Physical Address
304 North Cardinal St.
Dorchester Center, MA 02124
Disorders of the Ankle and Foot: Medial
Introduction
Due to the superficial location of many of the structures that contribute to medial sided symptoms, ultrasound plays an important role in their assessment. Abnormalities of the medial tendons predominate, but disorders of the neurovascular structures, ligaments and even bones need to be considered. The technique for examining the medial ankle has already been discussed. Important points include the dominant role that axial images play in the assessment of tendon disease and this is particularly important in the medial ankle where the tendons follow a curved course around the medial malleolus. Each of the conditions that can contribute to medial side of symptoms will be discussed in turn.
Tibialis Posterior Tendon
The tibialis posterior tendon (TPT) is the most powerful inverter of the foot and helps to stabilize the medial longitudinal arch. TPT dysfunction is one of the commonest causes of medial sided ankle pain and is particularly prevalent in the middle-aged and older population. The cause of tendinopathy is multifactorial. Intrinsic factors combine with extrinsic and abnormal biomechanics to lead to tendon degeneration. Intrinsic factors include strain on the tendon as it passes a curved course around the medial malleolus. A zone of hypovascularity is said to occur in the watershed area between the proximal portion of the tendon supplied by the posterior tibial artery and the distal portion of the tendon supplied by a combination of the posterior tibial and dorsalis pedis arteries. Other areas of relative hypovascularity occur as the tendon sheath does not extend the full length to its insertion and there is no associated mesotendon. The combination of these anatomical features may predispose to tendon degeneration in this location. Other intrinsic factors include systemic disease, particularly diabetes, renal disease and rheumatoid arthritis, hypertension and use of steroids. Histologically, tendinosis is associated with replacement of the normal collagenous architecture with mucinous material that lacks structure or fibre organization. There is a decrease in the ratio of type 1 to type 3 collagen, and a reactive vascular ingrowth. This maladaptive repair is associated with tendon dysfunction.
Tendinopathy of the TPT is most common in middle-aged females who complain progressively of pain followed by flat foot deformity. Classically patients describe difficulty with walking on uneven ground, climbing and descending stairs. Clinically, tenderness is found on the medial aspect of the ankle along the line of the tendon. With advancing disease, the patient is unable to carry out a single heel raise.
The action of tibialis posterior in plantar flexing and everting is to maintain congruity at the talonavicular and calcaneocuboid joints during walking. Failure of this mechanism leads to flexion stresses of the midfoot and ultimately failure.
Key Point
The TPT maintains the longitudinal arch of the foot and consequently its failure leads to flat foot deformity followed by sequential failure of the spring ligament and ligaments of the sinus tarsi.
Flat foot deformity is assessed with the patient standing. Looking from the posterior, more toes are visible lateral to the heel on the affected side.
Degenerate TPT tears usually occur at the level of the medial malleolus, whereas tears in athletes are usually at the navicular insertion.
Clinical and Radiological Staging
Both clinical and imaging staging has been described. The lower grades include the presence of pain without structural abnormality. This progresses through tendon degeneration to complete rupture when flat foot deformity is obvious. The clinical classification describes progressive dysfunction from stage I paratenonopathy, tenosynovitis and tendon degeneration with normal tendon length, through stage II with tendon elongation leading to correctable flat foot deformity, stage III with rigid flat foot deformity and finally stage IV with secondary medial ligament failure leading to valgus deformity. The imaging findings reflect clinical progression though is often normal in the early stages. Positive findings can be divided into those that involve the tendon sheath called tenosynovitis, and changes within the tendon itself.
Tenosynovitis
A small quantity of fluid is frequently found in the normal tendon sheath, particularly in the submalleolar region. A useful rule of thumb is that the cross-sectional area of fluid should not exceed that of the adjacent tendon. In the earliest stages, findings may be limited to excess fluid within the tendon sheath ( Fig. 27.1 ).
Practice Tip
| Distension often begins in the immediate submalleolar area as this is where the sheath has room to expand ( Fig. 27.2 ). |
As tenosynovitis progresses, synovial thickening as opposed to echo-free fluid becomes more apparent ( Fig. 27.3 ) and increased Doppler signal develops within it ( Fig. 27.4 ). Apart from the nutrient artery, Doppler signal will not under normal circumstances be found in the synovial lining and its presence is generally indicative of tenosynovitis. Synovial thickening may become quite marked, even mass-like ( Fig. 27.5 ). Even at this stage, the tendon may remain completely normal, although in most cases some degree of underlying tendon disease is apparent, especially if high-resolution equipment is used. Detecting even small degrees of tendinopathy may have important implications in planning treatment.
Hypertrophic, Atrophic and Calcific Tendinopathy
Key Point
The earliest ultrasound changes of tendinopathy are focal areas of decreased reflectivity within the tendon.
These are due to loss of the normal tendon architecture with areas of focal hypointensity representing tendon degeneration. The tendon may begin to delaminate and longitudinal splits appear. Progression leads to enlargement of the tendon and areas of further focal breakdown and partial tear. The name hypertrophic tendinopathy or type 1 partial tear is applied to this condition. Increased Doppler activity can be detected within the tendon at an early stage.
Practice Tip
| Under normal circumstances, blood vessels should not be found within a tendon apart from perhaps an occasional vessel close to the nutrient artery. |
Key Point
Signal changes within the tendon should be carefully sought as their detection indicates progression to a more significant form of the disease.
The detection of intrinsic tendon abnormalities also has a significant impact on therapeutic decision making and many feel that corticosteroid injection therapy for tenosynovitis is contraindicated when the tendon becomes abnormal. Others argue that minor signal changes within the tendon, particularly using sensitive ultrasound, are not a contraindication to corticosteroid injection; however, in all cases the patient should be warned about the potential for tendon rupture and protected against it.
These early abnormalities predominate in the submalleolar region and may be associated with other findings. There is a fibrous pulley enthesis on the posterior aspect of the medial malleolus where the TPT passes around it. Involvement of the enthesis may lead to bony hypertrophy and the formation of a spur on the posterior aspect of the medial malleolus ( Fig. 27.6 ). This may be visible on plain films and is a useful plain film clue to the underlying tendon disorder. It is also clearly visible on MR imaging, particularly in the axial plane.
As the tendon begins to further elongate and as the arch of the foot drops, the tendon becomes further stretched. In some cases, there is a decrease in the cross-sectional area of the tendon that now appears of equal size to or smaller than the adjacent flexor digitorum tendon. The appearance of atrophic tendinopathy, as it is called ( Fig. 27.7 ), has been likened to a fraying rope. As the individual strands begin to dissociate, they slide apart, reducing the tendon cross-sectional area in the most involved segment ( Fig. 27.8 ). As has previously been outlined …
Key Point
… the TPT is normally at least twice the size of flexor digitorum. Loss of this ratio is termed atrophic tendinopathy or type 2 partial tear.
In general this is a relatively straightforward diagnosis with ultrasound as the tendon sheath is frequently involved and the internal structure of the tendon is grossly abnormal. On MRI, however, the abnormalities of the tendon sheath may be less obvious and the degenerating tendon may preserve its low signal on both T1 and T2 weighting. An alteration in size is therefore often the only feature of type 2 partial tear and the diagnosis may be overlooked.
Other forms of tendinopathy include acute calcific ( Fig. 27.9 ) and insertional tendinopathy. Fibrosing tenosynovitis is uncommon in the TPT, although it has been described. Calcification in the tendon sheath leading to acute calcific tenosynovitis is rare. A few flecks of calcification within the tendon, particularly at tendon insertions, should not be regarded as significant and calcification of this type is frequently asymptomatic. As with the supraspinatus tendon, occasionally acute calcific tendinopathy presents very acutely. The skin is red, the subcutaneous tissues are swollen and the tendon is very tender to touch. Calcium may be seen as a conglomerate within the tendon that can be associated with an increase in Doppler signal.
Insertional tendinopathy involves the area of tendon close to its attachment onto the navicular. This is a more common area for overuse disease in the athlete; however, there is a potential pitfall.
Practice Tip
| Care should be taken when considering areas of decreased signal close to the insertion as pathological. |
Although a major component of the tendon inserts into the navicular, there are significant slips which pass inferiorly to insert in the undersurface of the cuneiforms even as far as the medial aspect of the cuboid. Diverging tendon fibres create anisotropic artifact, which is difficult to eradicate in this location. The presence of a normal Doppler pattern and the absence of local symptoms on sonopalpation are helpful to confirm that the tendon is normal. Abnormal fluid around the distal portion of the tendon is more strictly a paratenonopathy as opposed to tenosynovitis, as the tendon sheath ends at approximately the level of the midtalus.
Insertional Tendinopathy Accessory Navicular
Key Point
Insertional tendinopathy can occur in isolation but is more frequently associated with an accessory ossicle.
An accessory navicular is present in approximately 4% of the population but there is a higher association of TPT disease in this group. Three types of accessory ossicles have been described. Type 1 is a small, well-corticated bony ossicle fully contained within the distal portion of the tendon. It is rarely associated with symptoms. A type 2 accessory ossicle is larger and contains most of the TPT attachment. There is a fibrous or cartilaginous joint between the accessory ossicle and the navicular that is essentially a pseudarthrosis ( Figs 27.10 and 27.11 ). These can be a significant source of symptoms. Tenderness will be localized to the pseudarthrosis and this may be elicited by sonopalpation during the examination; increased Doppler signal may also be detected ( Fig. 27.12 ). On MRI, bone oedema may be detected on either side of the pseudarthrosis. Painful pseudarthroses are difficult to treat. Surgical options include fixing the accessory article onto the navicular. Prior to this, a corticosteroid injection can be attempted to alleviate symptoms. The patient should be warned that there is a significant risk of rupture that will precipitate surgical fixation.
The third type of accessory ‘ossicle’ is where there is an elongation of the medial aspect of the navicular, as though a type 2 had fused with its parent bone. This is also referred to as a cornuate navicular. This is the least troublesome variant, although it is also said to predispose to tendinopathy, due to shortening of the tendon and reduction of the curve around the medial malleolus.
Tibialis Posterior Rupture
The most advanced stage of TPT disease is tendon rupture which on imaging grading is referred to as a type 3 tear. As with tendinopathy the typical location is in the submalleolar region. The aetiology is generally chronic but can occur following an acute injury superimposed on an already damaged tendon. Axial images above the malleolus will demonstrate an intact but damaged tendon. As the tendon is followed distally it disappears at the level of the rupture ( Fig. 27.13 ). Tendon retraction is not a prominent finding as adhesions between the tendon sheath and the adjacent tibia occur. The distal portion of the tendon will appear lax helping to make the diagnosis.
One of the principal functions of TPT is to preserve the medial arch of the midfoot. If it fails, considerable stress is placed on the spring ligament and it is not uncommon that spring ligament failure follows TPT failure.
Tibialis Posterior Subluxation
Subluxation of the TPT is uncommon but has been described following trauma and following release of the flexor retinaculum for tarsal tunnel compression. The configuration of the torn retinaculum should be reviewed to determine whether the periosteum is also involved. Stripping of the retinaculum, with or without the attached periosteum, creates an elongated sulcus that allows medial subluxation of the TPT during flexion and inversion. The abnormality is best appreciated on dynamic ultrasound. Surgical treatment is generally advised.
Flexor Digitorum Longus
Disorders of flexor digitorum longus (FDL) are considerably less common than tibialis posterior disease. Many cases occur in conjunction with tibialis posterior disease if a common sheath is present ( Fig. 27.14 ). The ultrasound findings are similar to TPT disease, with tenosynovitis initially ( Fig. 27.15 ) followed by involvement of the tendon itself ( Fig. 27.16 ).
More distally a friction syndrome is described where FDL crosses flexor hallucis longus (FHL) on the undersurface of the foot. The area is referred to as the knot of Henry and is located between the superficial and second muscle layers. The crossover occurs at approximately the level of the navicular-cuboid joint. The medial plantar nerve lies in close proximity to the knot of Henry. Repetitive friction, such as might occur in runners, may underlie the syndrome, which is sometimes referred to as runner's foot.
You're Reading a Preview
Become a Clinical Tree membership for Full access and enjoy Unlimited articles
If you are a member. Log in here
