Plantar fasciitis is usually the cause of heel pain, which is the most common patient complaint about foot pain. Treatments for a variety of foot ailments are given, including bunions, hammer toes and claw toes. Ill-fitting shoes are often a cause of foot pain.
Under managed care, more and more patients with foot pain are appearing in your office first. What’s needed is a straightforward approach to plantar fasciitis, bunions, flatfoot, hammer toes, and other frequently seen problems.
In 1995, 15 million Americans sought medical care for foot complaints. More than half of them were seen initially by orthopaedists or podiatrists. The rest visited a primary care physician first.
Statistics for 1996 are showing a gradual shift toward primary care. As managed care places more onus on primary care physicians, formulating diagnoses and establishing office-based treatment protocols for foot problems have increasingly become priorities. Here’s what you need to know to evaluate and treat the clinical entities that encompass 90% of structural foot complaints: plantar fasciitis; bunions and bunionettes; mallet toes, hammer toes, and claw toes; fractures; tendinitis and bursitis; and the structural deformities of pes planus and pes cavus.
Heel pain is the most common foot complaint seen in an office setting, and by far the most common cause of heel pain is plantar fasciitis. The plantar fascia is a strong but elastic band of fibrous tissue that originates from the anteromedial calcaneal tubercle alongside but superficial to the short flexor muscles of the toes. It terminates in multiple slips that insert into the proximal phalanges in the forefoot.
Since the plantar fascia plays an important role in the support of the longitudinal arch, it is under constant strain during walking and standing. Any ambulatory patient can develop fasciitis, but it tends to be more common in athletes and active people older than 30 – probably because of a gradual loss of tissue elasticity and subsequent degeneration at the calcaneal attachment. Other risk factors are obesity, gout, rheumatoid arthritis, systemic lupus erythematosus, and positive findings on an HLA-B27 blood test. Chronic strain – or even the sudden off-balance impact at heel strike in a runner – can initiate an inflammatory response in the fascia. Ensuing microruptures, hemorrhages, and collagen degeneration lead to fibrosis of the plantar fascia and possible ossification between the origin of the flexor digitorum brevis and the fascia that manifests as a heel spur.
The patient usually describes the pain as nonradiating and well localized to the medial aspect of the heel pad. It may have been present for a short time, for months, or even for years, but in nearly all cases the pain is worse with the first step in the morning no matter how gingerly the foot touches the floor. This pain diminishes with each successive step but may return late in the afternoon after prolonged weight bearing or rising from a long period of sitting.
The runner often describes a stage of relative inactivity followed by intensive training in which pain appears at the beginning of the run, becomes bearable for a few miles, and then gradually increases again. The homemaker describes a period of excessive standing followed by a change in activity such as spring cleaning. The symptoms are predominantly unilateral, but bilateral involvement occurs in 10% of cases. If bilateral symptoms are persistent, consider the possibility of systemic collagen disease.
The most important physical finding is tenderness of the fascia] attachment on the medial tubercle of the calcaneus. Sometimes a fair amount of pressure is needed to reproduce the pain. This localized tenderness is quite distinct from any other cause of heel pain. Although the tenderness may extend about 1cm distally along the fascia, the remainder of the plantar fascia is not tender. If other tender points are elicited, the diagnosis of plantar fasciitis is doubtful.
In plantar fasciitis, passive dorsiflexion of the foot – and, specifically, the great toe – elicits a painful response. So does toe walking. If the plantar fascia is not involved, toe walking often relieves heel pain.
Check for tightness of the Achilles’ tendon and pronated (flat) or cavus (high) arch deformities. Any of these conditions may magnify the symptoms and predict a slow response to treatment.
The differential diagnosis of heel pain also should consider the following five conditions:
- Tarsal tunnel syndrome: Palpation for irritation of the posterior tibial nerve situated off the heel pad on the medial side of the heel produces a radiating pain pattern that follows the innervation of the nerve. This area of innervation is not tender in patients with plantar fasciitis.
- Heel pad atrophy: Symptoms arise from direct palpation of the bone through the atrophic fat pad.
- Stress fracture of the calcaneus: The entire heel is tender to pressure, both medially and laterally.
- Rupture of the plantar fascia: This acute process is accompanied by swelling and ecchymosis.
- Achilles’ tendinitis: Heel pain is on the posterior rather than plantar surface and can be elicited by squeezing the tendon.
The diagnosis of plantar fasciitis can usually be made from the history and physical findings; further studies are rarely needed. If the patient has brought x-ray films to the visit, examine them for stress fractures, cysts, tumors, and foreign objects such as needles. A very prolific periostitis indicates a systemic disease, and further studies may be necessary.
Horizontal calcaneal spurs are seen in more than half of patients with heel pain and in a few who are asymptomatic. These spurs are not a source of pain and should not influence management.
A lateral x-ray of the heel is warranted if the patient has not responded to treatment within two months and before corticosteroid injection is offered. Bone scans or electromyographic and conduction studies are of limited value in the differential diagnosis of heel pain.
Patient education is a primary goal in plantar fasciitis. Explain that the condition is self-limiting, usually lasting 2-3 months, but can persist for up to 10 months. A long trial of conservative treatment should be expected. Surgery is rarely contemplated before two years have passed, except sometimes for elite athletes with subacute plantar fasciitis who have fewer than 10 months to train for competition.
Treatment begins with a small, inexpensive heel pad to lift the heel, nonsteroidal antiinflammatory drugs (NSAIDs) taken for up to 2-3 weeks only, and exercises to stretch the plantar fascia performed for 20 seconds 4-5 times a day. Most patients are more comfortable using a heel pad in both shoes, even when plantar fasciitis affects only one foot. This regimen, combined with a decrease in activity for six weeks, relieves pain for 70% of patients. Emphasize to the patient that stretching is by far the most important part of this regimen.
If there is no improvement in six weeks, an ankle-foot orthosis placed in 10 degrees of dorsiflexion is used as a night splint. Hot and cold soaks – so-called contrast soaks – may help at this point. Recommend 15 minutes twice a day to start, with half of each 15 minutes given to a hot soak and the other half to cold. The exercise program stresses power building as well as stretching. Runners should be evaluated carefully for pronation deformities that need orthotic correction to decrease stress on the medial-based plantar fascia.
If improvement is only minimal after another 6-8 weeks, corticosteroid injection may be helpful. Use a medial injection parallel to the fascia, close to the bone and away from the fat pad. This approach is less painful and reduces the chance of fat pad atrophy. Use of a cryospray before injection can also help. As long as the patient is responding, three injections may be given 24 weeks apart; 95% of patients will do well with this treatment. The rest will have pain recalcitrant to treatment after two years. These 5% of patients may be surgical candidates and should be referred for further workup.
In patients with early, very resistant and diffuse heel pain, consider the diagnosis of calcaneal stress fracture. Although uncommon, it may occur in the early phases of conditioning after prolonged periods of standing. Look for swelling medial and lateral to the calcaneus. With persistent pain, a lateral x-ray obtained 6-8 weeks after initial symptoms may show evidence of a fracture or fracture healing. If stress fracture is likely, casting followed by limited weight bearing for three weeks may relieve symptoms.
The first metatarsophalangeal (MP) joint is the most complex in the forefoot. It anchors the distal end of the medial arch and plays a major role in the transmission of body weight during walking. Oddly enough, the muscle attachments at the joint bypass the metatarsal head and attach to the proximal phalanx. This configuration essentially leaves the metatarsal head supported only by the weak medial capsule, so any abnormal stress at this point may easily lead to deformity.
The term bunion – from the Greek word for turnip – has been used for any deformity or enlargement of the first MP joint. These include an enlarged bursa, inflammatory bursitis, an enlarged bony medial prominence, a ganglion cyst, and the proliferative changes of arthritis. Hallux valgus (HV) is a more demonstrative diagnostic term indicating a static subluxation of the first MP joint. This includes lateral deviation of the great toe and medial deviation of the first metatarsal. When push comes to shove, an HV deformity is a bunion, but a bunion is not necessarily an HV deformity.
HV deformities occur almost exclusively in people who wear shoes, with 35% of all shod persons having HV compared with only 7% of the unshod. Modern footwear is the principal cause of this condition, and there is as high as a 15:1 female to male predilection. One recent study reported that 88% of 356 healthy female subjects had often worn shoes that were at least one-half inch too narrow.Other studies indicate that as heel height increases, plantar pressure increases by 75%. Dr. Michael Coughlin, past president of the American Orthopaedic Foot and Ankle Society, has stated that 75% of the total number of surgical forefoot procedures probably result from women wearing ill-fitting shoes, with a conservative estimate of surgical fees, hospital costs, and time lost from work to be several billion dollars yearly
Some feet appear to be more vulnerable to the effects of footwear than others. Current studies show a high familial incidence, especially in juvenile HV. Transmission is apparently autosomal dominant. New studies are in the works to shed light on whether hereditary predisposition is the major underlying factor in bunion development, with constrictive footwear being the factor that precipitates a clinical condition. Other predisposing factors include contractures of the Achilles’ tendon, as seen in patients with cerebral palsy or stroke; joint hyperelasticity; and a pronated foot. Excessive foot width (greater than size B in females and D in males) seems to be a factor in 10% of patients.
Bunions are often staged as I-IV according to severity.
Stage I: Very little deviation of the toe is demonstrated, but affected patients have a large medial prominence at the MP joint. This prominence or bump is the uncovered medial aspect of the metatarsal head that has hypertrophied in response to pressure from years of wearing excessively constrictive footwear. The initial symptom of pain at this stage is often inflammation in a small bursa formed over the medial prominence. Thickening of the bursal wall accentuates the prominence and the pain.
Stage II: Mild deformity is seen. The toe is starting to deviate, but the angle formed by the intersection of lines bisecting the proximal phalanx and the first metatarsal – the HV angle – is less than 20 degrees and the intermetatarsal angle is less than 10 degrees. There is no associated lateral subluxation of the sesamoid bones as seen on anteroposterior x-ray.
Stage III: Moderate deformity has occurred. The HV angle is 20-40 degrees, and the lateral sesamoid is displaced about 75% from beneath the metatarsal head. As the deformity increases, the toe starts to pronate.
Stage IV: Severe deformity is present. The HV angle is greater than 40 degrees, with marked lateral deviation, overlapping of the second toe, and pronation of the great toe. X-rays show 100% subluxation of the lateral sesamoid; congruity at the metatarsophalangeal joint is completely lost.
After taking an adequate medical history, determine the patient’s main concern. When treating bunions, clinicians’ failure to follow this rule causes more patient unhappiness than anything else. Does the patient care mainly about cosmesis, second-toe deformity, problems with shoe fit, or pain? Make sure your treatment is aimed at the correct complaint – that is, don’t recommend a surgical evaluation to a patient whose bunions don’t hurt. The patient’s occupational and recreational requirements may also affect selection of treatment.
Education is paramount. The patient must understand precisely what can be achieved with treatment so that expectations do not exceed treatment goals. Staging of the deformity helps to set realistic goals.
Patients with stage I bunions have essentially an inflammatory condition. Since pain is the predominant concern, the treatment should be aimed toward relieving it. NSAIDs, contrast soaks, inexpensive OTC pads found in most drugstores, and wide, soft-soled shoes with an adequate toe box are the treatments of choice. As long as you have ruled out gout, 90% of patients with stage I bunions will probably be happy with your treatment. An occasional patient will require a bursal corticosteroid injection.
Stage II patients are usually starting to show early signs of toe deviation in addition to having pain. Family history becomes important in prognosis, and education figures prominently in the treatment. Place the patient’s shoe alongside the weight-bearing foot to emphasize that the first approach to treatment should be to buy shoes with a wider toe box. Another simple but effective measure is to modify shoes by stretching and eliminating pressure points such as seams or stitching. Bunion pads, night splints, bunion posts, and other commercial appliances seem to work better at this stage.
Stage III patients most often present with cosmetic concerns. Most of the early inflammatory pain has been treated or has responded to more comfortable shoes, but patients are still unhappy with how their foot looks. Treatment can be difficult because the condition is usually asymptomatic. Surgery is definitely not warranted, but a custom orthosis may be helpful. Stabilizing the heel, raising the medial arch, and providing a metatarsal pad often dramatically change the appearance of the foot. These interventions also allow a better shoe fit, especially when bunions are associated with a pronated foot.
Stage IV patients, with severe deformity of the great toe commonly associated with an overlapping second toe, are often surgical candidates. As a rule, pain is a concern and the progressive deformity is affecting quality of life. Usually by this time the patient has become dissatisfied with conservative treatment. Referral to a qualified foot specialist is appropriate, but stress that surgery is never a quick fix. Recovery from bunion surgery may take as long as 6-12 months.
The bunionette (tailor’s bunion) is a mirror image of the first metatarsal bunion occurring on the lateral side of the fifth metatarsal head. This enlargement develops from hypertrophy of the soft tissue or lateral deviation of the metatarsal head. Regardless of cause, pressure from too-tight shoes causes a thickened bursa to form over the enlargement, which in turn becomes painful and swollen. Treatment with a broad-toed shoe and relief pads is essential because continued pressure leads to an irreversible condition alleviated only by surgical correction.
MALLET TOES, HAMMER TOES, AND CLAW TOES
These clinical entities are often confused, a situation that isn’t helped by the tendency of Some physicians to use the terms mallet toe, hammer toe, and claw toe interchangeably. A clear understanding of the deformities is necessary before a sound treatment program can be established.
A simple nomenclature can be used to delineate these conditions:
* Mallet toe involves the distal interphalangeal joint with the distal phalanx flexed on the middle phalanx.
* Hammer toe involves the proximal interphalangeal joint with the distal and middle phalanges flexed on the proximal phalanx.
* Claw toe is a hammer toe deformity associated with dorsifiexion at the metatarsophalangeal joint. These deformities are acquired, with ill-fitting shoes playing the leading role in development of hammer toes and mallet toes.
Pay special attention to a claw toe, which is often neurologic in origin. As this deformity becomes more rigid and the hammer toe component strikes the shoe, the dorsiflexed proximal phalanx drives the metatarsal head down into the forefoot. Metatarsalgia and painful callosities may result. If prolonged, a claw toe produces ulcerations that are difficult to treat conservatively.
The secret to the successful management of mallet toes, hammer toes, and claw toes is to catch them early, while the deformity is still flexible. Once the patient’s joints have become rigidly contracted, extensive surgical correction will be required.
The most important conservative measure in the flexible hammer toe and mallet toe is to get the patient into spacious, well-fitted shoes. If there is pain beneath the metatarsal head, use a soft metatarsal pad inside or a metatarsal bar outside the shoe. Almost as important is to start the patient on a program of daily manipulation of the toes to maintain flexibility in the joints.
Fractures of the foot are among the most common of all musculoskeletal injuries seen in an office setting. Early recognition and proper management are critical to preventing a chronically painful foot. Even minimal, well-aligned fractures may lead to stiffness and loss of mobility, or a small bony projection can produce pressure when it comes in contact with the shoe. Remember that localized tenderness is a hallmark of foot fractures. This, together with knowledge of the common fracture sites, makes diagnosis less of a challenge.
Medilal-lateral tenderness and severe heel pain after an axial load point to a calcaneus fracture. Obtain a lateral plain radiograph to look for displacement at the fracture site and to see whether there is extension into the joint. Nondisplaced extra-articular fractures can be managed with a short leg walking cast or boot for 4-6 weeks. Displaced fractures should be referred.
Common midfoot fractures include stress fractures of the navicular and fractures of the base of the fifth metatarsal. The navicular, the apex of the longitudinal arch, is second only to the second metatarsal as a site of stress fractures of the foot. The usual picture consists of an active patient with vague, diffuse, dull midfoot pain that increases with activity. Persistent pain and tenderness over the navicular are suspicious even when an early x-ray is negative. A technetium bone scan will assist the diagnosis. With early diagnosis and no displacement at the fracture site, treatment consists of a non-weight-bearing short leg cast for 6-8 weeks. A displaced fracture requires surgical internal fixation.
Fractures of the base of the fifth metatarsal are the most common type of metatarsal fracture. Nonarticular fractures through the proximal tuberosity are treated with a wooden shoe until symptoms cease, even if there is displacement. If the fracture extends into the joint, the patient should use a short leg walking cast for 4-5 weeks.
Much more difficult to treat is the Jones fracture, occurring at the point where the base of the metatarsal becomes the shaft of the bone. This is an area of decreased blood supply and is prone to nonunion and persistent pain. Six weeks in a nonwalking cast is the preferred treatment, although surgical fixation is an alternative in the very active patient or competitive athlete. Acute fractures of the metatarsal shaft are usually minimally displaced and are treated with a short leg walking cast for six weeks.
The most common forefoot fracture is a stress fracture of the second or third metatarsal neck. Persistent forefoot pain and bone tenderness in an active person represent a stress fracture until proven otherwise. Treatment with a wooden shoe for 3-4 weeks should decrease symptoms; if not, consider Morton’s neuroma and look for a cause of metatarsaigia. Fractures of the great toe should be straightened and treated with a wooden shoe or cast with a toe plate – unless the joint is involved, when surgical correction is used to prevent painful arthritis of the toe. Fractures of the lesser toes should also be straightened, with the injured toe buddy-taped to the adjacent toe until tenderness ceases.
When treating injuries of the foot, concentrate on maintaining mobility. If the patient has a beautifully healed fracture and a foot that is stiff and painful, you have not accomplished your treatment goal.
Rehabilitation of the surrounding soft tissues is critical. Leaving the toes free in a cast, encouraging movement and early weight bearing when possible, and even bivalving a nonweight-bearing cast for mobility exercises can prevent chronic pain. Early motion, elevation, and weight bearing also decrease the incidence of reflex sympathetic dystrophy, a condition often difficult to diagnose until irreversible damage has occurred.
Extensive rehabilitation of the foot after casting is essential for a good result. This can be accomplished by formal physical therapy or by having the patient walk in the deep end of a swimming pool, where the resistance of the water provides the mobility. Exercise in a swimming pool is preferred to exercise in a whirlpool. Lastly, remember that a longitudinal arch support and a soft comfortable shoe encourage weight bearing in the rehabilitation of a painful foot.
TENDINITIS AND BURSITIS
Tendinitis in the foot is difficult to treat, especially when it has become chronic. Prompt attention is imperative to prevent stretching, degeneration, and rupture of the tendon. Because of the stresses of weight bearing, inadequately treated tendinitis commonly leads to foot deformities. The tendons most frequently affected are the posterior tibial, Achilles’, flexor hallucis longus, and peroneus longus and brevis.
Posterior tibial tendinitis
This condition is the most common cause of gradual, progressive, and chronic medial mid-foot pain, especially in women 50-70 years old. The posterior tibial muscle is a strong inverter and plantar flexor of the foot. It also supports the medial arch and keeps the foot from hyperpronating during the midstance phase of walking or running. Microtrauma to the tendon leads to inflammation, progressive degeneration, and possible rupture. The tendon acts much like a rope on a pulley around the medial malleolus and then attaches to the navicular at the apex of the medial arch. An accessory navicular bone may add to the pain picture and should be looked for.
Initially, the patient presents with medial ankle pain and swelling. There is localized tenderness over the tendon, notably in the portion from the medial malleolus to the navicular, and decreased inversion strength against resistance.
Conservative treatment at this stage consists of 4-6 weeks of cast immobilization holding the foot in slight inversion and plantar flexion. Oral NSAIDs are helpful as well. If immobilization is unsuccessful, you may consider a corticosteroid injection in the tendon sheath, being careful not to inject the tendon substance. Advise the patient to rest the foot for at least 10 days after any injection. No more than two injections should be given, with a two-week interval between them.
Excessive pronation must be prevented using a medial heel wedge or orthoses. When the tendon is stretched or ruptured, there is an abnormal forefoot pronation with accompanying heel valgus and abducted foot. This is best viewed from behind the standing patient and is often called the “too many toes” sign. In patients with this sign, pain may shift to the lateral ankle as a result of impingement of the lateral ligaments in the sinus tarsi. With any persistent signs of stretching or collapse of the medial foot, referral for surgical evaluation is necessary.
After plantar fasciitis, Achilles’ tendinitis is the most frequent hindfoot disorder in active people. The cause is usually overuse – a sudden increase in training mileage, a switch to uneven terrain, a long hike, or a hurried run to catch an flu’plane. Achilles’ tendinitis may also occur secondary to use of fluoroquinolone antibiotics: Although an uncommon adverse effect, it should be mentioned to active people taking these drugs.
Achilles’ tendinitis can present early as a peritendinitis in which the inflammation has a spongy feel. Upon movement of the foot, the pain tends to stay in one location. Tenderness is several centimeters proximal to the insertion of the tendon into the calcaneus. It’s important to recognize and treat the condition at this stage, before repeated microtrauma and restricted blood flow produce inflammation and degeneration in the tendon that can lead to rupture.
Initially, treatment includes contrast soaks, ice massage, and NSAIDs. As the inflammation starts to subside, a temporary 3/8-inch felt heel pad is placed inside the shoe and a program of gentle stretching is begun to take the stress off the tendon. The patient should warm up the tendon before starting the stretches and work below the limits of pain with slow, controlled movements against an elastic cord. Maximum benefit is usually achieved if the patient can work up to 5-6 stretches performed 3-4 times a day.
If the injury does not respond to this regimen and range of motion is being steadily lost, the patient can be referred for a rapid infiltration of 15 mL of 1% lidocaine HCI (Xylocalne HCI) into the sheath, which produces a mechanical lysis of adhesions. Gentle stretching is then resumed. If this approach also fails, open lysis of the adhesions may be performed.
Some patients may present later in the disease process with true Achilles’ tendinitis. Chronic repetitive stresses produce a fusiform swelling that is firm to palpation. Dorsiflexion of the ankle is decreased to less than 15 degrees (normal is 25 degrees). Strain causes pain within the substance of the tendon that moves with movement of the foot and increases with activity. Degenerative changes within the tendon predispose to rupture with repeated stress.
Treatment at this stage includes NSAIDs and 1-2 weeks in a non-weight-bearing cast, followed by ice, stretching, and assessment of the foot and leg alignment to determine if orthotic correction is needed. If symptoms persist beyond six months, referral for surgical evaluation is recommended.
This injury often occurs after an inversion injury of the ankle that produces a lateral ligament sprain. The sprain is treated successfully, but pain persists in the lateral midfoot and ankle. You may note clicking laterally with an occasional sensation of giving way. Tenderness is well localized to the section of peroneal tendons from the lateral malleolus to the base of the fifth metatarsal. The tendon sheath is usually swollen, and resisted eversion reproduces the pain.
Treatment is aimed at reducing the stress on the tendon by using lateral or eversion wedges or orthoses. If symptoms are severe, a cast is used for 2-3 weeks to rest the tendon, followed by extensive rehabilitation. For resistant symptoms, corticosteroid injection within the tendon sheath can be used, followed by the usual injection precautions.
If the tendinitis is secondary to subluxating or dislocating peroneal tendons, the predominant pain and tenderness will be proximal and behind the lateral malleolus. In your examination, attempt to palpate abnormal movement of the tendons. If findings are positive, referral is indicated.
Flexor hallucis longus tendinitis
This type of tendinitis is most commonly seen in persons who repeatedly execute push-off maneuvers – ballet dancers, for example. Excessive forces along the tendon cause irritation and inflammation in the tendon and sheath. Patients complain of pain and tenderness in the posteromedial aspect of the ankle and sometimes in the medial arch. Passive extension of the great toe is limited with the foot in neutral position and normal with the foot plantar-flexed.
Taping of the foot, use of longitudinal arch supports and oral NSAIDs, and contrast soaks afford relief for most patients. Occasionally, surgical release will be necessary.
Retrocalcaneal bursitis or tendo-Achillis bursitis may occur in the posterior aspect of the heel. The retrocalcaneal bursa located between the Achilles’ tendon attachment and the posterior angle of the calcaneus is the only consistent aharomic bursa in the foot. Together with the small, acquired subcutaneous bursa superficial to the tendon, it serves to protect the Achilles’ tendon from external pressures. As a result, these bursae are themselves subject to tension from a tight heel counter. When an excessively prominent calcaneal bursal projection, or Haglund’s deformity, is also present, inflamed bursae and pain localized to the Achilles’ insertion can result. The Haglund’s deformity is usually palpable, but a lateral x-ray of the heel demonstrates the prominence very nicely.
Retrocalcaneal bursitis produces diffuse swelling and fullness in an area directly in front of the tendon and posterior to the calcaneus. Tenderness is detected by applying pressure medially and laterally just anterior to and above the insertion of the tendon. Chronic inflammation of the tendo-Achillis bursa leads to a distinct, painful enlargement on the posterior aspect of the heel that is often called pump bump. This condition is most frequently seen in adolescent girls when they start wearing high heel shoes with restrictive heel counters. It may also develop in iceskaters, skiers, and hockey players secondary to poorly designed heel counters. Direct pressure over the enlargement will elicit pain.
Rest, ice, oral NSAIDs, and a change in footwear are the cornerstones of treatment and will control symptoms in most cases. Although corticosteroids should rarely be used near the Achilles’ tendon, a well-localized injection using a short needle and excellent technique will usually cure retrocalcaneal bursitis. Local corticosteroid injection, however, is never advised in tendo-Achillis bursitis as it may produce Achilles’ tendon rupture or skin and subcutaneous atrophy. Surgery may be an option in recalcitrant cases, but the results are frequently unsatisfactory.
The two most prevalent foot deformities encountered in office practice are the flatfoot (pes planus) and the foot with an excessively high arch (pes cavus).
The flatfoot is difficult to classify; there is no real standard as to how flat is fiat. The integrity of the medial plantar ligament (spring ligament) seems to be a primary determining factor in the shape of the longitudinal arch. In 10-20% of the population, this ligament does not tighten and varying degrees of flatfoot develop. Approximately 1 in 1,000 affected persons will have pain. The asymptomatic flexible flatfoot requires no treatment – except possibly in children, where some controversy still remains. You may need time, however, to convince a demanding patient of this.
At the age of 12-14 months, all children have fiat feet. At 24 months, the arch starts to develop, and by 5-7 years in girls and 8-10 years in boys the ligaments are starting to tighten significantly. The appearance of the parents’ feet, although often similar, is not a statistically proven determinant of what the child’s feet will look like and should not influence management.
Even older children with pes planus rarely have foot pain. If they do, it is usually in the legs and at night. The pain most often is coming from spasm in the posterior tibial muscle, which has been stretched during daytime play. Parents may be suffering sleepless nights, prompting them to show up in your office for answers.
Massage and warm soaks to the calves help, but if the child is older than 4 and the symptoms persist, scaphoid pads, inner heel wedges, or soft orthoses lessen or relieve the painful spasms. Some clinicians use this treatment protocol in asymptomatic flatfoot with severe deformity or in obese children. Rigid orthoses should be avoided unless the deformity is neurologic in origin.
Symptomatic flatfoot in a child older than 4 should be carefully evaluated and treated. Two congenital conditions frequently cause a painful flatfoot in an otherwise healthy child: the peroneal spastic flatfoot that is secondary to a coalition or bony bar between the calcaneus and navicular (sometimes the calcaneus and talus); and the prehallux (accessory navicular) that manifests as a painful prominence over the medial navicular bone.
* Peroneal spastic flatfoot In any painful flatfoot, the heel position, examined with the patient bearing weight and then on tiptoe, is the key to diagnosis and treatment. In the weight-bearing position, normal heel eversion is 5 degrees. On tiptoe, the peroneal spastic flatfoot will show heel eversion greater than 10 degrees that is rigid. In contrast, when the patient has symptomatic flexible flatfoot, the heel will revert to normal inversion on toe standing. Peroneal spastic flatfoot plus a finding of decreased or absent subtalar motion are clues for further work-up. This should include oblique x-rays and possibly tomograms or a CT scan looking for a bony bar.
When the diagnosis is made, initial treatment should be conservative, with casting for six weeks, followed by an ankle-foot orthosis. This approach affords relief in about 50% of patients, and, more often than not, surgery is not required.
* Accessory navicula? In an adolescent with a tender medial bump over the navicular and increasing foot pain, consider the diagnosis of accessory navicular. The pull of the posterior tibial tendon on the abnormal navicular attachment, plus increased rubbing of the shoe on the bump, causes the pain. A bursa over the prominence occasionally contributes to the pain pattern.
Treatment includes early casting and oral NSAIDs. If symptoms do not improve after about three weeks, referral for further treatment, which may include surgery, is indicated.
On occasion, an adult with a previously asymptomatic flexible flatfoot will become symptomatic. The history often includes prolonged weight bearing, changes in work environment, some type of minor trauma, or a sudden weight gain. A dull, achy, diffuse pain develops after 2-3 hours of standing that is relieved by sitting down. With the patient sitting, the arch appears normal, but it flattens on weight bearing and the heel deviates into valgus. With the patient on the toes, the heel reverts to normal varus and examination of the subtalar joint shows normal flexibility. Further examination usually demonstrates a tight heel cord.
Treatment should be conservative, starting with a spacious, comfortable shoe with an adequate arch support and a trial of medial heel wedges to tilt the calcaneus into varus. This alone, or in combination with heel cord stretching exercises if necessary, may be sufficient treatment for most patients. Any modifications inside the shoe should be made gradually, allowing the foot to adapt to change. If symptoms persist, the foot is placed into a University of California Biomechanics Laboratory type insert. Surgical evaluation is a last resort.
The cavus foot, because of its multitude of possible deformities, is much more difficult to treat than the flatfoot. Pes cavus varies widely in severity, from a mild, flexible high arch to a rigid, extremely deformed neurologic foot. Symptoms increase with severity but appear early and are resistant to treatment.
More than 65% of patients with a diagnosis of cavus foot have a neurologic lesion. The most common are Charcot,Marie-Tooth disease, followed by myelodysplasia and polio. In idiopathic pes cavus, half of patients have a positive family history and one third have abnormal electromyographic and nerve conduction studies. Most remaining patients have sustained trauma and a postcompartment syndrome, crush injury, or fracture malunion. The clinician’s first duty is to establish the classification, which may require referral to a neurologist.
Whatever the cause, the basic problem is muscle imbalance. A dorsal tilt of the calcaneus of more than 30 degrees is seen on a lateral x-ray, and the plantar fascia is extremely thick and prominent. The foot cannot absorb the impact of running without severe pain, which limits repetitive activities such as sports. The foot tires easily and readily forms huge calluses; the patient is susceptible to lateral ankle sprains.
Treatment aims to provide pain relief by maintaining as much of a plantigrade foot as possible to even out pressure distribution. If the foot has potential flexibility, a stretching program is essential. A spacious shoe with a well-molded, flexible fiberglass orthosis is recommended. Custom shoes may be necessary. If a plantigrade foot cannot be maintained and the foot starts collapsing, referral for surgical correction is appropriate.