This entry is part 3 of 3 in the series Achilles Tendon Dysfunction

Achilles Tendinosis

Background

Achilles tendinosis is characterized by intratendi-nous or mucoid degeneration of the Achilles tendon without evidence of paratenonitis (inflammation). The process starts with interstitial microscopic failure, which leads to central tissue necrosis with subsequent mucoid degeneration Achilles tendinosis most commonly occurs in mature athletes as the result of accumulated repetitive microtrauma from training errors. It is associated with an increased risk of Achilles tendon rupture.

The histology generally is noninflammatory, showing decreased cellularity and fibrillation of collagen fibers within the tendon. Along with the collagen fiber disorganization, there is scattered vascular ingrowth and occasional areas of necrosis and rare calcification.

Initially, the paratenon sheath may become inflamed, and with overuse, the tendon itself becomes inflamed or hypovascular because of the restriction of blood flow through the scarred paratenon.

Clinical Signs and Symptoms

Achilles tendinosis is often asymptomatic and remains subclinical until it presents as a rupture. It may elicit low-grade discomfort related to activities, and a palpable painless mass or nodule may be present 2 to 6 cm proximal to the insertion of the tendon. This can progress to gradual thickening of the entire tendon substance.

The painful arc sign is positive in patients with Achilles tendinosis. The thickened portion of tendon moves with active plantar flexion and dorsiflexion of the ankle (in contrast to paratenonitis, in which the area of tenderness remains in one position despite dorsiflexion and plantar flexion of the foot).

Paratenonitis and tendinosis can coexist when inflammation involves both the paratenon and intra-tendinous focal degeneration. This gives the clinical appearance of paratenonitis because the symptoms associated with tendinosis are absent or very subtle. Most patients seek treatment for symptoms related to the paratenonitis, and usually, the tendinosis is unrecognized until both processes are noted on MRI or at surgery (most commonly after a rupture). Conservative treatment is the same as for paratenonitis. MRI is very useful in preoperative planning, which must consider both entities.

Treatment

The initial treatment of Achilles tendinosis is always conservative and progresses as described for paratenonitis. If symptoms are severe, initial treatment may include 1 to 2 weeks of immobilization and crutch ambulation, in addition to NSAIDs, ice, and heel cord stretching. Foot and leg alignment should be carefully evaluated, with orthotic correction if necessary. Conservative treatment is continued for 4 to 6 months; surgery is indicated if this fails to relieve symptoms.

Operative Treatment

MRI is used to confirm the diagnosis and plan the operative procedure.

Technique

The patient is placed prone with a thigh tourniquet and the foot hanging off the end of the table. The incision is placed posteromedially just off the edge of the tendon (avoids the sural nerve). Full-thickness flaps are created with very careful soft tissue handling. The paratenon is inspected and any hypertrophic paratenon adherent to the tendon is excised. A longitudinal incision is made within the body of the tendon over the thickened, nodular parts to expose areas of central tendon necrosis. Degenerative areas are excised (should correspond with MRI). Débridement is followed by side-to-side closure to repair any defect. If the defect is too large to be closed primarily or lacks adequate substance after débridement, the Achilles tendon is reconstructed using the plantaris tendon, flexor digitorum longus, or a turndown flap.

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This entry is part 2 of 3 in the series Achilles Tendon Dysfunction

Achilles Paratenonitis

Background
Inflammation is limited to the paratenon without associated Achilles tendinosis. Fluid often accumulates next to the tendon, the paratenon is thickened and adherent to normal tendon tissue. Achilles paratenonitis most commonly occurs in mature athletes involved in running and jumping activities. It generally does not progress to degeneration. Histology of paratenonitis shows inflammatory cells, and capillary and fibroblastic proliferation in the paratenon or peritendinous areolar tissue.

Clinical Signs and Symptoms

Pain starts with initial morning activity. The discomfort is well-localized tenderness and sharp, burning pain with activity. The discomfort is present 2 to 6 cm proximal to the insertion of the Achilles tendon into the calcaneus. Pain is primarily aggravated by activity and relieved by rest. Pain is present with single-heel raise and absent on the Thompson test. Significant heel cord contracture will exacerbate symptoms.

Swelling, local tenderness, warmth, and tendon thickening are common. Calf atrophy and weakness and tendon nodularity can be present in chronic cases. Crepitation is rare.

Painful arc sign (Fig. 5–40) is negative in paratenonitis. It is important to localize the precise area of tenderness and fullness. In paratenonitis, the area of tenderness and fullness stays fixed with active ROM of ankle. The inflammation involves only the paratenon, which is a fixed structure, unlike pathology of the Achilles tendon itself, which migrates superiorly and inferiorly with ROM of the ankle.

In the acute setting, symptoms are typically transient, present only with activity, and last less than 2 weeks. Later, symptoms start at the beginning of exercising or at rest, and tenderness increases. The area of tenderness is well localized and reproducible by side-to-side squeezing of the involved region.

Partial rupture may be superimposed on chronic paratenonitis and can present as an acute episode of pain and swelling.

Operative Treatment for Paratenonitis

Operative treatment generally is indicated if 4 to 6 months of conservative treatment fails to relieve symptoms. Preoperative MRI usually is obtained primarily to evaluate for associated tendinosis and confirm diagnosis.

Technique

The patient is positioned prone and a thigh tourniquet is applied. A longitudinal incision is made postero-medially along the Achilles tendon. Full-thickness flaps are raised, with very gentle soft tissue handling. The thickened paratenon and adhesions are removed posteriorly, medially, and laterally as needed. Anterior dissection is avoided because the blood supply of the tendon is primarily within the anterior mesotenon and fat pad. The tendon is inspected for thickening and degeneration (tendinosis); if noted intraoperatively or on MRI, surgical treatment is as described for tendinosis.

Postoperative Protocol

  • Padded splint is applied in neutral position.
  • Non–weight-bearing motion is initiated immediately, both active ROM and gentle passive dorsiflexion with rubber tubing.
  • Crutch-assisted weight-bearing as tolerated after 7 to 10 days, when pain permits and swelling has decreased. If the wound is healing uneventfully at 2 to 3 weeks, ambulation is allowed as tolerated.
  • Exercises are begun on a stationary bike and stair climber when the patient can walk without pain. Swimming and aqua jogging are allowed, as tolerated by the patient and when the wound is healed.
  • Running can be resumed 6 to 10 weeks postoperative.
  • Return to competition is allowed after 3 to 6 months; calf strength must be at least 80% of the normal side.

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This entry is part 1 of 3 in the series Achilles Tendon Dysfunction

Achilles Tendon Dysfunction

Robert C. Greenberg, MD and Charles L. Saltzman, MD

The Achilles tendon is the largest and strongest tendon in the body. The tendon has no true synovial sheath but is encased in a paratenon of varying thickness. The vascular supply to the tendon comes distally from intraosseous vessels from the calcaneus and proximally from intramuscular branches. There is a relative area of avascularity 2 to 6 cm from the calcaneal insertion that is more vulnerable to degeneration and injury. Achilles tendon injuries are commonly associated with repetitive impact loading due to running and jumping. The primary factors resulting in damage of the Achilles tendon are training errors such as a sudden increase in activity, a sudden increase in training intensity (distance, frequency), resuming training after a long period of inactivity, and running on uneven or loose terrain. Achilles dysfunction can also be related to postural problems (e.g., pronation), poor footwear (generally poor hindfoot support), and a tight gastrocsoleus complex.

Diagnosis—Achilles Tendinitis

Pain is typically located in the area of the distal Achilles tendon approximately 2 to 6 cm from the calcaneal insertion. With initial morning activity, pain is noted that is described as sharp or burning pain. The pain is initially present only with vigorous activity and progresses to pain with activities of daily living. Pain is typically relieved with rest.

Examination

Examination is performed with the patient placed prone and the feet hanging off the edge of the table. Palpate the entire substance of the gastrocnemius-soleus myotendinous complex while the ankle is put through active and passive ROM. Evaluate for tenderness, warmth, swelling or fullness, nodularity, or substance defect. The Thompson test is performed to evaluate the continuity of the Achilles tendon (Fig. 5–39). A positive Thompson test (no plantar flexion of the foot with squeezing of the calf) indicates a complete rupture of the tendinoachilles. Note the resting position of the forefoot with the ankle and talonavicular joints held in the neutral position. Ankle and subtalar mobility may often be decreased. Calf atrophy is common in any Achilles tendon dysfunction.

While seated on the exam table, the patient’s foot shoud be passively dorsiflexed, first with the knee flexed and then with the knee fully extended. This will tell the examiner how tight the Achilles tendon is. Many females who have worn high heel shoes for years won’t be able to dorsiflex the foot to neutral with the knee in full extension.

Classification of Achilles Tendon Problems

Achilles tendon problems generally are classified as paratenonitis, tendinosis, or rupture.

Imaging

Most Achilles problems can be diagnosed with a thorough history and physical examination. Imaging helps confirm the diagnosis, assist with surgical planning, or rule out other diagnoses.

  • Routine radiographs are generally normal. Occasionally, calcification in the tendon or its insertion is noted. Inflammatory arthropathies (erosions), Haglund’s deformity (pump bump) can be ruled out on radiographs.
  • Ultrasound is inexpensive and fast and allows dynamic examination, but it requires substantial interpreter experience. It is the most reliable method for determining the thickness of the Achilles tendon and the size of a gap after a complete rupture.
  • MRI is not used for dynamic assessment, but it is superior in the detection of partial tears and the evaluation of various stages of chronic degenerative changes, such as peritendinous thickening and inflammation. MRI can be used to monitor tendon healing when recurrent partial rupture is suspected and is the best modality for surgical planning (location, size).

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This entry is part 2 of 2 in the series Inferior Heel Pain (Plantar Fasciitis)

Natural History

Although plantar fasciitis can seem quite debilitating during the acute phase, it rarely causes lifelong problems. It is estimated that 90 to 95% of patients who have true plantar fasciitis recover with conservative treatment. However, it may take 6 months to 1 year, and patients often require much encouragement to continue stretching, wearing appropriate and supportive shoes, and avoiding high-impact activities or prolonged standing on hard surfaces. Operative treatment can be very helpful in selected “failed” patients, but the success rate of surgery is only 50 to 85%.

Bilateral Heel Involvement

Bilateral plantar fasciitis symptoms require ruling out systemic disorders such as Reiter’s syndrome, ankylosing spondylitis, gouty arthropathy, and systemic lupus erythematosus. A high index of suspicion for a systemic disorder should accompany bilateral heel pain in a young male aged 15 to 35 years.

Signs and Symptoms

The classic presentation of plantar fasciitis includes a gradual, insidious onset of inferomedial heel pain at the insertion of the plantar fascia (Fig. 5–21). Pain and stiffness are worse with rising in the morning or after prolonged ambulation and may be exacerbated by climbing stairs or doing toe raises. It is rare for patients with plantar fasciitis not to have pain or stiffness with the first few steps in the morning or after a prolonged rest.

Evaluation of Patients with Inferior Heel Pain

  • History and examination
  • Biomechanical assessment of foot
  • Pronated or pes planus foot
  • Cavus-type foot (high arch)
  • Assessment of fat pad (signs of atrophy)
  • Presence of tight Achilles tendon
  • Squeeze test of calcaneal tuberosity (medial and lateral sides of calcaneus) to evaluate for possible calcaneal stress fracture.
  • Evaluation for possible training errors in runners (e.g., rapid mileage increase, running on steep hills, poor running shoes, improper techniques).
  • Radiographic assessment with 45-degree oblique view and standard three views of foot.
  • Bone scan if recalcitrant pain (> 6 wk after treatment initiated) or suspected stress fracture from history.
  • Rheumatologic work-up (Table 5–1) for patients with suspected underlying systemic process (patients with bilateral heel pain, recalcitrant symptoms, or associated sacroiliac joint or multiple joint pain).
  • Electromyographic (EMG) studies if clinical suspicion of nerve entrapment.
  • Establish correct diagnosis and rule out other possible etiologies (Tables 5–2 and 5–3).

Rupture of the Plantar Fascia

Background
Although not commonly reported in the literature, partial or complete plantar fascia ruptures may occur in jumping or running sports. Often, this is missed or misdiagnosed as an acute flare-up of plantar fasciitis. Complete rupture of the plantar fascia usually results in a permanent loss of the medial (longitudinal) arch of the foot. Such collapse is typically quite disabling for athletes.

Examination

Patients typically complain of a pop or crunch in the inferior heel area, with immediate pain and inability to continue play. This usually occurs during push-off, jumping, or initiation of a sprint. After an antecedent cortisone injection, the trauma may be much more minor (e.g., stepping off a curb).
Weight-bearing is very difficult, and swelling and ecchymosis in the plantar aspect of the foot occur fairly rapidly. Palpation along the plantar fascia elicits marked point tenderness. Dorsiflexion of the toes and foot often causes pain in the plantar fascia area.

Radiographic Evaluation

Diagnosis of a plantar fascia rupture is a clinical one. Pain radiographs are taken (three views of the foot) to rule out a fracture. MRI may be used but is not necessary for diagnosis (Fig. 5–37). MRI may miss the area of the actual rupture but does typically pick up the associated hemorrhage and swelling surrounding the rupture.

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This entry is part 1 of 2 in the series Inferior Heel Pain (Plantar Fasciitis)

Inferior Heel Pain (Plantar Fasciitis)

S. Brent Brotzman, MD

Clinical Background

Heel pain is best classified by anatomic location (see box following). This section discusses plantar fasciitis (inferior heel pain). Posterior heel pain is discussed in the section on Achilles tendinitis.

Anatomy and Pathomechanics

The plantar fascia is a dense, fibrous connective tissue structure originating from the medial tuberosity of the calcaneus (Fig. 5–18). Of its three portions—medial, lateral, and central bands—the largest is the central portion. The central portion of the fascia originates from the medial process of the calcaneal tuberosity superficial to the origin of the flexor digitorum brevis, quadratus plantae, and abductor hallicus muscle. The fascia extends through the medial longitudinal arch into individual bundles and inserts into each proximal phalanx.

The medial calcaneal nerve supplies sensation to the medial heel. The nerve to the abductor digiti minimi may rarely be compressed by the intrinsic muscles of the foot. Some studies, such as those by Baxter and Thigpen (1984), suggest that nerve entrapment (abductor digiti quinti) does on rare occasions play a role in inferior heel pain (Fig. 5–19).

The plantar fascia is an important static support for the longitudinal arch of the foot. Strain on the longitudinal arch exerts its maximal pull on the plantar fascia, especially its origin on the medial process of the calcaneal tuberosity. The plantar fascia elongates with increased loads to act as a shock absorber, but its ability to elongate is limited (especially with decreasing elasticity common with age). Passive extension of the metatarsophalangeal (MTP) joints pulls the plantar fascia distally and also increases the height of the arch of the foot (Fig. 5–20).

Myth of the Heel Spur

The bony spur at the bottom of the heel does not cause the pain of plantar fasciitis. Rather, this is caused by the inflammation and microtears of the plantar fascia. The spur is actually the origin of the short flexors of the toes. Despite this, the misnomer persists in the lay public and the literature.

Heel spurs have been found in approximately 50% of patients with plantar fasciitis. This exceeds the 15% prevalence of radiographically visualized spurs in normal asymptomatic patients noted by Tanz (1963). However, spur formation is related to progression of age. The symptomatic loss of elasticity of the plantar fascia with the onset of middle age suggests that this subset of patients would be expected to show an increased incidence of spurs noted on radiographs.

Etiology

Inferior (subcalcaneal) pain may well represent a spectrum of pathologic entities including plantar fasciitis, nerve entrapment of the abductor digiti quinti nerve, periostitis, and subcalcaneal bursitis.

Plantar fasciitis is more common in sports that involve running and long-distance walking and is also frequent in dancers, tennis players, basketball players, and nonathletes whose occupations require prolonged weight-bearing. Direct repetitive microtrauma with heel strike to the ligamentous and nerve structures has been implicated, especially in middle-aged, overweight, nonathletic individuals who stand on hard, unyielding surfaces, as well as in long-distance runners.

Some anatomic features seem to make plantar fasciitis more likely. Campbell and Inman (1974) noted that in patients with pes planus, heel pronation increased the tension on the plantar fascia, predisposing the patient to heel pain. Pronation of the subtalar joint everts the calcaneus and lengthens the plantar fascia. A tight gastrocnemius (with increased compensatory pronation) also predisposes patients to plantar fasciitis. Cavus feet with relative rigidity have been noted to place more stress on the loaded plantar fascia. Several studies have shown an association with plantar fasciitis and obesity. However, other researchers have not obtained similar findings.

Bone spurs may be associated with plantar fasciitis, but are not believed to be the cause of it. Many studies show no clear association between spurs and plantar fasciitis. Studies of patients with plantar fasciitis report that 10 to 70% have an associated ipsilateral calcaneal spur; however, most also have a spur on the contralateral asymptomatic foot. Anatomic studies have shown the spur is located at the short flexor origin rather than at the plantar fascia origin, casting further doubt on its role in contributing to heel pain.

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This entry is part 5 of 5 in the series Ankle Sprains

Treatment for Lateral Collateral Sprains

The current literature supports functional rehabilitation as the preferred method of treatment for ankle sprains, allowing an earlier return to work and physical activity without a higher rate of late symptoms (ankle instability, pain, stiffness, or muscle weakness) when compared with cast immobilization.

Immediately after injury in the acute phase, the PRICE (protection, rest, ice, compression, and elevation) principle is followed (see rehabilitation protocol). The goal is to reduce hemorrhage, swelling, inflammation, and pain. A period of immobilization is initiated, depending on the severity of the injury. Some authors stress the importance of immobilizing the ankle in neutral rather than in plantar flexion because the ATFL is stretched out during plantar flexion. For grades 1 and 2 sprains, an ankle brace (Fig. 5–8) is used for immobilization. For grade 3 sprains, a removable cast boot offers more stability and protection and allows earlier weight-bearing with less pain. Immobilization is continued for several days in mild sprains and up to 3 weeks in severe grade 3 sprains. As grade 3 sprains improve, the cast boot is replaced with an ankle brace.

In the subacute phase, goals include continued reduction of swelling, inflammation, and pain, while some motion, strengthening, and appropriate controlled weight-bearing are started. This is the period of collagen fiber proliferation, and too much stress on the ligaments at this point could result in weaker tissue.

The rehabilitative phase focuses on improving strength, endurance, balance, and weight-bearing proprioception. During this maturation phase of the healing ligament, about 3 weeks after the injury, controlled stretching of the muscles and movement of the joint promote a more normal orientation of the collagen fibers parallel with the stress lines. Repeated exercise during this phase has been shown to increase the mechanical and structural strength of the ligaments.

Prevention of Ankle Sprains

Proper strengthening and rehabilitation are critical to help prevent inversion ankle injuries; however, some patients require additional biomechanical support. We routinely use ankle braces in athletes prone to ankle injuries in high-risk sports like basketball and volleyball. We prefer a lace-up brace with figure-of-eight straps or a functional stirrup brace that is placed beneath the insole of the shoe. The Ultimate Ankle Brace (Bledsoe Brace Company) effectively limits inversion injuries, but still allows the ankle to dorsiflex and plantar flex. However, some athletes, such as ballet dancers, may not be able to perform in a brace, which limits its usefulness in some sports. Another effective means of preventing inversion injuries is to apply a slight lateral flare to the sole of the tennis shoe or a lateral wedge to an insole. This, again, is effective only in certain sports in which a tennis shoe is worn.

Ankle taping may be of some benefit, but much of the strength is lost with loosening of the tape within the first 10 minutes. We use a closed basketweave technique (Fig. 5–16).

  1. Have the seated athlete position the ankle at 90 degrees (A.)
  2. Spray a tape adherent (e.g., Tuf-Skin, QDA) over the area to be taped.
  3. Apply a heel and lace pad with skin lubricant on the anterior and posterior aspects of the ankle (B.)
  4. Apply pre-wrap, starting at the midfoot and continuing up the leg, overlapping by half until approximately 5–6 inches above the medial malleolus (C.)
  5. Apply an anchor strip at the proximal (#1) and distal (#2) ends of the pre-wrap with half of the tape covering the pre-wrap and the other half adhering to the skin (D.)
  6. Starting posteromedially on the proximal anchor, apply a stirrup covering the posterior third of the medial malleolus and then under the foot and up the lateral side to the proximal anchor (#3) (Ei and ii).
  7. Starting at the distal anchor (#4), apply a horseshoe around the heel (approximately 2 inches from the plantar surface) to the other side of the distal anchor (F.)
  8. Repeat steps 6 and 7 twice. Each time, overlap the previous strip by half the width of the tape (G.)
  9. To apply a figure-of-8, start medially (Hi) at the position of the first stirrup (#5), pull the tape at an angle toward the medial longitudinal arch (approximately where the third stirrup goes under the foot), under the foot, across the anterior aspect of the ankle, and around the ankle (just above the third horseshoe strip) (Hii).
  10. Close up the tape by applying single strips of tape around the leg, overlapping by half until the area from the ankle to the proximal anchor is covered (#6) (I).
  11. To apply a heel lock, start at the anterior aspect of the proximal anchor laterally. Pull the tape at an angle (arrows) toward the posterior aspect of the lateral malleolus, around the posterior aspect of the ankle, under the heel, up the lateral side of the foot, and across the anterior aspect of the ankle (Ji–iii). To continue and apply a continuous double-heel lock, make one complete loop around the ankle (#7), continue around the ankle, then down around the posterior aspect of the ankle, under the heel, and up the medial side of the foot (K), across the anterior aspect of the ankle, and complete with another full loop around the ankle.
  12. Apply one or two closure strips (dark tape) around the foot (#8) to hold the horseshoes down to the foot and the anchor strip (Li–v).

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This entry is part 4 of 5 in the series Ankle Sprains

Chronic Lateral Ankle Instability: Rehabilitation after Lateral Ankle Ligament Reconstruction

Mark Colville MD, and Ken Stephenson, MD
It is estimated that 20 to 40% of patients with ankle sprains develop long-term sequelae such as pain, swelling, or instability. Interestingly, the severity of the ankle sprain does not seem to correlate with the development of chronic symptoms. If a patient has received appropriate treatment for an ankle sprain and has completed a rehabilitation program but continues to have significant symptoms, another etiology of the symptoms must be sought. Etiologies to be considered in patients with chronic ankle pain include occult bony injuries such as fractures, osteochondral defects, or bone contusions; cartilage damage; ankle, subtalar, or syndesmosis instability secondary to ligament rupture; tendon pathology such as a peroneal tendon or posterior tibial tendon longitudinal tear; a neuropraxia of the superficial peroneal or sural nerves; or soft tissue problems such as anterolateral ankle soft tissue impingement.

Radiographic Examination

If the patient has a history or examination consistent with instability, stress radiographs (talar tilt and anterior drawer) are indicated. Although there is some controversy in the literature regarding normal values for stress radiographs, in general, a positive talar tilt is more than 15 degrees or more than 10 degrees difference from the contralateral side. A positive anterior drawer is 5 to 10 mm anterior subluxation of the talus or more than 5 mm difference from the contralateral side. MRI is useful for delineating bone contusions, avascular necrosis, osteochondral defects, and tendon or ligament injuries. The diagnosis of chronic lateral ankle ligament instability is based on a history of multiple inversion ankle sprains, often with fairly minor provocation (such as stepping off a curb). Instability, not pain alone, should be the primary criterion for ligament reconstruction.

Ankle Ligament Reconstruction

Numerous surgical procedures have been described for lateral ankle instability, but the most commonly used is the modified Brostrom procedure. This involves an anatomic repair of the ATFL and CFL augmented by suture of the superior edge of the inferior peroneal retinaculum to the anterior edge of the fibula. This procedure is particularly indicated in ballet dancers or patients whose livelihood depends on a full ROM and in most patients undergoing reconstruction for the first time. It is not the procedure of choice for revision surgery or patients with generalized ligamentous laxity or a connective tissue disorder. The use of the peroneus brevis tendon to augment the repair is indicated for revision surgery. The Watson-Jones, Chrisman-Snook, and Evans procedures have good success rates (80 to 85%) but each limits subtalar and ankle motion.

The goal of ankle ligament reconstruction in an unstable ankle is to restore stability while preserving normal ankle and subtalar motion whenever possible. Most patients with chronic instability have laxity of the ATFL and CFL and increased subtalar joint motion.

General Principles of Rehabilitation after Ankle Ligament Reconstruction

Postoperatively, a short-leg, well-padded splint is applied with the ankle in slight eversion, and the patient remains non–weight-bearing. One to 2 weeks after surgery, the patient is placed into a removable cast boot or short-leg walking cast with the foot in neutral position and is allowed to begin partial weight-bearing, progressing to full weight-bearing as tolerated. Four weeks postoperative, the patient is placed into a functional brace or removable cast boot, and active rehabilitation is started with gentle ROM exercises and isometric strengthening exercises. Usually at 6 weeks, proprioception and balancing exercises are started. In athletes, sport-specific exercises are started at about 8 weeks postoperative. Return to sports or dancing is allowed when peroneal strength is normal and the patient is able to perform multiple single-leg hops on the injured side without pain. A lace-up brace (such as the Rocket Sock) or functional stirrup brace should be worn for at least the first season, and most athletes prefer bracing or taping for sports indefinitely.

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This entry is part 3 of 5 in the series Ankle Sprains

Treatment for Lateral Collateral Sprains

The current literature supports functional rehabilitation as the preferred method of treatment for ankle sprains, allowing an earlier return to work and physical activity without a higher rate of late symptoms (ankle instability, pain, stiffness, or muscle weakness) when compared with cast immobilization.

Immediately after injury in the acute phase, the PRICE (protection, rest, ice, compression, and elevation) principle is followed (see rehabilitation protocol). The goal is to reduce hemorrhage, swelling, inflammation, and pain. A period of immobilization is initiated, depending on the severity of the injury. Some authors stress the importance of immobilizing the ankle in neutral rather than in plantar flexion because the ATFL is stretched out during plantar flexion. For grades 1 and 2 sprains, an ankle brace (Fig. 5–8) is used for immobilization. For grade 3 sprains, a removable cast boot offers more stability and protection and allows earlier weight-bearing with less pain. Immobilization is continued for several days in mild sprains and up to 3 weeks in severe grade 3 sprains. As grade 3 sprains improve, the cast boot is replaced with an ankle brace.

In the subacute phase, goals include continued reduction of swelling, inflammation, and pain, while some motion, strengthening, and appropriate controlled weight-bearing are started. This is the period of collagen fiber proliferation, and too much stress on the ligaments at this point could result in weaker tissue.

The rehabilitative phase focuses on improving strength, endurance, balance, and weight-bearing proprioception. During this maturation phase of the healing ligament, about 3 weeks after the injury, controlled stretching of the muscles and movement of the joint promote a more normal orientation of the collagen fibers parallel with the stress lines. Repeated exercise during this phase has been shown to increase the mechanical and structural strength of the ligaments.

Prevention of Ankle Sprains

Proper strengthening and rehabilitation are critical to help prevent inversion ankle injuries; however, some patients require additional biomechanical support. We routinely use ankle braces in athletes prone to ankle injuries in high-risk sports like basketball and volleyball. We prefer a lace-up brace with figure-of-eight straps or a functional stirrup brace that is placed beneath the insole of the shoe. The Ultimate Ankle Brace (Bledsoe Brace Company) effectively limits inversion injuries, but still allows the ankle to dorsiflex and plantar flex. However, some athletes, such as ballet dancers, may not be able to perform in a brace, which limits its usefulness in some sports. Another effective means of preventing inversion injuries is to apply a slight lateral flare to the sole of the tennis shoe or a lateral wedge to an insole. This, again, is effective only in certain sports in which a tennis shoe is worn.

Ankle taping may be of some benefit, but much of the strength is lost with loosening of the tape within the first 10 minutes. We use a closed basketweave technique (Fig. 5–16).

  1. Have the seated athlete position the ankle at 90 degrees (A.)
  2. Spray a tape adherent (e.g., Tuf-Skin, QDA) over the area to be taped.
  3. Apply a heel and lace pad with skin lubricant on the anterior and posterior aspects of the ankle (B.)
  4. Apply pre-wrap, starting at the midfoot and continuing up the leg, overlapping by half until approximately 5–6 inches above the medial malleolus (C.)
  5. Apply an anchor strip at the proximal (#1) and distal (#2) ends of the pre-wrap with half of the tape covering the pre-wrap and the other half adhering to the skin (D.)
  6. Starting posteromedially on the proximal anchor, apply a stirrup covering the posterior third of the medial malleolus and then under the foot and up the lateral side to the proximal anchor (#3) (Ei and ii).
  7. Starting at the distal anchor (#4), apply a horseshoe around the heel (approximately 2 inches from the plantar surface) to the other side of the distal anchor (F.)
  8. Repeat steps 6 and 7 twice. Each time, overlap the previous strip by half the width of the tape (G.)
  9. To apply a figure-of-8, start medially (Hi) at the position of the first stirrup (#5), pull the tape at an angle toward the medial longitudinal arch (approximately where the third stirrup goes under the foot), under the foot, across the anterior aspect of the ankle, and around the ankle (just above the third horseshoe strip) (Hii).
  10. Close up the tape by applying single strips of tape around the leg, overlapping by half until the area from the ankle to the proximal anchor is covered (#6) (I).
  11. To apply a heel lock, start at the anterior aspect of the proximal anchor laterally. Pull the tape at an angle (arrows) toward the posterior aspect of the lateral malleolus, around the posterior aspect of the ankle, under the heel, up the lateral side of the foot, and across the anterior aspect of the ankle (Ji–iii). To continue and apply a continuous double-heel lock, make one complete loop around the ankle (#7), continue around the ankle, then down around the posterior aspect of the ankle, under the heel, and up the medial side of the foot (K), across the anterior aspect of the ankle, and complete with another full loop around the ankle.
  12. Apply one or two closure strips (dark tape) around the foot (#8) to hold the horseshoes down to the foot and the anchor strip (Li–v).

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This entry is part 2 of 5 in the series Ankle Sprains

Syndesmosis Injury

Disruption of the syndesmosis ligament complex (tibiofibular ligaments and interosseous membrane) may occur in as many as 10% of all ankle ligament injuries (Fig. 5–6). The examiner should always test for this injury (see squeeze test and external rotation test, p. 377). Rupture of the syndesmosis is often associated with deltoid (medial) ligament rupture, and concomitant fracture of the fibula is common (see ankle fracture section). The mechanism may be pronation and eversion of the foot combined with internal rotation of the tibia on a fixed foot, such as occurs in football players who have an external rotation force applied to the foot (stepped on) while lying prone on the field.

Point tenderness and pain are located primarily on the anterior aspect of the syndesmosis (not over the lateral collaterals as with an ankle sprain), and the patient is usually unable to bear weight. These injuries are typically more severe than ankle sprains, with more pain, swelling, and difficulty in weight-bearing. Stress radiographs taken with the ankle in external rotation (in both dorsiflexion and plantar flexion) often display the diastasis (gap) between the tibia and the fibula. Bone scanning is useful if the diagnosis is suspected but hard to confirm.

Partial isolated syndesmosis tears are typically treated nonoperatively in a removable cast for 6 to 8 weeks (partial weight-bearing with crutches). With complete syndesmosis rupture, the fibula may shorten and externally rotate. A complete tear is treated by suture of the ligament and temporary fixation of the tibia and fibula with a syndesmosis screw. The syndesmosis screw must be placed with the ankle dorsiflexed to neutral (the widest portion of the talus) to avoid postoperative limited dorsiflexion. A walking boot is used (touch-down weight-bearing) for 6 to 8 weeks postoperative. Early active and passive motion out of the boot is encouraged from day 7, and full weight-bearing is allowed at 6 weeks. An aggressive rehabilitation program stressing vigorous range of motion (ROM), strengthening, and proprioception exercises is undertaken (see ankle sprain rehabilitation protocol, p. 381). The patient should be informed about the longer recovery compared with ankle sprains and the potential for pain and late sequelae, such as heterotopic ossification.

Factors crucial for a good outcome after syndesmosis injuries are recognition of the injury and obtaining and maintaining an anatomic reduction of the ankle mortise and the distal lower extremity syndesmosis. Syndesmosis fixation is usually indicated to avoid the more catastrophic complications of mortise widening and joint incongruity (e.g., early post-traumatic arthritis).

Radiographic Evaluation

Radiographs are taken to rule out fractures of the medial and lateral malleoli, the talus, and the fifth metatarsal base. Radiographs should include three views of the ankle on long cassettes that include the entire length of the fibula: anteroposterior [AP], lateral, and mortise views (Fig. 5–7A) and three views of the foot (AP, lateral, and oblique) (see Fig. 5–7B–D). Stress radiographs can be used to quantify instability during the anterior drawer and talar tilt stress tests. Anterior taluar subluxation of more than 10 mm or more than 5 mm difference from the contralateral ankle indicates a positive anterior drawer stress test. Talar tilt of 15 degrees or 10 degrees difference from the contralateral ankle indicates a positive talar tilt test.

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This entry is part 1 of 5 in the series Ankle Sprains

Ankle Sprains

Ken Stephenson, MD

Ankle sprains make up about 15% of all athletic injuries, with a reported 23,000 ankle ligament injuries occurring each day in the United States. They are particularly common in basketball, volleyball, soccer, modern dance, and ballet. Most patients fully recover, but an estimated 20 to 40% develop chronic symptoms of pain and instability.

Relevant Anatomy

The stability of any joint depends on the inherent constraints provided by the bony configuration and the active and passive soft tissue restraints. The ankle joint is quite stable in the neutral position because the wider anterior portion of the talus fits snugly into the ankle mortise. Plantar flexion of the ankle rotates the narrower posterior talus into the mortise, resulting in a much looser fit, with a particular tendency toward inversion. Active soft tissue restraint depends on the muscle-tendon units involved in movement and support of the joint. The talus, however, has no tendinous insertions and must rely in an indirect way on the muscular actions on other bones adjacent to the ankle joint. Passive support of the ankle is provided by the medial, lateral, and posterior ligaments and the syndesmosis. The lateral ankle ligament complex is the structure most commonly involved in ankle sprains.

The three main components of the lateral ligament complex are the anterior talofibular ligament (ATFL), the calcaneofibular ligament (CFL), and the posterior talofibular ligament (PTFL) (Fig. 5–1). The ATFL is relaxed in neutral and taut in plantar flexion. It is the primary restraint against inversion while the foot is plantar flexed. The CFL is also relaxed in neutral, but it is taut in dorsiflexion.

The most common ankle injury involves an isolated tear of the ATFL, followed by a combined tear of the ATFL and the CFL. The mechanism of injury is usually inversion of the plantar flexed foot (Fig. 5–2).

Classification of Lateral Collateral Ligament Sprains

A grade 1, or mild ankle sprain, is a stretch of the ligament with no macroscopic tear, little swelling or tenderness, minimal or no functional impairment, and no joint instability. A grade 2, or moderate ankle sprain, involves a partial tear of the ligament with moderate swelling and tenderness, some loss of joint function, and mild joint instability. A grade 3, or severe sprain, involves a complete tear of the ligaments (ATFL and CFL) with severe swelling, ecchy-mosis and tenderness, inability to bear weight on the extremity, and mechanical joint instability (Fig. 5–3).

Diagnosis

An inversion injury is commonly associated with a tearing sensation or a pop felt by the patient over the lateral ankle. Swelling can be immediate in grades 2 and 3 sprains, and the initial intense pain subsides after a few hours, only to return more intensely as the hemorrhage continues 6 to 12 hours after the injury.

Physical Examination
Physical examination reveals mild swelling in grade 1 sprains and moderate to severe swelling in a diffuse pattern in grades 2 and 3 sprains. Tenderness is usually elicited at the anterior edge of the fibula with ATFL injuries and at the tip of the fibula with CFL injuries. The region of the syndesmosis and the base of the fifth metatarsal should also be palpated to rule out injuries to these structures.

The anterior drawer test and the talar tilt test are commonly used to identify signs of joint instability (Fig. 5–4 A and B). The anterior drawer test is performed by stabilizing the distal tibia anteriorly with one hand and pulling the slightly plantar flexed foot forward with the other hand from behind the heel. A positive finding of more than 5 mm of anterior translation indicates a tear of the ATFL. The talar tilt test is performed by stabilizing the distal tibia with one hand and inverting the talus and calcaneus as a unit with the other hand. A positive finding of more than 5 mm with a soft endpoint indicates a combined injury to the ATFL and CFL (see Fig. 5–4C). It is important to always compare the affected ankle with the contralateral side because some patients are naturally very flexible (generalized ligamentous laxity), and this could result in a false-positive test.

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