Porter & Schon: Baxter's The Foot and Ankle in Sport, 2nd ed.

Section 2 - Sport Syndromes

Chapter 8 - Posterior tibialis tendon dysfunction

  1. Grant Braly

  

 

Introduction

  

 

Anatomy and biomechanics

  

 

Diagnosis

  

 

Disease staging

  

 

Treatment

  

 

Perils and pitfalls (with illustrative case reports)

  

 

Summary

  

 

References

Introduction

Acute posterior tibialis tendon injury in the athlete is rare [0010] [0020] but must be considered in the differential diagnosis of a patient who presents primarily with tenderness, swelling, and pain over the medial ankle or plantar medial midfoot. Antecedent to the acute presentation, there often is a history of less severe prodromal symptoms more consistent with a chronic interstitial rupture with tendinosis. The chronic picture is seen more often in the middle-aged to elderly patient, athlete or not, that was especially popularized by the late Kenneth A. Johnson, MD, [0030] [0040] [0050] with whom I had the honor of fellowship training. Others, [0010] [0020] [0060] [0070] [0080] [0090] of course, also have contributed to a further understanding of the diagnosis and treatment of this condition.

Although most of the literature emphasizes chronic posterior tibialis tendon disease, the ultimate presentation of the acutely injured athlete may be very similar to the chronic form. Therefore given the rarity of acute injury versus the more commonly seen chronic presentation, posterior tibialis tendon “dysfunction,” rather than “injury,” probably is a more accurate description and title for this chapter.

 

Anatomy and Biomechanics

The posterior tibialis muscle is a resident of the deep posterior compartment of the leg, originating along the proximal one third of the tibia and intraosseous membrane. Distally, its tendon travels posterior, then inferior, through the medial malleolar groove, changing direction abruptly almost 90 degrees. The stout retinaculum of the long flexors prevents the tendon from subluxating over the medial malleolus.[10] Because the posterior tibialis tendon is without a mesotenon, there is an area of relative hypovascularity from this acute turn at the medial malleolus to the medial navicular insertion. These factors of hypovascularity and the mechanical stress of an acute turn of the tendon as part of a strong, weight-bearing leg muscle (second only to the gastrocnemius) make the tendon predisposed to injury in this area.

Because the posterior tibial tendon travels posterior to the axis of the ankle and medial to the axis of the subtalar joint, it serves as an ankle plantarflexor and foot invertor via the transverse tarsal joint (talonavicular and calcaneocuboid joints).[11] The tendon also has multiple slip attachments to the capsule of the naviculocuneiform joint, all three of the cuneiforms, the cuboid, and their respective metatarsal bases in the plantar arch. [0040] [0120] The posterior tibialis tendon therefore is primarily a midfoot invertor and dynamically supports and elevates the medial longitudinal arch. It also indirectly supports the hindfoot because of its medial malleolar pulley action and intimate relationship to the deep deltoid ligament, plantar medial talonavicular joint capsule, and spring ligament (calcaneonavicular ligament).[13] With relatively little elongation because of rupture, the tendon becomes incompetent to support the medial longitudinal arch initially, resulting in the acquired adult flatfoot with forefoot pronation and abduction ( Fig. 8-1 ). However, over time other ligamentous structures are affected, including the talonavicular joint capsule, deltoid ligament, and spring ligament. The stretching out or even frank rupture of these structures eventually leads to a valgus inclination of the hindfoot and external rotation of the calcaneus, also resulting in contracture of the Achilles tendon as it becomes a hindfoot everter[11] ( Fig. 8-2 ). Clinically, this may result in impinging pain and swelling in the subfibular or sinus tarsi area as the calcaneus abuts against the lateral malleolus. In very severe or neglected cases, a valgus tilt of the ankle may be seen as the deltoid ligament becomes incompetent.

 
 

Figure 8-1  Dorsal-plantar view demonstrating the normal foot (A) and the posterior tibialis tendon incompetent foot (B). With external rotation or abduction of the forefoot, the medial talar head becomes more uncovered by the navicular as it rotates externally. The calcaneus also secondarily rotates externally and tilts into more valgus.

 

 

 
 

Figure 8-2  Posterior-anterior view of the normal (A) and posterior tibialis tendon incompetent ankle and hindfoot (B). With external calcaneal rotation, the talar head translates plantarward. This also leads to increased valgus tilting of the calcaneus and subfibular or sinus tarsi impingement.

 

 

 

Diagnosis

Usually, a detailed history, conscientious physical examination, and x-rays will establish the diagnosis of a posterior tibialis tendon injury.

History and questions to be answered

Sometimes the history alone will provide the examiner with enough information to suggest the diagnosis.

  

   

What was the mechanism of injury? Specifically, did the foot sustain an eversion twisting injury, especially on impact from tripping or a fall? Or, was there a sudden increase in the level of athletic activity temporally related to the onset of symptoms?

  

   

Were there prodromal symptoms of possible tendon degeneration before the acute injury?

  

   

Has the athlete noticed that the arch on the involved side is “flatter,” the foot is “turned out,” the ankle “turned in,” or complained that the injured foot is “weaker”?

  

   

When unshod on a hard, wet floor surface, such as at bath time, does the patient notice a different footprint or a “sucking sound” because of a vacuum effect of the collapsed arch on the symptomatic side?

  

   

Has the athlete noticed more medial shoe sole wear or “running over” the medial vamp?

  

   

Is there any history of gout, pseudogout, or autoimmune disease?

  

   

Are there sensory (dysesthesias or paresthesias) complaints?

  

   

In terms of predisposing risk factors, is there a history of oral steroid use, injected steroids in the area of the tendon, diabetes, smoking, vasculopathy, obesity, or worsening of a preexisting pes planus deformity?

Physical examination and questions to be answered

For comparison, both unclothed and unshod lower extremities from the midthigh distally to the toes should be carefully examined.

  

   

Is there a valgus knee deformity (genu valgum) of the symptomatic side? (This may precipitate or exacerbate posterior tibialis tendon dysfunction, especially if chronic.)

  

   

Is there tenderness and swelling along especially the terminal course of the tendon, generally between the medial malleolus and the navicular insertion or, less commonly, in the posterior aspect of the medial malleolus ( Fig. 8-3, A and B )?

  

   

Is there tenderness in the insertional area of the anterior tibialis tendon?

  

   

In viewing the weight-bearing patient from behind, is there increased forefoot abduction or pronation (the so-called “too many toes sign”) ( Fig. 8-4 )?

  

   

Does the patient have difficulty heel rising with all of his or her weight on the injured side (“single foot heel rise” test), or if he or she is able to heel rise, does the hindfoot fail to invert or invert less than the normal side ( Fig. 8-5 )?

  

   

Is there tenderness and swelling laterally in the sinus tarsi or subfibular area, suggesting impingement, especially in the patient with deformity ( Fig. 8-6 )?

  

   

Is the Achilles tendon contracted?

  

   

Are there abnormal sensory findings that might suggest peripheral neuropathy, especially in the diabetic patient?

  

   

Is there a positive Tinel's sign over the tibial nerve in the medial ankle or plantar foot sensory deficits that might suggest a tarsal tunnel syndrome?

  

   

Is there a tender and swollen bony prominence in the area of the medial navicular, suggesting an accessory navicular or stress fracture?

  

   

Is the medial malleolus itself tender, thus suggesting a stress fracture?

  

   

Are there any dysvascular findings (absent posterior tibial or dorsalis pedis pulses, delayed capillary refill, cyanosis, toe hair loss, and dystrophic nail changes)?

 

 
 

Figure 8-3  Usual area of maximal tenderness and swelling along the terminal course of the posterior tibialis tendon between the medial malleolus and medial navicular insertion. Occasionally, this can extend to the area posterior to the medial malleolus.

 

 

 
 

Figure 8-4  The positive “too many toes” sign in the posterior tibialis dysfunctional right foot is appreciated when examining the weight-bearing patient from behind. The forefoot is abducted/pronated and the hindfoot is in greater valgus, resulting in more toes seen laterally in the right foot when compared with the left.

 

 

 
 

Figure 8-5  Notice hindfoot inversion in the normal left foot. Although patients with posterior tibialis tendondysfunction may be able to perform the single-foot heel-rise test, notice that the hindfoot does not invert, orinverts less, than the normal foot. This may be due to some residual function of the posterior tibialis muscletendon unit with assistive recruitment of the long toe flexors.

 

 

 
 

Figure 8-6  Zone of tenderness and swelling indicative of impingement in the subfibular or sinus tarsi area, often seen with more severe posterior tibialis tendon dysfunction with hindfoot valgus deformity.

 

 

X-rays and questions to be answered

Ideally, weight-bearing x-rays of the symptomatic foot and ankle should be taken. Also, comparison views of the other foot and ankle often are helpful diagnostically.

Ankle x-rays

  

   

Do films demonstrate a medial or valgus tilt ( Fig. 8-7, A )?

  

   

Are there arthritic changes with joint space narrowing, osteophytes, or loose bodies medially?

  

   

Is there any evidence of a medial malleolar stress fracture or medial talar dome osteochondritis dissecans ( Fig. 8-7, C )?

  

   

Is there major arterial (anterior and posterior tibial) calcification?

 




 

Figure 8-7  Radiographs of patients with medial ankle or midfoot pain and swelling demonstrating medial talar tilt because of primary deltoid ligament incompetency (A) accessory navicular (B) medial talar dome osteochondritis dissecans with a coronal magnetic resonance imaging (MRI) view (C) and medial column arthiritis. (D) all of which can mimic to varying degrees the clinical presentation of posterior tibialis tendon dysfunction.

 

 

Foot x-rays

  

   

Is there an accessory navicular or possible avulsion fracture of the medial navicular (see Fig. 8-7, B )?

  

   

Do the films of the foot reveal arthritic changes of the medial subtalar (additional Broden's views may be helpful), talonavicular, naviculocuneiform, or medial tarsometatarsal joints ( Fig. 8-7,D )?

  

   

Is there any evidence of a tarsal coalition, especially in the periadolescent athlete?

  

   

On the lateral view, is the talo-first metatarsal angle negative, especially if it is more so than a comparison view of the contralateral foot ( Fig. 8-8 )?

  

   

On the anteroposterior (AP) view, is there an increased talo-first metatarsal angle or increased “uncovering” of medial talar head at the talonavicular joint, thus indicating forefoot abduction, again especially when compared with the contralateral foot ( Fig. 8-9 )?

  

   

As in the ankle, is there arterial calcification of the dorsalis pedis or posterior tibialis arteries?

 

 
 

Figure 8-8  Lateral weight-bearing views demonstrating the midfoot sag of the posterior tibialis incompetent right foot. I prefer this more simplistic measurement of the angle between the long axis of the talus (a) and the I metatarsal (b). The resultant angle (c) is greater in the involved foot. In this case in the normal left foot, these lines are virtually parallel. Also, notice that the subtalar joint is less clearly seen in the symptomatic right foot because of superimposition of the talus and calcaneus from a hindfoot valgus deformity.

 

 

 
 

Figure 8-9  Anteroposterior (AP) weight-bearing views demonstrating abduction deformity resulting from posterior tibialis tendon incompetency in the right foot. Again, I prefer this more simplistic measurement of the ankle between the long axis of the talus (a) and the I metatarsal (b). The resultant angle (c) is great in the involved right foot. Also, notice that the medial talar head is more uncovered by the navicular in the involved foot (d).

 

 

Magnetic resonance imaging (MRI)

Although rarely necessary, if the history, physical examination, and x-rays fail to conclusively determine the diagnosis of a posterior tibialis tendon injury, or to confirm the diagnostician's impression, then an MRI may be indicated. [0140] [0150] An MRI also is helpful to determine the extent of acute injury or chronic tendinosis and thus guide treatment, especially if surgery is planned, and may predict the postoperative clinical outcome.[15] Finally, the MRI may help to determine other conditions that may mimic, be concomitant with, or even contribute to posterior tibialis tendon disease [0080] [0100] [0130] [0160] [0170] ( Table 8-1 ). Perhaps of historical interest, others have proposed the diagnostic use of tenography[7] or ultrasound,[18] but their sensitivity is significantly less than that of a high-quality MRI.


Table 8-1   -- Differential diagnosis

Medial ankle arthritis

Medial subtalar joint or medial column arthritis

Medial ankle instability with deltoid ligament rupture/laxity

Symptomatic accessory navicular with synchondrosis disruption

Medial malleolar or talar stress fracture

Medial navicular bony avulsion or stress fracture

Medial talar dome osteochondritis dissecans

Acute injury or tendinosis of the flexor hallucis longus or flexor digitorum longus tendons

Tarsal tunnel syndrome

Peri-insertional anterior tibialis tendon rupture or tendinosis

Tarsal coalition, especially in periadolescent athletes

Medial ankle or hindfoot/midfoot crystalline or autoimmune arthritis

 

 

Generally, the MRI will reveal fibrous tendinotic longitudinal hypertrophy or bulbous enlargement of the tendon, sometimes with cystic or longitudinal voids ( Fig. 8-10, A ). Also, there usually is increased tenosynovial fluid within the sheath surrounding the tendon [0180] [0190] ( Fig. 8-10, B ). These findings usually are seen between the medial malleolus and navicular but also can extend proximally into the posterior medial malleolar area.

 
 

Figure 8-10  Magnetic resonance imaging (MRI) findings of posterior tibialis tendon dysfunction. (A) Sagittal view at the level of the medial malleolus (MM) demonstrating longitudinal void within the tendon. (B) Transverse view at the level of the talus (T) also demonstrating intratendinous voids and increased fluid around the tendon.

 

 

 

Disease Staging

Once the diagnosis is firmly established, the stage of posterior tibialis tendon disease, as popularized by Kenneth A. Johnson's seminal work, is important to determine the proper course of treatment. Johnson initially described stages I to III,[5] but a stage IV [0110] [0200] has more recently been described that involves a valgus inclination of the talus with degenerative arthritis of the ankle joint ( Table 8-2). This is exceedingly rare in the active athlete and will not be elaborated upon beyond its mention.

Table 8-2   -- Disease stages

Stage I Peritendinitis and/or tendon degeneration (tendinosis)

No deformity

Stage II Tendon elongated/incompetent

Mild flexible deformity

Stage III Findings of Stage I and II

Moderate-to-severe deformity that may be rigid with possible subfibular or sinus tarsi impingement

Radiographic arthritic changes of triple joint complex and/or naviculocuneiform joints

(Stage IV, which involves a valgus talar tilt and early ankle joint degeneration, also has been described but probably is not applicable to this discussion, given its extreme rarity in the active athlete.)

 

 

Stage I is essentially peritendinitis and/or tendon degeneration (tendinosis) with a normal tendon length and no deformity. Stage II is characterized by an incompetent or lengthened tendon with a mild flexible deformity. Stage III encompasses the findings of the preceding stages, but with a greater degree of deformity that also may be rigid. X-rays of the stage III foot may further reveal significant arthritic changes in any or all of the triple joint complex (subtalar, talonavicular, and/or calcaneocuboid joints) or naviculo-cuneiform joints, as well as clinical signs and symptoms of subfibular or sinus tarsi impingement.

 

Treatment

Conservative

In general, conservative treatment is recommended initially, especially for the stage I and II presentation in the otherwise healthy athlete. However, in the patient who has significant comorbid conditions (e.g., diabetes, smoking, vasculopathy, obesity, etc.) that makes surgical treatment ill advised, conservative treatment may be the definitive treatment. In the young, competitive athlete, these comorbidities are uncommon, but, in the middle-aged athlete, they are not rare.

As with any inflammatory condition or injury, immobilization is therapeutic. Either casting or rigid bracing is recommended for several weeks, the length of immobilization depending on the response of such treatment with diminution of the associated swelling or tenderness. The cast that is well molded to support the arch or the incorporation of an arch support and/or medial wedge if a brace is chosen is further recommended. Weight bearing during the immobilization treatment period is allowed as tolerated. In the less acute or chronic presentation, or after a positive response to immobilization, custom-molded arch supports, perhaps with medial wedging incorporated either in the orthotic and/or on a supportive shoe on the symptomatic side are advised for several months.

Nonsteroidal anti-inflammatory medications also are helpful, but chronic oral steroids should be avoided. Steroid injections also should be shunned because these may lead to complete rupture [0070] [0210] or at least exacerbate a tendinotic condition, especially if an injection is inadvertently intratendinous.

In terms of athletic activity during the conservative treatment period, and perhaps for several weeks after, the injured athlete also should avoid any repetitive impact-loading sports or conditioning. Cross training (e.g., bicycling, swimming, perhaps walking and/or primarily upper-extremity bench weight training) is advised.

In the athlete with a tight Achilles tendon, stretching is helpful,[22] especially to avoid reinjury once he or she has been successfully treated conservatively and returns to the preinjury level of activity. Also, ideal long-term management includes supportive and often-replaced, high-quality athletic shoes. Finally, if it is an issue in the overweight athlete, weight loss obviously is recommended. Other comorbid conditions also should be addressed, for example smoking cessation and good control of diabetes and autoimmune disease.

Surgical treatment

The following discussion includes surgical treatment of the stages of posterior tibial tendon rupture gleaned from the literature but also is biased by my own experience ( Table 8-3 ).

Table 8-3   -- Surgical Management

Technique

Postoperative regimen

Return to sports postoperative

Stage I

 

 

Tenosynovectomy

Cast: 3 weeks

3 months

Repair of interstitial rupture

Rigid brace: 3 weeks

 

Possible medial shift calcaneal osteotomy for severe cases?

Supportive shoes with custom-molded arch supports: until 3 months postoperative

 

Stage II

 

 

Repair and advance/shorten tendon

Cast: 6 weeks

6 months

Imbricate talonavicular joint plantar medial capsule

Rigid brace: 6 weeks

 

Flexor digitorum longus tendon transfer

Supportive shoes with custom-molded arch supports: until 6 months postoperative

 

Medial shift calcaneal osteotomy with flexible deformity

 

 

Possible Achilles tendon lengthening or gastrocnemius recession

 

 

Stage III

 

 

Repair/reconstruction of tendon may not be necessary?

Cast: 9-12 weeks

9-12 months

Medial shift calcaneal osteotomy and/or lateral column lengthening if deformity is flexible

Rigid brace: 6-9 weeks

 

Arthrodesis if deformity rigid and/or arthritic changes present

Supportive shoes with custom-molded arch supports?

 

Possible Achilles tendon lengthening or gastrocnemius recession

 

 

 

 

Stage I—tendon length normal

Intraoperative findings include tenosynovitis, often with granulation tissue, increased tenosynovial fluid, and an interstitial longitudinal rupture, usually between the medial malleolar tip and the navicular insertion of the tendon. [0050] [0090] Fusiform hypertrophy with tendinotic “crabmeat” tissue often is encountered, as well as possible cystic degeneration, especially in a more chronic presentation.

Surgical treatment involves opening the tendon sheath from at least the medial malleolus to the navicular insertion. If disease is noted proximal to the medial malleolus, then it is important to preserve, if possible, an approximately 1-cm section of the sheath at the medial malleolar level to prevent subluxation of the tendon. (If this is not possible because of extensive proximal disease, then that portion of the tendon should be repaired after the tendon itself is addressed.) Tenosynovitis and granulation tissue are debrided with a small rongeur. The hypertrophied portion with tendinosis within the tendon then is debrided and debulked sharply via a longitudinal incision in the tendon itself. The incision then is repaired with absorbable, interrupted suture with inverted knots.

Postoperatively, cast immobilization is recommended for 3 weeks, followed by rigid bracing, stirrup bracing, or a short articulating AFO for another 3 weeks. After immobilization, supportive shoewear with a custom-made arch support is recommended for 3 months. In the athlete, repetitive impact-loading sports or conditioning endeavors are avoided until at least 3 months postoperatively.

Stage II—tendon elongated, deformity mild and flexible

Similar, but more severe, pathologic findings as seen in stage I are encountered in stage II disease. There usually is a longer area of interstitial rupture with accompanying bulbous enlargement of the tendon that may even extend proximal to the medial malleolus. The tendon is found to be elongated, and thus incompetent, allowing excessive pronation and abduction of the forefoot. (The function of the posterior tibialis is easily compromised with even a small increase in length because the normal excursion in the healthy tendon rarely exceeds 1 to 2cm.)

The tendon is repaired as described for stage I. Also, shortening of the tendon is advised by advancing its plantar medial insertion on the navicular. It usually is necessary to detach the medial insertion and excise excess peri-insertional tendon before securing it to the decorticated plantar medial aspect of the navicular with nonabsorbable sutures incorporated in bone anchors[9] or through drill holes [0040] [0050] [0090] [0110] [0130] [0230] [0240] ( Fig. 8-11, F, H, and I ). The surgeon also may consider elliptically excising a transverse segment and imbricate the attenuated plantar medial capsule of the talonavicular joint in severe cases, [0110] [0230] or, obviously, repair it if it is torn ( Fig. 8-11, B, D, and G ).









 

Figure 8-11  Intraperative photographs and corresponding schematic drawings demonstrating my preferred method of reconstruction of a complete rupture of the posterior tibialis tendon. This patient had a flexible deformity without degenerative triple joint arthritis. A medial shift calcaneal osteotomy was added to the medial soft-tissue reconstruction. (A) Complete rupture of the posterior tibialis tendon. The two ends could not be approximated because of proximal migration of the proximal end. (B) Subsequent to debridement of the distal end of the posterior tibialis tendon, the plantar medial talonavicular joint capsule was incised and an elliptical segment removed to the later imbricate it. (C) The flexor digitorum longus tendon is harvested as distally as possible. It is not necessary to tenodese the distal end of the flexor digitorum longus of the flexor hallucis longus tendon to maintain adequate lesser toe flexor function. (D) Heavy absorbable stay sutures are placed and tagged in the plantar medial talonavicular joint capsule. (E) The flexor digitorum longus tendon is passed through and tenodesed with maximal tension to the proximal end of the posterior tibialis tendon. (F) A bone anchor is placed in the decorticated medial aspect of the navicular. (G) The plantar medial talonavicular joint capsular stay sutures are tied. (H) The flexor digitorum longus tendon is secured to the medial navicular under tension with the nonabsorbable sutures from the bone anchor. (I) Final appearance of the reconstruction. Heavy absorbable sutures also are used to further secure the flexor digitorum longus tendon transfer to the fibrous tissue of posterior tibialis tendon sheath and the surrounding periosteum.

 

 

With extensive stage II findings, and especially if the tendon is completely torn, a tendon transfer is recommended ( Fig. 8-11, A ). Most surgeons harvest the flexor digitorum longus [0030] [0040] [0050] [0070] [0090] [0100] [0110] [0130] [0190] [0230] [0240] for this purpose, which is in close proximity to the posterior tibialis tendon ( Fig. 8-11, C and E ). Within the same surgical incision, the flexor digitorum longus is cut sharply as distally as possible and is secured to the navicular or as a side-to-side transfer to the repaired and advanced posterior tibialis tendon. It generally is not necessary to sew the distal stump of the flexor digitorum longus tendon to the flexor hallucis longus tendon because of the many soft-tissue connections between them distal to the level of flexor digitorum longus cut. Other tendons have been suggested for transfer, but these transfers may be of historical interest only. Although the flexor hallucis longus has a stronger muscle than the flexor digitorum longus, its transfer is not recommended because the dissection associated with its harvesting is technically challenging and risky, given its close proximity to the neurovascular bundle. Also, the resultant weakness of great toe flexion may be a significant problem for a high-performance athlete.

More recently, as primarily popularized by Myerson [0110] [0230] and described by others, [0100] [0190] [0220] [0260] a medial shift or slide calcaneal osteotomy has been advocated for stage II disease. (There also may be an indication for this osteotomy in severe stage I cases.[11]) The effect of this osteotomy is to translate the pull of the gastrocsoleus muscle via the Achilles tendon more medial to the axis of the subtalar joint, which enhances the varus force on the hindfoot. Another indirect, beneficial effect therefore is to decrease tension on the reconstructed posterior tibialis tendon. The medial displacement also may at least partially reestablish the height of the medial longitudinal arch.

The osteotomy is a straight cut from the lateral hindfoot at an angle of approximately 45 degrees to the plantar surface of the heel roughly equidistant between the posterior facet of the subtalar joint and the posterior plantar edge of the calcaneal body, thereby avoiding the insertion of the Achilles tendon and the plantar fascia origin. [0110] [0190] [0230] [0240] A slightly curved incision is made, and great care is taken to protect the sural nerve in the lateral approach to the calcaneal wall ( Fig. 8-12, A ). A power saw can be used until the surgeon approaches the medial calcaneal wall, but an osteotome is recommended to complete the osteotomy medially to prevent injury to the neurovascular bundle ( Fig. 8-12, B and C ). A medial shift of approximately 10mm is recommended. [0110] [0190] [0230] [0240]Provisional fixation is achieved with two percutaneous pins in the sinus tarsi area until definitive internal fixation is placed ( Fig. 8-12, D ). A partially threaded cannulated cancellous screw via a separate plantar posterior heel incision can be used for internal fixation. The proper placement of this screw should be guided fluoroscopically to avoid penetration of the subtalar joint and medial or lateral calcaneal wall. Countersinking the screw head is advised to prevent symptomatic hardware.




 

Figure 8-12  Medial shift calcaneal osteotomy. (A) Recommended location of lateral incision. (B) Power saw used initially for osteotomy. Multiple retractors are recommended to protect the surrounding soft tissues. (C) Osteotomy completed through the medial calcaneal wall using an osteotome to minimize any potential damage to the neurovascular bundle. (D) Temporary percutaneous smooth pin internal fixation until definitive internal fixation is placed.

 

 

Recently I have been using two dynamic compression nitinol step staples for definitive internal fixation ( Fig. 8-13, A through C ). This eliminates the need for a second incision associated with the screw placement, is technically less challenging and time consuming, and decreases the likelihood of symptomatic hardware. Also, there is potentially less fluoroscopic radiation exposure because usually only intraoperative radiographic demonstration of the final proper staple position in the axial heel and lateral planes is necessary, versus perhaps multiple fluoroscopic guidance images that may be required for screw placement.

 

 

Figure 8-13  Intraoperative photograph (A) and lateral (B) and axial (C) heel views demonstrating nitinol step staple internal fixation of the medial shift calcaneal osteotomy of approximately 10mm for patients with primarily stage II and III posterior tibialis tendon dysfunction.

 

 

If, after the reconstruction of the posterior tibialis tendon, the foot cannot be passively dorsiflexed to at least 10 degrees with the knee fully extended, then a percutaneous Achilles tendon lengthening or gastrocnemius recession is indicated.[22] This procedure serves to diminish the stress on the reconstruction and may help to prevent recurrent rupture and deformity postoperatively.

Postoperatively, casting is advised for 6 weeks, initially with the foot in plantarflexion and inversion for the first 2 weeks. The foot is brought to a neutral position gradually by the end of the fourth week, when partial weight bearing is permitted. If a medial shift calcaneal osteotomy is performed, then serial axial and lateral x-rays of the heel are taken to monitor healing. Following casting, rigid bracing with an arch support is recommended for 6 weeks, with progression to full weight bearing as tolerated. The patient may remove the brace for bathing, sleeping, and active ankle range of motion exercises. Supportive shoewear with a custom-made arch support is worn until 6 months postoperatively. Return to repetitive impact-loading sports or conditioning is ill advised before 6 months postoperatively.

Stage III—Tendon Elongated, Flexible or Rigid Moderate to Severe Deformity

Stage III presentation is rare, especially in the younger athlete. Intraoperative pathologic findings often eclipse those of stage II, and the tendon is grossly incompetent even if still intact or may be completely ruptured with retraction of the proximal end of the tendon in the distal medial leg. Surgical repair or reconstruction of the tendon as described in stage II disease may not be necessary when a bony stabilization procedure (fusion or opening wedge osteotomy) is performed in stage III disease. A soft-tissue reconstruction alone, even with a medial shift calcaneal osteotomy, probably will not prevent recurrent deformity and associated symptoms, especially in the heavier patient.

If the deformity, although moderate to severe, is still flexible and there are no significant degenerative arthritic changes, then the surgeon may consider a medial shift calcaneal osteotomy combined with a lateral column lengthening, with either a calcaneocuboid joint distraction arthrodesis or anterior calcaneal opening wedge with bone graft proximal to the calcaneocuboid joint. [0200] [0220] However, a calcaneocuboid distraction arthrodesis usually will limit hindfoot motion significantly and unduly stress the articulations of the synchronous function of the talonavicular and subtalar joints, possibly leading to early degenerative arthritis, which may be the result of diminution of circulating synovial fluid delivery of nutrition to the cartilage of these unfused, but now stiffer, joints. Theoretically, an anterior calcaneal opening wedge osteotomy may have an advantage in preserving more motion and thus preventing long-term arthritic disease.[22] An opening wedge plantarflexion osteotomy with bone graft of the dorsal medial cuneiform also has been described[20] to further correct residual forefoot varus deformity with restoration of a more balanced, “tripod,” weight-bearing foot. These procedures are technically challenging, and overcorrection can be a problem. Also, if autogenous iliac tricortical bone graft is chosen, the surgeon must consider the associated morbidity. Finally, as with any distraction arthrodesis or opening wedge osteotomy, the delayed or nonunion rates may be significantly higher.[22] Rigid internal fixation may lessen this complication.

However, if degenerative arthritis also is an issue, then an arthrodesis is indicated. There are many proponents of an arthrodesis of the subtalar [0050] [0200] [0250] or talonavicular joint alone, calcaneocuboid and talonavicular joint arthrodesis (double arthrodesis),[9] or triple arthrodesis.[26] Perhaps it may not make much difference which type of arthrodesis is chosen, because, again, the fusion of even one of these joints severely limits the motion of the other two, thus maintaining the desired correction. However, long-term pain and eventual arthritis may develop because of the limited motion in the remaining unfused joints for the same reason as an isolated calcaneocuboid distraction arthrodesis as previously described. A triple arthrodesis with deformity correction would, of course, prevent this, but over time may lead to usually valgus ankle instability and arthritis. [0110] [0220] This is the result of long-term attenuation of the deltoid ligament usually resulting from undercorrection of hindfoot valgus that is rigid and therefore incapable of inversion/eversion torque conversion, thus translating those forces to the medial ankle. On rare occasions, especially if the hindfoot is overcorrected to varus, or in the preexisting cavovarus foot that is undercorrected, just the opposite can occur, with lateral talar tilt, instability, and arthritis.

Converse to the argument against a limited versus triple arthrodesis, a case can be made, especially in the younger patient, for selected arthrodesis of one of the joints of the triple joint complex if the deformity is severe but still flexible, because limitation of motion in the other unfused joints, even if they are somewhat cartilage deficient, may prevent arthritic symptoms from developing. Based on that rationale, I prefer an isolated talonavicular joint arthrodesis with bone graft and believe that it better corrects the abduction/pronation deformity and may indirectly correct a flexible hindfoot valgus deformity. Others feel that the subtalar joint, [0040] [0050] [0240] and not the talonavicular, is the “keystone” to correction of the deformity. Rather than proceeding with a subtalar or triple arthrodesis, I feel that if hindfoot valgus still is an issue intraoperatively after a talonavicular joint arthrodesis, then a medial shift calcaneal osteotomy can be added.

As with stage II cases, and regardless of the chosen arthrodesis or osteotomy for stage III disease, a percutaneous Achilles tendon lengthening or gastrocnemius resection[22] is further indicated if the foot cannot be passively dorsiflexed beyond 10 degrees with the knee fully extended.

Postoperatively, cast immobilization generally is in the 9- to 12-week range, depending on the progress of healing of the osteotomy or arthrodesis. Some limited weight bearing usually is allowed at 6 weeks postoperatively, depending on the level of healing on serial x-rays. Rigid bracing after casting is advised for 6 to 12 weeks. Supportive shoes with custom-molded arch supports may not be necessary, especially if a fusion is performed. Return to athletic activity is allowed 9 to 12 months postoperatively.

 

Perils and Pitfalls (with Illustrative Case Reports)

Lack of recognition or misdiagnosis of posterior tibialis tendon injury in the athlete can be avoided with a conscientious history, physical examination, and weight-bearing x-rays. The differential diagnostic possibilities (see Table 8-1 ) also should be kept in mind when encountering the athlete with a suspected posterior tibialis tendon injury to prevent the perils and pitfalls of misdiagnosis and to aid selection of the proper treatment. If the presenting patient's diagnosis then is still in question, then an MRI is recommended. However, even the most astute diagnostician can fail to determine the proper diagnosis.

Case Study 1  

One dilemma of determining the correct diagnosis and treatment is especially evident in the patient who may have preexisting bilateral pes planus, because unilaterality of the traumatically acquired pes plano valgus deformity with a positive “too many toes” sign may not be a conclusive physical finding. Also, in the patient who has a more chronic presentation, swelling and tenderness may not be impressive. Furthermore, because of the abnormal biomechanics in the patient with bilateral pes planus, the single-foot heel-rise test (or lack of hindfoot inversion if the patient is successful in heel rise) may be positive in both feet.

I recently encountered such a case in a 58-year-old healthy man who had been an active runner until he began experiencing medial right ankle and midfoot pain and swelling 1 year before presentation. Conservative treatment by the referring physician had included cessation of running and impact-loading exercise, immobilization for 6 weeks, nonsteroidal anti-inflammatory medication, physical therapy, and the use of bilateral, custom-molded, soft, longitudinal arch supports with medial posting for the involved foot in supportive shoes.

Physical examination revealed mild tenderness and a modicum of swelling in the area of the terminal course of the posterior tibialis tendon. The “too many toes” sign was inconclusive, and he was able to perform the single-foot heel-rise test bilaterally, although neither hindfoot inverted. Bilateral flexible pes planus was noted. There was no clinical evidence of subfibular or sinus tarsi impingement. The Achilles tendon was not contracted with passive dorsiflexion of the foot to 20 degrees.

Weight-bearing x-rays of the involved foot were essentially unremarkable, save for pes planus. There was no evidence of an accessory navicular, tarsal coalition, or triple joint degenerative arthritis. A recent MRI suggested an interstitial rupture with tendinosis of the posterior tibialis tendon and excess fluid around it but otherwise was unremarkable.

Given the chronicity of the patient's symptoms and failed response to conservative treatment, he was scheduled for surgical reconstruction for severe stage I or early stage II disease.

Intraoperatively, there was indeed mild attenuation and incompetency of the posterior tibialis tendon with a small longitudinal interstitial rupture and tenosynovitis. Also, the plantar medial capsule of the talonavicular joint was completely ruptured ( Fig. 8-14, A and B ). This pathology had not been detected in the preoperative MRI. In addition to repair and imbrication of the capsular tear, the posterior tibialis tendon was repaired and advanced, and a medial shift calcaneal osteotomy was performed. After 6 weeks of casting and 6 weeks of bracing postoperatively, the patient was fitted with bilateral, custom-molded, soft, longitudinal arch supports, especially in his running shoes, and returned to running at 6 months.

This case points out that other traumatic pathology may mimic (see Table 8-1 ) and other conditions (e.g., pes planus) may contribute to posterior tibialis tendon insufficiency. More specifically, the examiner and surgeon should consider diagnostically and surgically repair a ruptured plantar medial talonavicular joint capsule.

 
 

Figure 8-14  Intraoperative photograph (A) and schematic drawing (B) of complete rupture of the plantar medial talonavicular joint capsule as seen in Case 1. The hyperemic interstitially torn posterior tibialis tendon is retracted inferiorly.

 

 

Case Study 2  

Another case serves to illustrate the importance of the differential diagnosis (see Table 8-1 ).

A 17-year-old presented with a several-month history of pain, swelling, and stiffness of the left foot after a twisting eversion injury was incurred while he was playing soccer. As reported by his mother, the patient also had recently experienced a “growth spurt” several months before the injury. Before referral to my office, conservative treatment had been rendered by his pediatrician that included bracing, over-the-counter nonsteroidal anti-inflammatory medication, physical therapy, and “arch supports.” A report of x-rays of the left foot taken recently was described as “normal.”

Physical examination revealed normal ankle range of motion but a rigid pes plano valgus deformity with peroneal muscle spasm. The uninjured right foot was flexible, with a normal range of hindfoot motion. Tenderness and swelling was appreciated along the terminal course of the posterior tibialis tendon. The “too many toes” sign was positive and the hindfoot failed to invert in the left-foot single-foot heel-rise test.

Save for the rigidity of the hindfoot, the physical findings and perhaps much of the history would have suggested that the patient had sustained a posterior tibialis tendon injury with dysfunction. However, x-rays taken in my office clearly were not “normal” and demonstrated a skeletally mature left foot with an obvious bony calcaneonavicular tarsal coalition and significant degenerative arthritis of the triple joint complex ( Fig. 8-15 ).

Given the severe rigidity of the hindfoot, pes planus deformity, triple joint degenerative arthritis, and failure of conservative treatment, the patient underwent a triple arthrodesis with corrective joint osteotomies. It was felt that a resection of the mature bony coalition, given the degree of the deformity and arthritic changes of the triple joint complex, would not have resulted in a successful outcome. One year postoperative from the triple arthrodesis, the patient was asymptomatic and had returned to some limited, repetitive, impact-loading sports.

 
 

Figure 8-15  Bony calcaneonavicular tarsal coalition in Case 2.

 

 

Case Study 3  

The final case further emphasizes the differential diagnosis and potential diagnostic pitfalls of posterior tibialis tendon injury and dysfunction.

A 16-year-old patient presented to my office with the recent history of an eversion injury of the right foot when she twisted it running to first base while playing softball. There were no prodromal symptoms before the injury. She complained of swelling and pain along the distal medial navicular insertional area of the posterior tibialis tendon.

Physical examination confirmed tenderness, swelling, and ecchymosis in the anatomic area of her symptoms as described. The “too many toes” sign was negative, but she complained of pain in the plantar medial midfoot with the single-foot heel-rise test, although the injured side hindfoot inverted normally when compared with the uninjured foot.

X-rays demonstrated a medial navicular avulsion-type fracture versus a small, nonunited accessory navicular with presumed synchondrosis disruption ( Fig. 8-16 ).

Comparison x-rays of the other foot also revealed a similar small, nonunited accessory navicular, thus suggesting the latter diagnosis. (Serial x-rays during the treatment period did not reveal bony healing of the possible avulsion fracture to the main body of the navicular, thus again suggesting that this was a synchondrosis disruption of a nonunited accessory navicular and not a fracture.)

Treatment consisted of immobilization and a well-molded, short-leg, nonweight-bearing cast for 3 weeks, followed by rigid bracing with an arch support with progressive weight bearing as tolerated for another 3 weeks. She returned to sports, asymptomatic, 3 months postinjury.

This case also demonstrates the importance of comparison x-rays in determining the correct diagnosis and thus the appropriate treatment.

 
 

Figure 8-16  Coned down and magnified view of nonunited accessory navicular with presumed synchondrosis disruption in Case 3.

 

 

 

Summary

Again, although rare, the acute rupture or dysfunction of the posterior tibialis tendon in the athlete demands timely diagnostic recognition and proper treatment. Conservative treatment is recommended initially, especially in the patient without deformity (stage I). Surgical treatment is advised if conservative treatment fails in any stage, but especially if there is significant deformity (stage II and III). Prompt treatment, whether conservative or surgical, may prevent the development of primarily triple joint or even ankle degenerative arthritis and resultant need for an arthrodesis, which may spell the end of an athlete's participation in repetitive, impact-loading conditioning and sports.

 

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