertional part of the TA, as the treatment of the two areas differs. Tendinopathy of the main body of the tendon is associated with tenderness and swelling, which may be discrete or involve a long section of the tendon. Tenderness and swelling that remains in the same location when the ankle is put through a full range of dorsiflexion and plantar flexion is due to inflammation of the paratenon rather than the tendon itself. Paratendinitis is relatively uncommon. This clinical sign is sometimes known as the Royal London Hospital test. Other soft tissue swellings may present around the TA and may be benign or very rarely malignant.
The insertion of the TA is relatively complex in anatomical terms (Figure 14.1). Pathology here may be seen in the retrocalcaneal bursa, superficial bursa, bursal projection, or the insertion of the TA itself. It is in fact usually a combination of these structures, but if tenderness is marked to the medial or lateral sides of the tendon then retrocalcaneal bursitis most likely predominates. Distinct midline tenderness is more indicative of calcific tendinopathy. A sports person will occasionally present with tenderness at the widest reaches of the tendon’s expansion due to a small avulsion injury.
Figure 14.1 Posterior heel anatomy.
Classification
After clinical and radiological assessment it should be possible to accurately classify the nature of the problem (Table 14.1). As in all fields of medicine, a precise diagnosis allows targeted treatment and should lead to improved results.
Logistics
The self-limiting nature of the symptoms in the majority of cases, and the need for the prudent use of healthcare resources, means that it is appropriate to triage patients presenting with heel pain. The protocol outlined in Table 14.2 is practical, rather than scientific, but in the authors’ opinion steers a sensible path between masterful inactivity and overinvestigation. Using this protocol only 4% of those patients who seek medical attention will ever require assessment in secondary care. The majority of the discussion below will focus on this group.
1. Less than three months | Home stretches | 80% |
2. More than three months | Physio eccentric stretches | 80% |
3. More than six months | Heel pain clinic | 80% |
Biomechanics | ||
Images |
Less Than Three Months of Symptoms
Patients presenting to primary care with heel pain of relatively recent onset can reasonably be expected to improve with simple “home stretches,” time, and activity modification. Stretches should focus in the calf muscle. Lowering the heel over the edge of a step is a simple stretch that patients can easily understand.
A gel heel cushion can be helpful for plantar heel pain. It is important that the patient understands that it is necessary to perform the stretches regularly. Failure to improve should prompt referral for physiotherapy.
More Than Three Months of Symptoms
If symptoms persist then physiotherapy is indicated, and very likely to help. Formal calf stretching programs are widely considered to be the best first-line treatment for both plantar fasciitis and non-insertional achilles tendinopathy11, 22. The TA even recovers its normal structure after eccentric stretching4. With plantar fasciitis there are further benefits from stretches targeting the fascia itself5–6. We believe that treatments in primary care should focus upon, and be restricted to, these stretches. There is little or no evidence for acupuncture, orthoses, or steroid injection.
More Than Six Months of Symptoms
Optimum management of stubborn cases of both plantar fascia pain and disorders of the TA requires a thorough clinical assessment and appropriate radiological investigation. Many patients have suffered for years while trying to relieve their symptoms. Multiple interventions have usually been tried without success. Our heel pain clinic is devoted to the investigation and treatment of these recalcitrant plantar fascia and TA problems. Patients are assessed and most commonly investigated by US scan, with color-Doppler capability. A critical part of the clinical examination is assessment of the calf muscle tension. There is a strong association between isolated tightness of the gastrocnemius and complaints of plantar fasciitis or TA pain. We believe that local treatments for heel pain are much less likely to be of benefit in the face of the adverse biomechanics consequent upon gastrocnemius tightness. Initial emphasis is therefore placed upon correcting this. Physiotherapy treatment is prescribed, but a proportion of cases are subsequently offered surgical gastrocnemius lengthening (Figure 14.2).
Figure 14.2 Gastrocnemius shortening is a malign influence and sometimes requires operative correction.
After clinical and US assessment, patients can be divided into groups on the basis of their biomechanical profile and the exact nature of their tendinopathy or fasciopathy. Treatment can be tailored accordingly.
Those who do not exhibit tight gastrocnemius, or remain symptomatic after gastrocnemius release, are candidates for local therapy (Table 14.3).
ESWT: extra-corporeal shockwave therapy; USS: ultrasound scanning.
Plantar Fasciopathy
Heel pain is common7–8. Pain, especially after a period of rest or with the first steps of the morning, is characteristic. Other complaints include difficulty standing for long periods, reduced ability to walk long distances, and an inability to play sport or run. Plantar heel pain is most commonly caused by plantar “fasciitis.” This term implies acute inflammation and is therefore something of a misnomer. We prefer the term plantar fasciopathy, which is consistent with the current nomenclature used for disorders of the TA.
Examination
Patients with recalcitrant plantar fasciopathy are nearly always either sedentary and overweight, often with a very high body mass index, or, conversely, very athletic.
An assessment of the overall foot shape, when standing, is important. There is a strong association between planovalgus foot posture, gastrocnemius contracture, and heel pain. Hallux valgus or hallux rigidus impair the function of the medial column of the foot and should be noted. Careful examination of the whole plantar fascia is imperative. The site of maximal tenderness is most commonly at the medial calcaneal tuberosity (Figure 14.3). Any tenderness more distally in the fascia is particularly relevant. Pulses and sensation should be documented, paying particular attention to the presence of altered sensation or a positive Tinel’s sign behind the medial malleolus, as this raises the possibility of a diagnosis of tarsal tunnel syndrome. The calcaneum is squeezed between the examiner’s two hands; tenderness may indicate a calcaneal stress fracture, but the squeeze is often mildly tender in patients who have had plantar fascia pain for months or years. Calcaneal stress fracture is commoner in running athletes who have increased their training or in older female patients.
Figure 14.3 Tenderness at the medial calcaneal tuberosity.
Imaging
Plantar fasciopathy is not routinely imaged and treatment is started empirically. Recalcitrant cases benefit from investigation when first-line treatments have failed. A plain lateral weightbearing radiograph of the foot and ankle allows assessment of foot shape and may show: a healing calcaneal stress fracture; erosions to suggest inflammatory arthropathy; and a plantar heel spur, which confuses both the patient and many practitioners – as it can be absent in the presence of disease, or present in the absence of disease!
We use USS as our primary imaging modality for all recalcitrant cases (Figure 14.4). Experience with this has led to an improved ability to distinguish between plantar fasciopathy affecting the insertion of the fascia at the os calcis, and patients with “atypical” findings.
Figure 14.4 Ultrasound scan of plantar fascia.
A cohort of patients was followed prospectively with USS, and the scans were reviewed noting the characteristics of their plantar fascia disease.
This study included 125 feet, in 120 patients9. Sixty-six percent had only “typical insertional” pathology on USS (Figure 14.5). The remaining 34% had “atypical distal fascia disease” or a combination of insertional and distal disease. Patients with distal disease had either distal thickening or, occasionally, discrete fibromata.
Figure 14.5 Thickening of the calcaneal insertion of the plantar fascia.
The proportion of atypical, non-insertional disease was higher than expected and indicates that USS is valuable both for determining location and characterizing the nature of pathology in the plantar fascia. Atypical cases are harder to treat and so the information is useful when counseling patients and deciding about management options.
We advocate the classification of plantar heel problems into insertional fasciopathy or non-insertional fasciopathy. This mirrors the current classification of Achilles tendinopathy, and it is important to remember that the treatment of insertional disease is more predictable than that of non-insertional fasciopathy.
Empirical treatment is not adequate for recalcitrant cases of plantar fasciopathy and we advocate USS to confirm the clinical picture and classify the pathology.
Treatment
There are many different treatments that are used for plantar fasciopathy. The evidence for most is weak7–8. Formal calf stretching with additional stretches for the plantar fascia is the best first-line treatment5–6. The mechanism by which these stretches help is not well established10. Calf contracture is associated with a variety of clinical problems in the foot and ankle11–12. There is also laboratory evidence that increased plantar fascia strain is seen with increased calf muscle tension13. Many patients who have already “had physiotherapy” or “done stretches” have, on close questioning, either not performed the stretches properly or, more commonly, have not been sufficiently diligent with the program. Even after months or years of symptoms we advocate further intensive stretching efforts, including plantar fascia stretches and gastrocnemius-specific calf stretches. Night splints are a useful adjunct to the stretching program but may not be well tolerated.
For many years steroid injections have been used to alleviate pain from plantar fasciitis. Currently many orthopedic foot and ankle surgeons recommend that this is done under image guidance. The imaging modality can be fluoroscopy, sometimes under anesthetic as a day-case procedure, or alternatively under US guidance as an outpatient. Anecdotal experience is that this is a satisfactory treatment. However, a recent published randomized controlled trial showed no benefit of steroid over placebo after one month14. It is important to remember that cortisone injections are not free from side effects – thinning of the plantar fat pad and rupture of the plantar fascia can be particularly difficult to treat as there is no answer to the chronic pain that both these problems can cause.
Extra-corporeal shockwave therapy (ESWT) is a non-invasive treatment that administers pulsed, radial waves of energy that penetrate body tissues. Originally it was used to break up kidney stones. Lower energy ESWT has been used to treat calcific tendinitis of the shoulder, tennis elbow, plantar fasciitis, and both insertional and non-insertional tendinopathy of TA. There have been several modifications of the technology and this has led to confusion within the literature regarding the effectiveness of ESWT in treating musculoskeletal complaints.
The few well-designed studies that do exist have shown that radial ESWT is effective in the management of tendinopathy of TA and plantar fasciitis15–17.
The UK’s National Institute for Care and Health Excellence (NICE) has reviewed the available evidence for the use of shockwave therapy in plantar fasciitis and tendinopathy of TA. Their recommendation is that further high-quality research is needed.
Our experience has been favorable when using ESWT for the treatment of plantar fasciopathy affecting the insertion of the fascia onto the calcaneum. However, in the face of persistent biomechanical imbalance – contracture of the gastrocnemius – there is a much lower success rate. Patients who have gastrocnemius shortening are likely to fail to improve with ESWT, and yet the same patients are greatly improved after surgical gastrocnemius release. For this reason we advocate that gastrocnemius contracture that persists in spite of three months of proper stretching, ideally supervised by specialist physiotherapists, is treated surgically before considering the use of ESWT.
Non-insertional or atypical plantar fasciopathy is difficult to manage. ESWT does help a proportion of cases, usually when the USS demonstrates a short segment of fusiform swelling. More widespread abnormalities or discrete fibromata are probably best served with the provision of a relief orthotic.
What about the patient for whom all this still proves ineffective? Firstly, it is important to reconsider the diagnosis. There are very rare distal entrapment syndromes of the tibial nerve or its plantar branches18. More proximally an accessory soleus muscle may be responsible for plantar heel pain, which is usually exercise related, by exerting a mass effect upon the neurovascular bundle. Tarsometatarsal arthritis can also masquerade as arch pain with plantar tenderness located over the main body of the plantar fascia in the midfoot.
If the plantar fascia does still seem to be the cause of the pain then Topaz (radiofrequency needle ablation) treatment can be considered, and may be performed under tibial nerve block or general anesthesia. There are few published series19 and although sometimes beneficial the results in our experience are unpredictable.
When all conservative measures fail, surgical release of the plantar fascia has traditionally been performed, sometimes in combination with release of the first branch of the lateral plantar nerve20. Success rates as high as 90% have been reported in the literature20–21, but there are risks of plantar fascia rupture, plantar nerve injury, wound complications, and lateral column pain. In one study of 47 heels undergoing a plantar fascia release only 48% of patients were satisfied22. In light of the uncertain results and significant complications surgical plantar fasciotomy is not a treatment that we recommend.
Tendinopathy of Tendo Achillis
Posterior heel pain not arising from the TA is rare. Tendo Achillis pain was classified by Clain and Baxter as being either from the insertional or from the non-insertional portion of the tendon23. This division is helpful clinically as the management of the two different tendinopathies is very different.
Non-insertional TA pathology is much commoner than the insertional variety. As with tendinopathies elsewhere (knee, shoulder, elbow, and hip) there is degeneration within the substance of the tendon, thickening of the paratenon, and sometimes both. Modern research emphasizes that the changes seen in cases of tendinopathy are attributable to a “failed healing response,” rather than an acute inflammatory process.
Terminology
Maffulli proposed a logical system (Table 14.4) for describing TA pathologies. This reduced the use of the many terms that have confused the literature. The triad of pain, swelling, and impaired function is best referred to as tendinopathy of TA24. The pathology seen in chronic tendinopathy is of necrosis and mucoid degeneration. There is no inflammatory response and granulation tissue is rarely seen histologically. Thus the term tendinitis should be abandoned25.
Clinical
1. Tendinopathy – pain, swelling, and impaired function
2. Paratenonopathy – affects the paratenon clinically
3. Pantendinopathy – affects both tendon and paratenon clinically
Histological
1. Tendinosis – mucoid degeneration and collagen disorganization
2. Paratenonitis – hyperemia and inflammatory cells; fibrosis and thickening; more common in younger patients
Demographics
Although tendinopathy of TA is known to be common, reliable epidemiological data are not available26. The association with sports and athletic training suggests that overuse is the principal cause. Age also plays a role. Young athletes have a lower incidence of TA pain than older individuals participating in the same sport. Tendo Achillis pain is also seen in sedentary individuals39. Older athletes have a higher prevalence of insertional tendinopathy than their younger counterparts27. Symptomatic non-insertional tendinopathy is four times more prevalent than symptomatic insertional tendinopathy.