Volume 17, Issue 1, Pages 3-9 (March 2007)

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Degenerative plantar fasciitis: A review of current concepts

Abstract

Plantar fasciitis is a common cause for heel pain and is the result of a degenerative process of the plantar fascia at its calcaneal attachment. Age, obesity, excessive weight bearing and tight Achilles tendon are the common predisposing factors. Though this is a self-limiting condition, the time for resolution of symptoms is highly variable. Commonly used treatments are rest, analgesics, heat and cold application, stretching exercises, splints and orthoses. Local infiltration with steroids, radiotherapy, extracorporeal shock wave treatment and surgery are used in more resistant cases. We review the current understanding and concepts in the treatment of this condition.

Keywords: Plantar fasciitis, Degenerative process, Biomechanical alterations, Non-operative options, Surgery

Article Outline

• Abstract

• 1. Introduction

• 2. Aetiology and mechanics

• 3. Clinical features and diagnosis

• 4. Natural history and treatment options

• 4.1. Radiotherapy (RT)

• 4.1.1. Extracorporeal shock wave therapy (ESWT)

• 4.1.2. Local steroid infiltration

• 4.1.3. Surgery

• References

• Copyright

1. Introduction

Plantar fascia is the principle static and dynamic stabiliser of the longitudinal arches of the foot [1]. It also acts as a shock absorber and helps to protect the underlying soft tissues. Degenerative changes can cause acute and chronic inflammation and may also cause calcification at the origin of the plantar fascia and bony traction spur formation. Ten percent of the population experience plantar heel pain at some point during their lifetime and plantar fasciitis accounts for approximately 1% of all outpatient visits to orthopaedic clinics [2]. Traditionally the first line of treatment of plantar fasciitis has been rest, analgesics, night splints and orthoses. Patients not responding to this treatment are usually advised infiltration with corticosteroids, such as triamcinolone [3], [4], betamethasone [5] or iontophoresis with dexamethasone [6]. Surgery in the form of fasciectomy, neurolysis of the nerve to abductor digiti minimi and excision of the heel spur has been successfully used in resistant cases [7], [8], [9], [10], [11]. We review the current understanding and concepts in the management of degenerative plantar fasciitis.

2. Aetiology and mechanics

Plantar fasciitis results from a degenerative process in the central cord of the plantar fascia at its calcaneal attachment and is commonly seen in obese, middle-aged individuals. The etiology is multifactorial; mechanical overload is generally believed to be fundamental to the development of the condition. Obesity not only increases the risk of plantar fasciitis, but also increases the level of disability, which is proportional to the body mass index [12]. Work related weight bearing and biomechanical abnormalities in the foot such as tight Achilles tendon and reduced ankle dorsiflexion are common predisposing factors [13], [14]. During stressful activities, a greater force is transmitted along the medial side of the plantar fascia. With the knee extended, 10° of ankle dorsiflexion is required during normal walking. If the Achilles tendon is shortened, thereby limiting the amount of ankle dorsiflexion, excessive pronation of the foot may occur to compensate for the limited ankle dorsiflexion. Excessive pronation of the foot increases tensile loads on the plantar aponeurosis [14]. Kwong et al. have found excessive pronation of the foot is an important mechanical cause of structural strain which can result in plantar fasciitis [15]. These factors cause repetitive microtrauma and microtears, which impair normal healing processes thereby resulting in chronic inflammatory reaction.

Low arch or abnormal arch movements have not been found to be the cause of chronic plantar fasciitis but once present, abnormal arch mechanics can influence the severity of heel pain [16]. In unilateral disease, toe flexors have been found to be weaker than the normal side [17]. Electromyography studies have demonstrated increased levels of muscular activity [16]. This is an antalgic response. Digital flexion due to flexor activity acts as an additional brace for the medial longitudinal arch, thereby reducing stress within the plantar fascia [16]. Patients also tend to place the foot in a plantigrade position early during the stance phase. This protective mechanism reduces force transmitted beneath the calcaneus and forefoot and increases the load beneath the digits [18].

Theory of heel spur as a primary cause of heel pain has been discarded. However if of significant size, it could be secondarily responsible for pain by entrapping the nerve to abductor digiti minimi quintis, a direct branch from the lateral plantar nerve. The nerve is at risk where it passes dorsal to the plantar fascia and heel spur. The other possible site of entrapment is beneath the deep fascia of the abductor hallucis muscle. This is the basis for neurolysis and heel spur excision in resistant cases. Histological examination of the nerve has revealed findings consistent with chronic nerve compression and the excised plantar fascia has shown chronic inflammatory changes, pointing towards a multifactorial cause for heel pain [8].

3. Clinical features and diagnosis

The main symptoms of plantar fasciitis are pain, swelling and difficulty in walking. Pain is particularly severe with the first few steps taken in the morning or after a period of rest, and usually lessens after a period of warming up. Occasionally the pain may spread to the whole of the foot including the toes. Tenderness can be elicited over the medial calcaneal tuberosity and the pain exaggerates on dorsiflexion of the toes or standing tip toe [19]. The diagnosis is usually clinical and rarely needs to be investigated further. Ultrasonography [20], [21], bone scintigraphy [22] and MRI [23] have been used to evaluate plantar fasciitis. Increased thickness, hypoechogenecity, and biconvexity are the main diagnostic findings on sonography. Partial rupture, perifascial edema and intratendinous calcification are also observed [20]. Three phase bone scintigraphy shows diffuse increased activity along the fascia during dynamic and blood pool stages and focal increased activity at the inferior calcaneal surface in the late static phase [22]. Common MRI findings are thickened plantar fascia, peritendinous edema, bone marrow edema of the calcaneus, and fascial tears [23]. Perifascial edema is the most consistent finding in post-fasciotomy patients who have persistent or new onset heel pain. MRI is more helpful in evaluating patients with failed conservative management, postoperative pain, and other causes of heel pain such as tarsal tunnel syndrome, ganglion, osteomyelitis and stress fractures [24].

4. Natural history and treatment options

Plantar fasciitis is generally considered to be a self-limiting condition. However the time taken for the symptoms to resolve is highly variable. Prolonged symptoms, increased disability and limitation of activity is most often seen in obese patients, patients with bilateral symptoms and in those who had symptoms for more than 6 months before seeking medical advice [25]. Various treatment modalities available at present are rest, ice, heat, nonsteroidal anti-inflammatory drugs (NSAIDs), stretching exercises, heel cushions, heel cups, magnetic insoles, runner's shoe, night splints, taping, short leg walking cast, steroid injections, shock wave, radiotherapy and surgery.

Rest relives pain by avoiding further soft tissue injury, reducing inflammation, and aids faster healing. Ice therapy aims at reducing inflammation. Heat alleviates pain by increasing the Aβ nerve impulses and dampening pain transmission at the spinal level [26]. NSAIDs reduce chemical mediators of pain. Orthotics, casts, and insoles act by supporting the medial longitudinal arch of the foot and prevent excessive pronation of the foot thus reducing the strain on the plantar fascia. Splints keep the foot in neutral or dorsiflexed position and thus help to passively stretch the contracted tendo Achilles. Stretching exercises are done to actively increase and maintain the length and integrity of the plantar fascia and Achilles tendon. Steroids and radiotherapy reduce the local inflammation and pain. The precise mechanism of action of extracorporeal shock waves is not known but faster soft tissue healing, reduced calcification, increased blood circulation, inhibition of pain receptors and denervation have been thought to be responsible for the clinical effects [27]. Surgery aims at releasing the tight contracted plantar fascia, excision of the inflamed tissue, neurolysis of the entrapped nerve to abductor digiti quinti, and excision the spur that may mechanically stretch the fascia or compress the nerve.

The standard protocol for treating acute onset plantar fasciitis is nonsteroidal antiinflammatory agents, rest, stretching exercises, and heel cushions. Physiotherapy is directed towards weight bearing tendo Achilles stretching and non-weight bearing plantar fascia-stretching exercises. Tendo Achilles stretching (more appropriately termed as calf stretching) is done by standing and leaning into the wall with the affected leg placed behind the contralateral leg. The heel is kept firmly on the ground and knee is fully extended. Plantar fascia-stretching is done by passive extension of the metatarsophalangeal joints. Although Achilles tendon-stretching exercise has a beneficial effect, plantar fascia-stretching program has been found to yield better results. Stretching is commenced prior to weight-bearing in the morning, as weight-bearing without stretching may result in microtears and inflammation [28].

Foot orthotics used in the treatment of plantar fasciitis can be classified as rigid, semi rigid or soft. Rigid orthotics aim to control motion of the foot joints. By preventing pronation at the forefoot, they bring about the desired change in biomechanics of foot. They are made up of carbon fiber or firm plastic material that do not deform with weight bearing. Due to their compact size, they can be worn in most closed shoe and need little shoe modification. The primary function of soft orthotics is protection of the foot. They act as shock absorbers and improve comfort within the shoe. They are made up of soft compressible materials and hence they are bulky, requiring shoe modification. Semi rigid type performs an intermediate role of both dynamics control and protection. Well fitting and well cushioned, customized heel pads and soft moulded orthotics can provide good pain relief and are effective first-line treatment for the heel pain and loss of function associated with plantar fasciitis [29]. In resistant cases splints such as ankle dorsiflexion dynasplint may be used. When used alone and worn throughout the sleeping hours they produce long-term symptomatic relief [30]. However if the symptoms are of less than 12 months duration, addition of night splint to a standard regime will not provide any added advantage. Due to low cost and low morbidity, this may be tried in appropriately chosen recalcitrant cases [31].

There is renewed interest in taping the foot to relieve plantar heel pain. In a modification of low Dye’ taping a 2.5cm tape is applied along the skin sole junction starting from the fifth metatarsal head and ending at first metatarsal head. Additional tapes are used on the plantar aspect of the foot starting just proximal to the first MTPJ following a path diagonally beneath the foot, passing underneath the calcaneal-cuboid joint, around the heel, then diagonally back beneath the foot passing over the sustentaculum tali and finishing just proximal to the fifth MTPJ. Finally, stirrup strapping are also applied transversely across the plantar aspect of the foot starting level with the malleoli and finishing level with the MTPJs. Presumably taping supports longitudinal arches of the foot, resists elongation of the foot and absorbs stress resulting in reduction of stress on the plantar fascia. Pedobarographic analysis has also shown reduced peak pressure in the transverse arch. Also the area beneath the pressure/time curves in the region of the second and third metatarsal heads is reduced with increase in these values in the region of fourth and fifth metatarsal heads. This shift in pressure distribution at the forefoot level indicates reduced forefoot pronation, reduces load transmission along the first ray and reduced tensioning of the plantar fascia [32].

4.1. Radiotherapy (RT)

Multiple forms of low dose radiotherapy have been used by various investigators in the treatment of recalcitrant plantar fasciitis. Micke et al. have reported the largest pattern of care study on radiotherapy for plantar fasciitis. Most patients referred for RT had undergone extensive pretreatments including shoe modifications, nonsteroidal antiinflammatory drugs, local injections with corticosteroids or local anesthetics, various physiotherapeutic measures, extracorporeal shock wave treatment, and surgical interventions. Tiny fractions ranging between 0.3 and 1.5Gy were applied two to three times a week, to a total dose of 2.5–18.75Gy. Technical equipment used for RT consisted of linear accelerators, orthovoltage units, Co-60 machines or other treatment units. Despite this variation in radiotherapy application, a very large number of painful and refractory cases were effectively treated. Pain reduction for at least 3 months was reported in 70%, and persistent relief for a period of over 12 months was reported in 65% of the treated patients. Favorable prognostic parameters were pain of less than 6 months duration, fewer than two previous treatment attempts, and relief of symptoms with one RT series [33]. Single fraction radiotherapy with a dosage of 8Gy has also been found to be effective and is probably more acceptable than multiple dose regimes due to simplicity, convenience and low cost [34]. No side effects attributable to the treatment have been recorded. There are no reports on the predictable long-term and short-term complications of radiotherapy. Thus it could be a cheap, effective, reliable and a safe option available for the treatment of resistant cases.

4.1.1. Extracorporeal shock wave therapy (ESWT)

Shock waves are commonly used in renal stone fragmentation, avoiding the need for open surgery. They are characterized by a high positive pressure and a tensile wave. The energy of positive pressure is responsible for the direct shock wave effect. It is released at the interface between two different materials with different acoustic impedance. The tensile wave is known to cause cavitation effect. Shock waves are generated through electrohydraulic, electromagnetic, or piezoelectric principles and electrohydraulic method has been shown to be superior to other methods [35]. Though the precise mechanism of action is not known, effects such as accelerated soft tissue healing, reduced calcification, increased blood circulation, inhibition of pain receptors and denervation, are possibly responsible for the clinical effects [27]. It is usually applied under intravenous sedation with or without local infiltrative anaesthesia; either as a single large dose or in multiple divided doses, using a standard or a mobile lithotripter [36], [37], [38]. Ultrasonic localisation is usually done before the application of shock waves. ESWT is indicated if there is failure of other conservative modalities such as stretching exercises, casting or night splinting. Prior steroid injections of over three times appear to be a poor prognostic factor for good recovery following ESWT. As this is a relatively safe procedure with no clinically relevant side effects, it could be considered before any surgical treatment and may be preferable to try before steroid infiltration [39], [40]. Bilateral cases can be treated under a single anesthetic and full weight bearing may be started immediately. Normal activities of daily living and work may be resumed usually within 24h, an advantage over open or endoscopic fascial release [41]. Presence of calcaneal bone marrow edema on MRI has been found to be a good predictive indicator for a satisfactory clinical outcome following ESWT [42]. After shock wave treatment, the thickness of the plantar fascia in patients is known to decrease to that of controls level, with statistically significant improvement in walking time [43]. Unlike other conservative modalities, the duration of symptoms had little effect on the positive response to ESWT [44]. In fact the outcome of treatment has been found to be better in patients with long standing symptoms than in those with shorter duration of symptoms [45]. Good long-term effect has also been reported [46]; and the outcome is not dependent on the presence of heel spur and ESWT does not change the radiographic appearance of the heel spur [47].

A recent multicenter, randomised, placebo-controlled, prospective, double-blind trial has shown short-term improvement in the VAS and, pain and activity self-assessment scores. One hundred and fourteen patients who were resistant to other methods of treatment were randomised into two groups. A single dose of 1300mJ/mm2 of shock wave energy was applied to the foot under medial calcaneal nerve block. In the placebo group, shock wave penetration was prevented using a thin foam cushion. At 3 months post treatment, improvement in pain during the first few minutes of walking as measured by a visual analog scale was seen in both groups; with statistically significant improvement in the treatment group. There were also statistically significant differences between treatments in the number of participants whose changes in VAS scores met the study definition of success (>60% improvement from baseline in VAS scores for pain during the first few minutes of walking) and in the distribution of Roles and Maudsley pain and activity self-assessment scores. Pain, paresthesia, oedema and peripheral neuritis occurred more frequently with shock waves than with placebo [36].

In a double blind randomised trial to evaluate the role of ESWT, Speed et al. have found no treatment effect of moderate dose ESWT in subjects with plantar fasciitis. The results of their study indicate that moderate dose ESWT delivered using an electromagnetic generator has no significant benefit over placebo. The improvement shown with the placebo may explain the significant improvements noted by others in uncontrolled studies. It is not unreasonable that such a placebo effect can be noted, since pain, the cardinal symptom of musculoskeletal disorders, is the feature most responsive to a placebo effect. However, other factors that can lead to false impressions of a placebo effect are spontaneous improvement and fluctuation of symptoms. Although the technique is widely reported to be safe, there is a potential for haemorrhage and local soft tissue damage through cavitation. This appears to be more likely with higher doses of shock waves [27].

4.1.2. Local steroid infiltration

Local infiltration of steroids such as Triamcinolone or Betamethasone to the plantar fascia can produce short-term (weeks to months) alleviation of pain [3], [4], [5]. The point of maximum tenderness, which is usually along the medial heel border, is approached either from the plantar aspect or from the medial side and a mixture of local anesthetic with a steroid is injected. Ultrasonography and Technetium-labelled bone scans have also been used to precisely localise the inflamed area and guide the needle placement [5], [48]. Iontophoresis is another method of steroid delivery. Dexamethasone (0.4%) used by this route can produce early relief of symptoms when used in conjunction with other modalities such as stretching and strengthening exercises, and orthoses, but it has not shown any long-term advantages over direct infiltration. This may thus be useful in active patients requiring immediate relief of pain. Skin burning, sensory symptoms, prolonged erythema at the electrode site and metallic taste in tongue are the immediate complications associated with this procedure [6]. Infection has also observed following steroid infiltration, and one case of calcaneal osteomyelitis has been so far reported in the literature [49]. Serious life threatening infections such as necrotising fasciitis has been reported with steroid infiltrations to shoulder and it remains a possibility in heel infiltrations as well [50].

Long-term complications of steroid treatment are fat pad atrophy and rupture of plantar fascia [51], [52]. About 10% of patients develop either sudden or gradual symptomatic tear. In most of these patients the medial calcaneal pain disappears significantly but they may develop dorsal and lateral midfoot pain and swelling, stress fracture, weakness, lateral plantar nerve dysfunction and hammer toe deformity. The diagnosis is essentially clinical; based on symptoms, diminishing tension in the plantar fascia and flattening of the arches. A lateral plain radiograph shows significant decrease in the calcaneal pitch angle. Bone scan may reveal increased activity in the areas of pain [51]. The treatment is mainly conservative; NSAIDs, rest, and supportive orthoses. Though the majority of patients show improvement in their symptoms, the recovery is gradual and unpredictable.

A critical review of the randomised control trials conducted to evaluate various treatment modalities has shown that there is evidence to suggest a short-term improvement in symptoms following steroid injections. The role of ESWT, orthotics, heel cushions, stretching exercises and night splints is limited. There was no evidence to support effectiveness of therapeutic ultrasound, low-intensity laser therapy, and exposure to an electron generating device or insoles with magnetic foil. Well designed and conducted randomised trials are suggested to evaluate the role of these treatment modalities [53]. A review of literature, has found that all trials report some improvement in patient's mean pain scores in both treated and non-treated populations. This could possibly be due to the placebo effect experienced from simply participating in a trial. It is thus suggested that, trials evaluating a treatment modality should be designed to eliminate these biases [54].

Recently investigators have used botulinum toxin in the treatment of resistant cases of degenerative plantar fasciitis. Botulinum toxin inhibits presynaptic release of acetylcholine; and is mainly used to relieve intractable muscle spasms in various ophthalmological and movement disorders. Short-term results of a prospective randomised trial involving injection of Botulisn toxin A (BTX-A) in the treatment of resistant plantar fasciitis has been encouraging. Patients who failed to respond to most of the treatment methods except shock wave and surgery were involved in the trial. A total of 40 units of BTX-A was injected at the medial calcaneal tuberosity and 30 units to the most tender point of the arch of the foot (between an inch anterior to the heel to the middle of the foot). At 3 and 8 weeks, there was a statistically significant improvement in the pain visual analogue scale, Maryland foot score and Pressure algometry response. No known complications were noted in these patients [55].

4.1.3. Surgery

Recalcitrant cases where symptoms persist for more than 6–12 months, even after adequate conservative treatment are usually selected for surgery. Open release, endoscopic fasciectomy, percutaneous and radiofrequency lesioning are various modes of plantar fascia release described. Earlier reports were of open release of plantar fascia with either a longitudinal or transverse incision, neurolysis of the nerve to abductor digiti minimi and excision of the heel spur [7], [9], [56]. Percutaneous release of plantar fascia has been reported to be a simple and cost-effective method with results comparable to other techniques [57]. Emphasis is placed on partial release of the fascia to avoid biomechanical complications of complete release. The results of partial release of plantar fascia have also been found to be satisfactory. This procedure combined with the neurolysis of the nerve to abductor digiti minimi has been shown to produce better results with average recovery time of 1.5 months [8], [58]. Endoscopic release of plantar fascia is less painful, minimally traumatic, allows early return to physical activities and has yielded excellent results. It is usually performed by a two portal technique with the medial portal along the line of posterior border of the medial malleous. The cannula is placed superficial to the fascia and release is done from superficial to deep to avoid neurovascular damage [59], [60]. Endoscopic treatment leads to slightly enhanced recovery time compared to the traditional open release, but the long-term results seem to be equivalent [61]. Good results following endoscopic procedure indicate that entrapment neuropathy may not be a significant etiological factor [62].

A triad combination of plantar fasciitis, posterior tibial tendon dysfunction and tarsal tunnel syndrome has been recognised in 5% of patients presenting with chronic heel pain. It is postulated that failure of static and dynamic stabilisers of the medial longitudinal arch, (i.e., plantar fascia and posterior tibial tendon), resulted in traction injury to the posterior tibial nerve or tarsal tunnel syndrome. These patients typically have collapsed medial longitudinal arch and heel valgus. They have been treated effectively by complete release of the plantar fascia, decompression of the tarsal tunnel, and augmentation of tibialis posterior with flexor digitorum longus tendon. Additional hind foot stabilisation procedures such as subtalar arthrodesis, osteotomy or triple arthrodesis was required to correct heel valgus and restore medial arch depending on the stage of posterior tibial tendon dysfunction [63].

Biomechanical alteration is the main concern of plantar fascia release. Complete release can lead to significant loss of windlass mechanism and increase bony stress reactions of the calcaneus [1], [64]. Equinus rotation of the calcaneus and a drop in the cuboid develop after complete release of plantar fascia. This increases strain on the plantar calcaneocuboid joint capsule and the plantar ligaments and is probably the likely cause of lateral midfoot pain that develop in these patients [65]. Pain is present in the area of the sinus tarsi, extensor digitorum brevis muscle, between the fourth and fifth metatarsals, and calcaneocuboid joint [66]. This complication can be prevented by partial release of the fascia and is particularly effective if the release is less than 50% [67]. When compared to partial medial third release, complete release will lead to collapse of medial arch by 62% and lateral arch by 100% [65]. Following complete plantar fascia release, the tension stresses carried by the long plantar ligament increase significantly, and may exceed by more than 200% of the normal average stress [68]. Upon loading of the sequentially released plantar fascia, the force in the remaining fascia increased significantly, and the force was shifted later in propulsion. The subtalar joint was unable to resupinate as the amount of fascia release increased, indicating a direct relationship between the medial band of the plantar fascia and resupination of the subtalar joint during late midstance and propulsion [69]. Increase in lateral length, decrease in the height of the medial longitudinal arch and widening of the inferior sinus tarsi space have also been documented. It is postulated that consequent upon this, straining the bifurcate and cervical ligaments, the lateral talocalcaneal ligament, and interosseous talocaneal ligaments may account for the lateral column pain. Reduced arch height also increases the incidence of acute tear of posterior tibial, peroneus longus and brevis tendons and the structural integrity of the foot could be maintained if 75% of plantar fascia is intact [66]. The stress under the metatarsal heads particularly the second metatarsal increase with increase in release of the fascia [70].

Other reported complications of plantar fascia release are scar tenderness, superficial cellulitis, deep vein thrombosis, superficial phlebitis [8], partial wound dehiscence, mild dorsal midfoot pain [58], lateral heel pain, superficial wound infection, and transient lateral paresthesia [62], [71].

A particular complication that may follow an endoscopic procedure is the neurovascular injury. A case of traumatic pseudoaneurysm of lateral plantar artery that followed endoscopic plantar fascia release has been reported. Weight bearing precipitated recurrent bleeding that resulted in severe hypotension, which was treated by exploration and ligation of the vessel. Meticulous attention to the plane of dissection could avoid such a complication [72].

Due to prolonged natural history and, self-limiting and fluctuating nature of the condition, resolution of symptoms after surgery may not be attributable to surgery itself [25]. However some of the patients may well genuinely be surgical candidates with nerve entrapment and posterior tibial tendon dysfunction. Chronic bilateral heel pain in obese individuals with failed conservative treatment who have reported late for medical treatment, and those who present with resting heel pain and paresthesia of the sole of the foot, suggesting entrapment neuropathy and/or with evidence of posterior tibial tendon dysfunction may well qualify as surgical candidates.

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a Department of Trauma and Orthopaedics, George Eliot Hospital, Nuneaton CV10 7DJ, Warwickshire, United Kingdom

b Department of Trauma and Orthopaedics, Warrington General Hospital, Warrington, United Kingdom

Correspondence to: 34, Chester Place, Chelmsford CM1 4NQ, United Kingdom

PII: S0958-2592(06)00086-1

doi:10.1016/j.foot.2006.07.005

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