Stabilizing Pain - Ankle diagnosis focuses on chronic care

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BioMechanics January 2006

Stabilizing Pain - Ankle diagnosis focuses on chronic care

By: P. SanGiovanni, MD

When patients present with acute ankle pain, often the diagnosis is

pretty straightforward. For those who present with chronic pain, in

contrast, arriving at a clear diagnosis can be challenging. The

etiologies are numerous and can involve either isolated or combined

injury to joint cartilage, bone, tendon, ligament, and/or nerves.

Evaluation of this patient population requires close attention to

detail in the patient's history-taking and clinical exam. Besides

plain radiographs, advanced imaging studies such as MRI, CT scan,

and/or bone scan play an integral role in the diagnostic workup.

With a focused history and exam the differential diagnosis can often

be narrowed. Advanced imaging studies or diagnostic lidocaine

injections are used to either confirm or negate the practitioner's

initial impression.

Effective treatment depends on arriving at the correct diagnosis.

When a patient is not improving in a timely manner, there may be more

involved than initially thought or one treatment may be directed at

an incorrect condition. A structured history-taking is essential. The

key factor is localization of the painful area to a specific region

of the ankle on history and exam. Focusing the patient on describing

where exactly the pain is; what activities or movements bring it on;

what are its quality, intensity, and frequency; what the aggravating

and relieving symptoms are; what treatments have been tried and what

response he or she has had to them will help the diagnosis. All of

these questions can easily be put on a patient's intake form.

The single most important item is localization of the pain. In the

initial clinical exam, the practitioner should try to pinpoint the

area of maximal tenderness to a specific region within the ankle. In

general, this can be divided into anterior and lateral pain, and

posterior and medial pain. From these general areas further narrow

the region down to one of the following: anterior joint line,

anterior lateral joint line, proximal syndesmotic region, lateral

gutter, subfibular region, retrofibular region (peroneal tendons),

sinus tarsi, lateral hindfoot/subtalar region, medial joint line,

medial hindfoot, posterior tibial region, posterior ankle joint line,

retrocalcaneal region, or noninsertional and insertional Achilles

region. The importance of taking the time to specifically localize

the pain to one of these areas cannot be overemphasized; then using

knowledge of the regional anatomy of the ankle will greatly

facilitate narrowing of the differential diagnosis. The more common

etiologies of chronic ankle pain, categorized by region, are listed

in Table 1.

Anterior and lateral causes of chronic ankle pain

It has been estimated that more than 9 million ankle sprains occur in

the U.S. every year.1 Contrary to what has previously been thought, a

significant number of these patients are left with residual pain

following a " routine ankle sprain. " Recent studies indicate that

residual painful symptoms are present in approximately 20% to 40% of

patients at six months post-injury.2 These symptoms may be a

manifestation of residual laxity of the lateral ankle ligament

complex or may represent other, associated, etiologies. The most

common cause of persistent pain following an ankle sprain is

inadequate rehabilitation. Many patients do not undergo a guided

therapy program and failure to recover peroneal strength and/or

proprioception can lead to these chronic symptoms.

Chronic lateral ankle instability. Chronic lateral ankle instability

can be categorized as either mechanical or functional. It is

imperative to differentiate between these two entities as their

treatments vary. A patient's subjective complaint of " giving way "

sensations indicates functional instability. An ankle that is

functionally unstable displays symptoms of instability despite having

a normal range of laxity. Once again this appears to be caused by

peroneal muscle weakness and/or poor proprioception. Mechanical

instability, on the other hand, occurs in an ankle in which the

laxity goes beyond the normal physiologic range. These patients will

have gross laxity on clinical exam and abnormal stress radiographs.

An MRI is not required for the diagnosis as it is not uncommon to

have irregularities in this region from previous injury. An MRI does

play a role in ruling out any concomitant injuries such as peroneal

tendon pathology/tears, osteochondral lesions of the talar dome,

intra-articular loose bodies, or occult fractures.

The majority of patients will respond to nonsurgical treatment

following acute ankle ligament injury. Initial treatment is focused

on shortening the inflammatory phase followed by a functional

rehabilitation program emphasizing peroneal muscle strengthening and

proprioceptive training. An ankle brace may be used to prevent

inversion-type injuries if subtle residual instability exists.

Reconstructive ligament repair is indicated for chronic mechanical

ankle instability if nonoperative treatment fails to provide the

stability required for the patient's desired activities. The ligament

repair used most often is the modified Brostrom repair.3,4 This

procedure essentially shortens the attenuated anterior talofibular

and calcaneofibular ligaments to provide stability; the modification

involves reinforcing the repair by suturing the extensor retinaculum

to the lateral fibular periosteum.5 Nonanatomical repairs involve

using the split half of the peroneus brevis tendon and weaving this

through the distal fibula and calcaneus to create a tenodesis effect.

Although similarly effective, this type of repair can sometimes lead

to some restriction of subtalar joint motion, which is not well

tolerated in certain athletes. The trend has recently returned toward

the modified Brostrom procedure since this provides enough stability

for the vast majority of cases with reduced risk of overtightening

the subtalar joint. If a Brostrom procedure does not provide the

stability required or if the soft tissue is of significantly poor

quality, then either a nonanatomic repair (i.e., a Chrisman-Snook or

procedure) or a new alternative, which involves a hamstring

tendon autograft or allograft woven through drill holes simulating

the anatomic origins and insertions of the lateral ligaments, can be

used.6-8

For those patients who have persistent pain following an ankle sprain

but who do not have significant laxity on exam, other sources of

pathology must be sought. Sources of residual lateral pain include

peroneal tendon pathology, syndesmotic ligament sprain, anterior

lateral impingement syndrome, sinus tarsi syndrome, occult fractures,

and traction nerve injuries.

Peroneal tendon pathology. The spectrum for peroneal tendon pathology

ranges from tendinitis to tendon tears or ruptures to tendon

subluxation/dislocation. Unlike lateral ankle ligament instability,

the tenderness is generally in the retrofibular area along the course

of the peroneal tendons. Often these injuries are mistaken for a

ligament injury due to their location. Patients will generally

present with swelling and tenderness localized to the retrofibular

area or from the distal end of the fibula to the fifth metatarsal

base. Provocative tests demonstrate pain on passive inversion,

resisted eversion, and decreased eversion strength testing.

Subluxation or dislocation can often be elicited with various motions

of the ankle joint causing a palpable snapping sensation as the

tendons displace out of the retrofibular groove and flip lateral and

anterior to the fibula.

X-rays will generally be normal with the exception of an occasional

finding of fracture of the os peroneum or alteration of its normal

position. An os peroneum is present in 7% of the population.9 This is

generally seen at the level of the calcaneal cuboid joint on an

oblique view of the foot. If this has migrated proximally, it

generally represents a rupture of the peroneus longus tendon distal

to the os or a fracture through the os. A " fleck sign " may sometimes

be seen with peroneal tendon subluxation if a small piece of fibula

bone has avulsed off the superior peroneal retinaculum insertion. An

MRI has been found to be the most useful imaging study for

demonstrating pathology of the peroneal tendons.10

Peroneus longus tendon tears or ruptures are generally treated

surgically with either direct repair or, if significantly diseased

tendon tissue exists with a normal-appearing peroneus brevis tendon,

the peroneus longus can be tenodesed to the peroneus brevis. Peroneus

brevis tendon tears are generally longitudinal split tears, either

isolated or associated with tendon subluxation and/or ankle

instability. Nonsurgical treatment revolves around reducing the

associated inflammation with nonsteroidal anti-inflammatory drugs

(NSAIDs), immobilization, and/or footwear modifications such as a

lateral heel wedge. Although the tendon tear may not heal from an

anatomical standpoint, the symptoms may be relieved by the above

measures. If symptoms persist or if there is associated ankle

ligament instability or tendon subluxation, surgical intervention is

required. This entails either repair or excision of the split tear

followed by tubularization of the tendon.

Peroneal tendon dislocation or subluxation is often missed on initial

exam due to swelling in the area and confusion with a lateral ankle

ligament sprain. The condition occurs when the superior peroneal

retinaculum is disrupted or stripped off the distal fibula, which

acts as a restraint to anterior lateral dislocation of the peroneal

tendons. Patients with a shallow retrofibular groove may be

predisposed to this injury. Nonoperative treatment for this entity,

which entails casting or boot immobilization, has a high incidence of

failure. Surgical repair depends on the anatomical pathology. If the

groove appears normal in depth, then reduction of the dislocated

tendons and repair of the superior peroneal retinaculum to the distal

fibula are performed. If the groove is shallow, then a fibular

osteotomy through the posterior aspect of the distal fibula is

performed to deepen the groove. This is followed by repair of the

superior peroneal retinaculum.

Impingement syndromes

Impingement syndromes of the ankle joint can result from bony or soft

tissue conditions. Anterior bony impingement presents with a history

of previous trauma. Distal tibial or talar neck osteophytes develop

along the anterior aspect of the ankle causing painful impingement on

ankle dorsiflexion. The symptoms are similar to those of an early

arthritic condition, with a dull, aching-type pain. At times the pain

will be sharp, usually when the patient first walks after a period of

rest. Conservative treatment for bony impingement includes physical

therapy, cortisone injection, and footwear modifications. A heel lift

will lessen ankle dorsiflexion and can sometimes alleviate some

symptoms. Surgical treatment involves excision of the anterior bony

osteophytes via arthroscopy or an open procedure.

Anterolateral soft tissue impingement is generally seen following a

sprain involving the anterior inferior tibiofibular or anterior

talofibular ligament. Tenderness is along the anterolateral joint

line or lateral gutter. Nonoperative treatment with NSAIDs, cortisone

injection, and physical therapy are various recommended treatment

options.11 If persistent symptoms continue, MRI will often

demonstrate synovitis, thickening, or a partial tear of the

anteroinferior tibiofibular ligament. In cases in which the pain

responds to injection but then symptoms return, arthroscopic

debridement of the synovitic scar tissue has been found to relieve

patients' symptoms in more than 80% of cases.12 On arthroscopic

evaluation, synovitis is generally noted at the anterolateral joint

line and hyalinized hypertrophic scar tissue stemming from a flap of

frayed anteroinferior tibiofibular ligament ends is sometimes seen.

Sinus tarsi syndrome. Sinus tarsi syndrome is a poorly understood

clinical entity with painful symptoms localized directly over the

sinus tarsi and is generally thought to be a diagnosis of exclusion.

Although the exact pathophysiology of this condition remains unclear,

the pain is thought to be secondary to synovitis in the area from

previous interosseous talocalcaneal ligament tear.13 Other theories

suggest it arises from injury to the nerve endings of the fibrofatty

tissue within the sinus tarsi area.14 Symptoms are usually alleviated

by an injection of a local anesthetic and cortisone. If initial

relief is provided with the injection but symptoms recur, excision of

the sinus tarsi contents often relieve the pain in these patients.

Advanced flatfoot deformity due to posterior tibial tendon

dysfunction can also cause pain in the sinus tarsi. In fact, as the

foot deforms due to tendon dysfunction, the medial pain experienced

may shift location to the lateral side due to the lateral talar

process impinging on the calcaneus.

Subtalar joint pathology. Subtalar joint abnormalities may masquerade

as lateral ankle pain. The pain is generally more posterior and

lateral, in the hindfoot region, and is associated with difficulty

ambulating on uneven surfaces. On examination, the practitioner will

note restricted subtalar inversion/eversion motion on the affected

side. A lidocaine or marcaine injection within the subtalar joint

should alleviate the pain in patients with subtalar joint pathology.

Elimination of the pain following injection within a specific joint

(i.e., the subtalar joint) aids in the diagnostic work-up: if the

pain is eliminated, the pathology is within the joint rather than due

to a tendon or ligament. Certain clinical entities, such as an

osteochondral injury to the subtalar joint from a previous trauma,

subtalar joint arthritis, and tarsal coalitions, must be considered.

Conservative treatment with NSAIDs, footwear modifications, or

bracing can be employed. Surgical treatment should be considered for

patients who have exhausted nonoperative treatment options; the type

of surgery depends on the pathology. Subtalar joint fusion would be

reserved for those with extensive arthritic changes of the joint as

the cost of providing pain relief via this method is limited joint

motion. Subtalar joint arthroscopy has limited uses; the decision to

proceed with it would depend on the pathology present.

Nerve injury. Nerve injury can occur to the lateral aspect of the

ankle, though it is relatively uncommon. Traction nerve phenomenon

involving the superficial peroneal nerve and/or sural nerve has been

cited in the literature. Patients will present with burning-type

pain, often with associated paresthesias. A positive Tinel's sign can

be elicited on exam. A diagnostic injection with a local anesthetic

will often confirm the diagnosis. Various pharmacological nerve

agents, such as gabapentin or amitriptyline, can provide substantial

relief for many patients. While this is not the primary indication

for these agents, they have been used in low doses for pain

management in various nerve-related conditions to reduce

dysethesias.15 Physical therapy modalities (whirlpool treatments,

transcutaneous electrical nerve stimulation) to desensitize an area

have been used as well. Nerve decompression or excision should be

reserved for those who do not improve with time, though the vast

majority of patients do. Nerve entrapment, neuromas, or nerve injury

are sometimes seen following surgery for fixation of calcaneus

fracture (sural nerve) or fixation of ankle fracture, ligament

repair, or ankle arthroscopy (superficial peroneal nerve).

Posterior and medial ankle pain

Posterior tibial tendon conditions present with pain along the medial

ankle and hindfoot and often features associated swelling with loss

of strength and endurance during ambulation. Some patients may

display progressive flatfoot deformity. At times the medial pain will

resolve and be replaced by lateral pain in the sinus tarsi due to

impingement as the foot continues to deform. These conditions are

seen in two subsets of patients. More commonly it is seen in the

middle-aged adult who may have had some degree of preexisting

flatfoot deformity, though the affected side is usually asymmetric.

Onset is generally insidious without any specific preceding traumatic

event. The other patient subgroup is younger (in their 20s and 30s)

with tenosynovitis/tendinitis. This may represent early manifestation

of a systemic form of arthritis.

Posterior tibial tendon dysfunction.The posterior tibial tendon is

the main inverter of the foot. Degeneration or attenuation of this

tendon as a result of injury may lead to progressive flatfoot

deformity. As the hindfoot goes into valgus, the medial longitudinal

arch will progressively depress and the forefoot will then assume an

abducted position. On examination, patients will have tenderness

along the course of the posterior tibial tendon from the retromedial

malleolar area to its insertion into the navicular. Boggy swelling

may be noted within the medial hindfoot. On weight-bearing, patients

will have the classic " too many toes " sign when viewed posteriorly.

This sign indicates progressive forefoot abduction. Double and single

limb heel raises constitutes functional testing. Patients will

generally have difficulty or be unable to perform a single leg heel

raise on the affected side. An associated Achilles tendon contracture

is common in longstanding conditions due to the Achilles axis

shifting laterally upon hindfoot valgus.

Stages (I through IV) for these conditions have been described by

and Strom.16 Stage I signifies tendinitis without deformity,

stage II is a flexible deformity, stage III a rigid deformity, and

stage IV a rigid deformity with not only involvement of the hindfoot

but also a valgus deformity of the ankle secondary to deltoid

ligament insufficiency. Treatment is based on the stage at

presentation. During the acute inflammatory stage, immobilization and

the use of NSAIDs and therapy may be of benefit. Immobilization with

an ankle stirrup brace, walking boot, or cast may also be beneficial.

In the next stages, recognized conservative treatment is the use of a

semirigid orthosis with either medial posting or a medial heel wedge

and arch support or ankle bracing with either an AFO or a semirigid

lace-up brace (i.e., an Arizona or Baldwin brace).

Surgical treatment is indicated for patients who fail to respond to

nonoperative means or are developing a progressive deformity that may

lead to a more rigid deformity. For stage I disorders, a simple

tenosynovectomy can be performed. Stage II disorders have been

addressed with combined flexor digitorum longus tendon transfer and

calcaneal osteotomy, medial displacement osteotomy, and/or lateral

column lengthening. In the later phases of stage III or IV, tendon

transfer and osteotomies generally do not suffice because of the

rigidity of the involved joints. In these instances, fusion

procedures have generally been recommended, with either an isolated

hindfoot fusion or a triple arthrodesis.17

Flexor hallucis longus tenosynovitis. Disorders of the flexor

hallucis longus tendon are commonly found in patients who perform

activities involving the extremes of ankle motion such as ballet

dancers, gymnasts, and athletes involved in jumping sports. The

flexor hallucis longus passes through a fibro-osseous tunnel along

the posterior aspect of the ankle. Patients will generally present

with pain localized to the posterior medial hindfoot and a history of

triggering or a catching sensation. On examination the pain can be

reproduced by resisted active flexion of the great toe. Also, a

pseudo-hallux rigidus may be observed if the ankle is brought into

neutral dorsiflexion and limited passive extension of the great toe

secondary to stenosis of the tendon through its fibro-osseous sheath

is noted. X-rays are inspected for a long trigonal process or os

trigonum, generally seen on the lateral view.

Nonoperative treatment involves rest from the inciting activities,

NSAIDs, physical therapy, and possibly a short course of

immobilization. Cortisone injections are generally not recommended

due to their detrimental effects on tendon. If a trial injection is

performed, the patient should be immobilized in a boot or cast for

three to four weeks. Surgical treatment includes debridement of the

flexor hallucis longus tendon with decompression of the fibro-osseous

tunnel and resection or repair of any nodular thickening of the

tendon. Intraoperative inspection generally shows a nodularity of the

tendon within the fibro-osseous tunnel that catches on ankle plantar

flexion and dorsiflexion. There is occasionally an associated cyst

within the tendon sheath or posterior ankle/subtalar joint region.

Tarsal tunnel syndrome. Tarsal tunnel syndrome may result from

compression of the posterior tibial nerve at the level of the ankle

joint. The nerve and its terminal branches can be entrapped within

its course following trauma, vein varicosities, fibrosis, and cyst

formation. Patients will often complain of burning-type pain with

numbness and tingling along the plantar aspect of the foot.

Percussion over the tibial nerve (Tinel's sign) will reproduce

symptoms. EMG/nerve conduction studies may have variable results,

though in two series positive findings were revealed in 82% to 90% of

patients.18,19 The value of EMG depends on both the technician and

the interpretation.

When a space-occupying mass is identified as the cause, surgical

treatment consists of release of the tarsal tunnel and excision of

the mass. When no space-occupying lesion is noted, nonoperative

treatment would consist of NSAIDs, pharmacologic nerve agents,

orthoses, physical therapy, and/or immobilization.

Achilles tendinitis. Classification of Achilles tendon disorders as

insertional or noninsertional is based on location of the pain.

Anatomical studies have demonstrated a relatively hypovascular area

approximately 2 to 6 cm proximal to the Achilles calcaneal

insertion.20 This is where noninsertional Achilles tendinitis is

recognized. Overuse that causes microtears within the tendon may lead

to degeneration, which frequently results in noninsertional Achilles

tendinitis.

Insertional Achilles tendinitis occurs at the distal insertion into

the posterior aspect of the calcaneus. Tenderness is distal and a

bony prominence can often be felt along the posterolateral calcaneal

border. This is known as Haglund's calcaneal deformity and is

commonly associated with insertional Achilles tendinitis, as is

retrocalcaneal bursitis. Radiographs may be normal or show traction

osteophytes or calcific deposits, which are best noted on the lateral

views. An MRI may assist in determining the region and percentage of

tendinosis if surgery is contemplated, and may be used to assess for

edema within the posterosuperior calcaneal tuberosity and

retrocalcaneal bursa.

Nonsurgical treatment is similar to that for noninsertional Achilles

tendinitis but has been less successful. Estimates put patient

response to nonoperative treatment at only 50%.21 Surgical treatment

addresses both the Achilles tendon and, if present, the bony

deformity. If a bony prominence exists, a partial excision of the

posterosuperior aspect of the calcaneus is performed to decompress

this region and remove a source of mechanical irritation. If more

than 50% of the tendon requires excision due to its degeneration, the

repair should be augmented with a flexor hallucis longus tendon

transfer. Besides supplementing the strength of the repair, the

adjacent musculature of the FHL tendon is sewn into the remaining

tendon, bringing its valuable blood supply to the repaired segment.

It should be understood by the patient and therapist that the

recuperation process from this procedure is rather long; slow,

gradual improvement will peak at nine to 12 months postoperatively.21

A degenerative process within the tendon with no surrounding

inflammation is termed an Achilles " tendinosis. " Patients present

with localized painful swelling several centimeters above the

Achilles tendon insertion. An area of nodular thickening can often be

visualized or palpated.

Conservative treatment focuses on relieving the stress/tension on the

tendon as well as decreasing any inflammation present. Physical

therapy, NSAIDs, a 3/8-inch tapered heel lift, night splints, or a

brief period of immobilization form the basis for conservative

treatment. Recent studies advocate a physical therapy program

incorporating a 12-week eccentric calf muscle strengthening

course.22,23 For patients for whom nonoperative treatment fails,

surgical management has traditionally been excision of the

degenerative segment with repair of the tendon. If inflammation of

the peritendinous sheath is noted, a tenosynovectomy is performed at

the same time.24 Some advocate microtenotomy of the tendon with small

longitudinal split incisions within the tendon to promote tendon

revascularization.25

Os trigonum syndrome. The os trigonum is described as a secondary

center of ossification that never fuses to the posterior aspect of

the talus in approximately 1.7% to 7% of the general population. It

may or may not have a cartilaginous connection and most of the time

is asymptomatic. It may be noted incidentally on x-rays. It forms the

lateral border of a groove where the FHL tendon passes along the

posterior aspect of the ankle. This bone becomes clinically

significant when it becomes symptomatic, most frequently in athletes

involved in activities requiring extreme plantar flexion. The classic

example is a ballerina en pointe. Patients will present with gradual

onset of pain in the area of the posterior aspect of the ankle. Pain

is experienced when the ankle is placed in maximal plantar flexion,

which causes the os trigonum to impinge on the posterior aspect of

the tibia. On examination pain is experienced with passive plantar

flexion of the ankle. The condition may or may not be associated with

a concomitant FHL tendinitis, therefore it is imperative to evaluate

pain on passive dorsiflexion of the hallux or resisted plantar

flexion of the hallux as well.

Imaging studies demonstrate an os trigonum on the lateral plain x-

ray. CT scan will better demonstrate the lesion though an MRI is

often more helpful as it can show bone marrow edema within the os

trigonum and adjacent increased inflammation when symptomatic. Bone

scan has also been a valuable study for this condition.

Nonsurgical options include restriction of the inciting activity,

NSAIDs, immobilization, and possible cortisone injection. If this

treatment fails, surgical excision of the os trigonum has been shown

to have a successful outcome in the majority of cases.26 It is

important to note whether a concomitant FHL tendinitis is present as

this may alter the surgeon's approach. In general, a posterior

lateral approach for os trigonum alone or posterior medial approach

when FHL tendinitis is present is preferred.

Summary

Arriving at the correct diagnosis of patients with chronic ankle pain

can be challenging. Strict attention to detail is paramount.

Knowledge of anatomy and the clinical entities that exist, based on

localization of the patient's signs and symptoms, helps narrow the

differential diagnosis. With a thorough history and a systematic

approach to physical exam, a diagnosis can often be reached.

Diagnostic x-rays, advanced imaging studies, and diagnostic

injections can further assist in pinpointing the diagnosis. Once the

correct diagnosis has been established, condition-specific treatment

can be initiated in an effort to relieve pain and thereby improve

function.

Tom SanGiovanni, MD, is director of the foot and ankle division for

UHZ Sports in Miami and is a voluntary assistant professor of

orthopedis and rehabilitation and a professor of exercise science and

sports medicine at the University of Miami.

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