TENDON DISORDERS OF THE FOOT AND ANKLE

The gastrocnemius muscle and the soleus muscles combine
in the posterior compartment of the leg to produce a common tendon, the
Achilles tendon, which inserts into the posterior tuberosity of the
calcaneus. The tendon does not

have
an accompanying synovial sheath, but it is surrounded by a peritenon or
fibrous covering that is derived from the crural fascia. During
steady-state walking, the primary function of the gastrocsoleus muscle
group is to decelerate the tibia as it passes over the foot. This is
accomplished with eccentric muscle contraction. Toe-off is a passive
event during steady-state walking and an active event during
steady-state running or acceleration (20).

Using pathologic criteria, the classification of
Achilles tendon dysfunction is best divided into paratenonitis,
tendinosis, and partial or complete rupture. Paratenonitis is defined
by inflammation of the tissues surrounding, but not including, the
Achilles tendon. Paratenonitis is commonly attributed to athletic
training errors, such as ineffective stretching or warm-up and overuse.
Mechanical factors, such as excessive foot pronation or a tight
Achilles tendon, have also been implicated. Tendinosis is defined by
degenerative changes within the substance of a tendon; these changes
are probably age related and may represent a precursor to partial
tears. Histologic examination of chronic Achilles tendinosis reveals
abnormal fibrous structure, focal hypercellularity, and vascular
proliferation. Curiously, inflammatory cells are not found (2).
Angiographic and microangiographic examinations reveal a paucity of
vasculature in the segment of tendon between 2 and 6 cm proximal to the
insertion (18). Clinical findings suggest that this same area is susceptible to tendinosis and rupture.

The goal of treating Achilles tendinosis is to alleviate
pain, prevent further degeneration, and preserve function. The goal of
treating Achilles tendon ruptures is to restore the functional
integrity to the gastrosoleus complex. For both conditions, surgical
and nonsurgical methods are used in an effort to maximize outcome.

The patient with Achilles tendinosis presents with pain
over the Achilles tendon that is aggravated by activity. Physical
examination begins with gait analysis; moderate to severe tendinosis
produces an antalgic pattern. Examine the patient in the standing
position to evaluate swelling or fullness related to the Achilles
tendon. Assess calf atrophy by comparison with the contralateral
extremity. Have the patient perform a repeated single-heel rise test.
This is accomplished by having the patient stand at a nearby wall using
hands for balance. The patient lifts the unaffected extremity while
performing repeated single-heel rises on the affected extremity. The
test is positive if the patient is unable to perform the maneuver owing
to pain or if the maneuver causes pain at the Achilles tendon. Then
seat the patient and palpate the posterior leg to assess swelling and
tenderness. Nodular or fusiform swelling typically accompanies
tendinosis.

Diagnostic imaging for the patient with Achilles
tendinosis begins with a lateral radiographic view of the distal leg
and hind foot. Look for intratendinous calcification associated with
tendinosis and check the topography of the posterior superior
calcaneus. The presence of a hyperconvex superior tuberosity of the
calcaneus may be associated with distal tendinosis. Although it is not
required for evaluation of Achilles tendinosis or rupture, magnetic
resonance imaging (MRI) is probably the most useful imagining modality.
On a T2-image sequence, tendinosis shows increased signal activity
within the tendon as well as localized thickening, cystic changes, and
even partial tears.

Rupture of the Achilles tendon may occur without
antecedent symptoms or may follow a period of pain associated with
Achilles tendinosis. Rupture is associated with the acute onset of pain
over the Achilles tendon and the loss of plantar flexion power, either
subtle or overt. Occasionally, the patient recalls sensing or hearing a
“pop” at the time of rupture. Examination of the standing patient may
reveal subtle to massive swelling along the posterior leg. With the
patient in a prone position, perform a Thompson’s test by squeezing the
calf at midsubstance and looking for the absence of foot
plantarflexion. When foot plantarflexion is not observed, the test is
considered positive and the diagnosis of ruptured Achilles tendon is
established (41). Palpation of the Achilles
tendon itself may reveal a defect. Failure to find this defect,
however, does not rule out tendon disruption.

Complete tears of the Achilles tendon are easily
identified on MRI, but the diagnosis is usually obvious on clinical
examination as well. MRI is not required for the routine evaluation of
Achilles tendon ruptures.

Achilles tendinosis consists of a spectrum of injuries
ranging from small focal areas of degeneration associated with mild
pain and minimal dysfunction through significant areas of degeneration
and partial tearing associated with significant discomfort and loss of
function. Furthermore, tendinosis can be classified with an anatomic
system based on the location of the degeneration relative to the
insertion. Noninsertional tendinosis includes degenerative changes of
the Achilles tendon between the musculotendinous junction to a point
proximal to the insertion. Insertional tendinosis is limited to
degeneration at the Achilles tendon insertion. This entity tends to be
more focal, but similar treatment principles apply.

Achilles tendon ruptures may occur de novo through a section of healthy tendon or through a section of tendinosis. Lacerations, ruptures through previously healed

tendon disruptions, and chronic ruptures are recognized as distinct entities.

Treat Achilles tendinosis initially with rest,
application of ice, and nonsteroidal anti-inflammatory medication.
Patients with moderate to severe symptoms require immobilization with a
weight-bearing cast or removable cast boot. Once the pain, swelling,
and tenderness have resolved, institute a rehabilitation program. Place
emphasis on stretching the gastrosoleus motor complex. Also correct
training errors related to intensity or frequency of activity.

Patients with acute, complete Achilles tendon rupture
may be treated by surgical or nonsurgical methods. The ideal treatment
of the acute, complete Achilles tendon rupture remains controversial.
Nonsurgical methods have the advantage of avoiding wound complications,
but they appear to have a higher rerupture rate (14,29).
Patients treated with surgical primary repair have a significantly
lower rerupture rate and a higher degree of satisfaction;
unfortunately, they are also prone to surgical complications such as
deep infection, fistula, and skin or tendon necrosis (14,29)

For nonsurgical treatment of acute, complete Achilles
tendon ruptures, use a non-weight-bearing equinus cast for 6 weeks,
followed by a weight-bearing cast boot for a second 6-week period, then
place a silicone heel wedge in the cast boot and subsequent shoewear.
On the resolution of local warmth and swelling, begin a motion and
strengthening program. Surgical treatment consists of primary repair of
the Achilles tendon. Achilles tendinosis that is recalcitrant to a
prolonged course of immobilization and conservative management requires
surgical debridement and possible reconstruction. Although it is not
required, an MRI may be obtained in order to better delineate the
extent of tendon degeneration.

Rerupture is a complication of Achilles tendon rupture
treated with either surgical or nonsurgical intervention. The rerupture
rate appears to be higher in those patients treated with cast
immobilization alone (14,29), particularly in those treated with less than 8 weeks of immobilization (19).

Skin slough and wound infection are serious
complications because of the subcutaneous position of the tendon.
Surgical technique requires preservation of full-thickness skin flaps,
gentle soft-tissue handling, and tension-free closure. Before
immobilization of the foot at surgery, verify the viability of the skin
overlying the Achilles tendon, with the foot in the proposed position
of immobilization.

With regard to the controversy surrounding acute,
complete Achilles tendon ruptures, we prefer early, primary repair for
healthy, active individuals. We believe that this treatment modality
allows a faster and more complete recovery.

From the deep posterior compartment of the leg, the
posterior tibial muscle forms a tendon that courses behind the medial
malleolus, turns anteriorly, and inserts directly into the navicular
tuberosity. The tendon is surrounded by a synovial sheath. The position
of the tendon relative to the ankle and subtalar joint axes of rotation
defines its function as an invertor and plantarflexor of the foot (Fig. 118.4) (22).
Insufficiency of the posterior tibial tendon (PTT) results in the
production of an asymmetric flatfoot identified by heel valgus, midfoot
collapse and abduction, and forefoot pronation. Insufficiency may be
related to acute or chronic tenosynovitis or partial or complete
rupture. It is unknown why the PTT is predisposed to injury, but it may
be related to a zone of relative hypovascularity within the tendon
located behind and distal to the medial malleolus (11).
PTT dysfunction occurs more frequently in patients with diabetes,
hypertension, and obesity compared with the general population (13).

The loss of PTT function results in significant
impairment to the lower extremity. The primary goal of treatment is to
re-establish the function of the PTT, when possible. For patients with
advanced disease, the substitution or addition of the FDL tendon may be
required. The most advanced stages of dysfunction are not amenable to
soft-tissue reconstruction and require identification and treatment of
fixed deformities.

Begin the physical examination with gait analysis. When
viewed from behind, the patient with PTT dysfunction may have decreased
heel inversion between flatfoot and toe-off, and in advanced cases, an
antalgic gait may be noted. Examination of the standing patient may
reveal varying degrees of swelling over the course of the PTT, as well
as heel valgus, midfoot collapse, and abduction. Ask the patient to
perform a repeated single-heel rise test. This is accomplished by
having the patient stand at a nearby wall, using the hands for balance.
The patient lifts the unaffected extremity while performing repeated
single-heel rises on the affected extremity. Patients with
tenosynovitis or mild degenerative changes are able to perform the
maneuver repeatedly with evidence of good heel height and heel
inversion, but this is typically a painful maneuver. In advanced
stages, heel height and heel inversion decrease. Finally, patients with
complete dysfunction of the PTT are unable to perform the maneuver.
Then seat the

patient
and palpate the posterior leg to assess swelling over the PTT and
associated tenderness. Tenderness at the sinus tarsi may indicate
lateral impingement in advanced cases. Early findings include supple
motion at the ankle, hindfoot, midfoot, and forefoot. With progression
of the disorder, subtalar motion becomes limited and the heel
eventually becomes fixed in a valgus position, midfoot abduction
increases with a concomitant decrease in midfoot adduction, and
forefoot pronation becomes fixed, which paradoxically produces fixed
forefoot varus when the heel is held in a neutral position. In the most
advanced cases, Achilles contracture produces equinus deformity, which
is most easily appreciated when ankle motion is evaluated with the heel
held in a neutral position. Manual motor testing reveals loss of
function varying from slight weakness associated with tenosynovitis to
complete loss of function associated with chronic tendinosis or
complete rupture.

Begin the radiographic examination with weight-bearing
views of the foot and ankle. Valgus tilt of the ankle mortise increases
the amount of chronic stress across the posterior tibial tendon. Loss
of ankle joint height, especially at the lateral joint line, is a risk
factor for rapidly progressive arthrosis after hindfoot fusion. An
enlarged or accessory tarsal navicular is a predisposition to PTT
dysfunction. Assess foot alignment, with particular attention to
midfoot collapse on the lateral view and midfoot abduction on the
anteroposterior view. Advanced imaging of the PTT is best accomplished
with MRI (4). The tendon is normally round to
oval in shape with a low, homogenous signal. Tenosynovitis is easily
identified by increased fluid surrounding the tendon. Degeneration and
partial and complete tears are identified on the T2 sequence by
thickening, increased signal activity, and cystic changes.

PTT dysfunction can arbitrarily be divided into
synovitis; tendinosis manifested by partial or complete tears, leading
to loss of the functional integrity; tendinosis with supple hind foot
valgus; and tendinosis associated with fixed deformity of the subtalar
and transverse tarsal joints.

Treat patients with posterior tibial tenosynovitis with
reduction or modification in activity. For advanced or recalcitrant
symptoms, immobilize the leg in a short-leg walking cast or removable
cast boot. For risk factors such as excessive pronation, use orthotic
devices.

Treat patients with tendinosis in a fashion similar to
that discussed earlier. Immobilization for 6 to 8 weeks may be
required. Occasionally, symptoms recur immediately on discontinuation
of treatment. For patients unwilling to pursue surgical treatment, a
custom ankle-foot orthosis is indicated.

For patients with a completely dysfunctional tendon,
nonoperative treatment is predicated on the presence of hindfoot and
forefoot deformity. Patients with mild to moderate deformity may be
treated in a custom ankle-foot orthosis. Patients with severe deformity
require more extensive bracing with a double upright brace and medial T-strap.

Evaluate patients with tenosynovitis and early
tendinosis with MRI to evaluate the extent of tendon degeneration.
Patients with advanced tendinosis with loss of PTT function do not
require evaluation by MRI. The presence of hindfoot valgus, supple or
fixed, along with the presence of any fixed deformity including
Achilles tendon

contracture, must be appreciated before surgical intervention.

Patients who have been successfully managed with
nonsurgical methods as well as those managed with soft-tissue
reconstruction are placed on programs designed to maintain motion of
the foot and ankle, and to increase strength of the posterior tibial
muscle or the transferred FDL muscle. Orthotics designed to resist
excessive pronation and hindfoot valgus are also prescribed as needed.

Care must be taken not to allow the patient with early
posterior tibial tendon dysfunction, synovitis, or mild tendinosis to
progress to a more advanced stage requiring more invasive and more
morbid intervention.

The peroneus brevis and longus muscles originate from
the lateral compartment of the leg. Distally, they form individual
tendons, which pass behind the lateral malleolus to turn anteriorly
toward their respective insertions at the base of the fifth metatarsal
and the base of the first metatarsal. At the lateral malleolus, the
peroneus brevis tendon remains anterior to the peroneus longus tendon.
The tendons are retained behind the lateral malleolus by the superior
peroneal retinaculum (14), a structure that originates from the periosteum on the posterolateral ridge of the fibula (5). The peroneal groove or retromalleolar sulcus is a shallow bony groove (9) that is deepened by a fibrocartilaginous ridge (Fig. 118.5).
The position of the tendons relative to the axis of rotation of the
ankle and subtalar joints determine their function as plantar flexors
and evertors of the foot (Fig. 118.4).

The peroneal tendons (PTs) share a common synovial sheath (35) that bifurcates above and below the lateral malleolus. The tendons receive vascular supply through a posterolateral vincula (37). Unlike the Achilles and posterior tibial tendons, the PTs do not have a demonstrable zone of hypovascularity.

Perhaps because of the intrinsic lack of bony stability, the PTs have a propensity to dislocate out of the peroneal

groove to a position anterior to the lateral malleolus. The injury
occurs as a result of sudden, forceful, passive dorsiflexion of the
inverted foot with reflex contraction of the PTs (8,27,39); an association with chronic lateral ankle instability has also been reported (12).
Dislocation of the peroneal tendons out of the peroneal groove is
associated with a variety of underlying pathoanatomic findings,
including a tear of the superior peroneal retinaculum, elevation of the
superior retinaculum off the lateral border of the fibula with
concomitant dissection of the tendon beneath the lateral fibular
periosteum, and fracture of the posterolateral margin of the fibula.

Chronic subluxation of the peroneus brevis tendon onto
the posterolateral border of the fibula may occur as a clinical or
subclinic entity. This condition has been implicated as a major
causative factor in the development of longitudinal tears of the
peroneus brevis tendon (17,36).
Anatomic factors associated with longitudinal tears of the peroneus
brevis tendon include laxity of the superior peroneal retinaculum,
compression of the peroneus brevis tendon by the overlying peroneus
longus tendon (17,32,36),
the presence of peroneal musculature at the peroneal groove, and
finally, the presence of an anomalous peroneal muscle such as the
peroneus quartus muscle (38). A longitudinal tear of the peroneal tendons has also been described after acute and chronic lateral ankle inversion injury (3,33).

When diagnosed acutely, the acute PT dislocation can be
maintained in a reduced position by a cast. Recurrent or chronic
dislocation requires surgical stabilization by soft-tissue or bony
reconstruction, or both. Longitudinal ruptures associated with chronic
subluxation of the peroneal tendons may respond to a period of
immobilization. Surgical treatment requires the identification and
correction of all pathoanatomic features in addition to the debridement
and repair of the longitudinal tendon rupture.

PT pathology has a tendency to evade diagnosis,
especially in the acute setting. Clinical findings are very similar to
that of a lateral ankle ligament sprain. Furthermore, peroneal tendon
injury can occur concomitantly with lateral ankle ligament injury.

The patient with acute PT dislocation complains of pain
over the course of the PTs as well as the lateral border of the fibula.
The patient may offer a history of forceful, passive, dorsiflexion of
the foot and the detection of a “pop” at the time of injury. Many
patients are able to describe accurately the translation of the tendon
out of the peroneal groove. The tendon typically reduces spontaneously.
Often, the patient presents after the condition becomes recurrent or
chronic. Examination of the acute injury reveals swelling and
tenderness behind the lateral malleolus (1,8,10,24,27).
This is in contrast to the inversion lateral ankle sprain, which is
associated with tenderness anterior to the lateral malleolus.
Observation of the contralateral extremity may reveal asymptomatic
physiologic subluxation. With the foot held in a plantarflexed and
everted position, active dorsiflexion may result in apprehension,
subluxation, and even dislocation. Dislocation is typically quite
painful and is not elicited as a routine part of our examination.
Gentle palpation of the PTs at the peroneal groove while the foot is
taken through active circumduction may reveal the presence of nodule
formation or snapping. Complete the examination with evaluation of
lateral ankle ligament stability.

Patients with partial longitudinal tears of the peroneus
brevis tendon associated with chronic subluxation present with acute or
chronic lateral ankle pain localized to the retrofibular region. This
pain may be associated with intermittent or persistent swelling, a
recurrent “popping” sensation, or lateral ankle instability.
Examination of the lateral ankle reveals mild to moderate swelling over
the course of the peroneal tendons at the peroneal groove.

Palpation
of the region while the ankle is actively circumducted reveals nodule
formation and possibly a “popping” phenomenon. Resisted ankle
dorsiflexion may confirm the presence of physiologic subluxation of the
peroneal tendons. Resisted manual motor testing may reproduce pain as
well as weakness of the respective muscles. Once again, lateral ankle
instability must be ruled out.

Routine radiographic evaluation after acute PT
dislocation rarely demonstrates an avulsion fracture off the rim of the
lateral malleolus (Fig. 118.6) (21).
Obtain stress views if lateral ankle instability is an associated
finding. For cases that present a diagnostic dilemma, use MRI to detect
tenosynovitis, partial or complete ruptures, subluxation, dislocation,
competency of the superior peroneal retinaculum, the presence of a
large distal peroneus brevis muscle insertion, the competency of
lateral ankle ligaments, and internal derangement of the ankle and
subtalar joints.

The pathoanatomic classification developed by Eckert and Davis (7) and subsequently modified by Oden (30) is based on the type of superior peroneal retinaculum injury (Fig. 118.7).
In a type I injury, the superior peroneal retinaculum remains in
continuity with the periosteum overlying the lateral border of the
fibula; the tendons translate out of the peroneal groove and dissect
beneath the periosteum, forming a false pouch. In the type II injury,
the superior peroneal retinaculum is disrupted by an anterior tear. The
type III injury is marked by an avulsion fracture off the posterior
fibular margin. Finally, the type IV injury is defined by a posterior
tear of the superior peroneal retinaculum.

Treat a single, acute dislocation of the peroneal
tendons with a well-fitted, non-weight-bearing, short-leg cast applied
with the foot in slight plantarflexion. Window the cast over the
peroneal tendons at the peroneal groove. Place one-quarter to one-half
inch of felt padding over the tendons and reduce the window. Instruct
the patient to adjust the thickness of the felt pad for comfort.
Immobilize the foot for 6 weeks, at which time, the stability of the
peroneal tendons should be checked. An additional 4 weeks of casting
may be necessary. Rehabilitation focuses on motion, strength, and
proprioception. Occasionally, the patient is able to detect recurrent
dislocation within the cast. These patients, as well as all patients
with recurrent or chronic dislocation, will not respond to nonsurgical
treatment methods (1,15,23,24,25,26 and 27,34,42).

The treatment for partial longitudinal tear of the
peroneal tendon is initially symptomatic. Treatment includes decreased
activity, application of ice, and oral nonsteroidal anti-inflammatory
agents. Patients that fail to respond

require enforced rest with a weight-bearing cast. A taping program may allow continued athletic activity.

Before surgical exposure, the prediction of pathologic
findings associated with peroneal tendon dislocation is very difficult.
Therefore, it is impossible to anticipate the exact nature of the
surgical repair and reconstruction. The patient must be prepared for
debridement of the peroneal tenosynovium; excision of excessive distal
peroneus brevis muscle insertion; resection of an anomalous peroneal
tendon such as the peroneus quartus; deepening of the peroneal groove;
imbrication and reconstruction of the superior peroneal retinaculum;
and finally, debridement, repair, or tenodesis of the peroneal tendons.
Failure to address contributing pathology or concomitant injury, may
result in the persistence of symptoms. An MRI and a computed tomography
(CT) scan can be used to delineate pathologic findings further, but
these are not used for routine evaluation of peroneal dislocation or
partial longitudinal tears.

After the completion of a nonoperative or operative
treatment program, focus rehabilitation on ankle and subtalar
range-of-motion, ankle and subtalar stability, peroneal motor
strengthening, and finally, lower extremity proprioception. Resume full
athletic activity only when local warmth and swelling have resolved and
the patient demonstrates full pain-free range of motion without
evidence of tendon or joint instability.

Occasionally, surgical exploration of the peroneal
tendons fails to reveal significant pathologic findings. At this point,
do not hesitate to extend the exposure distally beyond the tip of the
fibula. Again, take care to maintain a cuff of peroneal retinaculum and
synovial sheath to function as a distal pulley.

When performing a stabilization procedure, if
soft-tissue techniques fail to provide adequate stability, do not
hesitate to perform a sliding osteotomy of the fibula (6) or a reconstruction using a lateral slip of the Achilles tendon (15).

Early accurate diagnosis of PT pathology requires a high
degree of suspicion. When it is detected, concomitant injury must be
identified and treated in order to maximize the functional outcome.
Individualize surgical treatment and address each identifiable
pathologic condition.