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Surgical Techniques for Repair of Atraumatic Tibialis Anterior Tendon Ruptures: A Report of Two Cases
The Journal of Foot & Ankle Surgery 56 (2017) 1343–1349
Contents lists available at ScienceDirect
The Journal of Foot & Ankle Surgery journal homepage: www.jfas.org
Surgical Techniques for Repair of Atraumatic Tibialis Anterior Tendon Ruptures: A Report of Two Cases Romy Patel, DPM 1, Lawrence Fallat, DPM, FACFAS 2 1 2
Second-Year Resident, Podiatric Surgical Residency, Beaumont Hospital Wayne, Podiatric Surgery, Wayne, MI Director, Podiatric Surgical Residency, Beaumont Hospital Wayne, Podiatric Surgery, Wayne, MI
a r t i c l e i n f o
a b s t r a c t
Level of Clinical Evidence: 4
Tendon ruptures of the foot and ankle are overwhelmingly due to direct or blunt force trauma; however, spontaneous tendon ruptures have been less commonly documented in the published data. Surgical techniques for the repair of atraumatic ruptures differ from those for acute traumatic ruptures owing to the delayed patient presentation. Spontaneous tendon ruptures usually result from predisposing factors that have compromised the structural integrity of the tendon before the rupture occurs. We present 2 cases of atraumatic rupture of the tibialis anterior tendon, each repaired using a different surgical technique. A unique surgical procedure was selected after preoperative planning and individual patient considerations. Each patient had a minimum follow-up period of 12 months after surgery. Both patients returned to their previous functional status with no long-term sequela. Ó 2017 by the American College of Foot and Ankle Surgeons. All rights reserved.
Keywords: spontaneous tendon injury tendon reconstruction tendon rupture tibialis anterior
Ruptures of the tibialis anterior tendon (TAT) are quite rare, accounting for only 10 of 1014 foot and ankle tendon ruptures, as reported by Anzel et al (1). Most commonly, they are noted in males aged 50 to 70 years (2). Injuries to the TAT can occur from both traumatic and atraumatic mechanisms. Traumatic mechanisms usually involve direct injury such as an acute laceration or blunt trauma. These types of ruptures have frequently been reported. Spontaneous nontraumatic ruptures of the TAT have been sparingly reported, with the published data limited mostly to isolated cases. Often, spontaneous ruptures occur with concomitant factors that predispose the tendon to failure. These factors include diabetes mellitus, inflammatory arthropathy, a history of steroid injections, or the use of fluoroquinolones (3). A history of diabetes with poor glycemic control has also been associated with increased tendon glycation. The end products of tendon glycosylation contribute to changes in collagen crosslinking within the tendon, which increases the risk of spontaneous rupture from tendon contracture and rigidity. Patients with diabetic-induced neuropathy are also known to have an increased risk of rupture of the flexor tendons (4). Gout and other inflammatory arthropathies have been documented as a potential cause of a spontaneous TAT rupture. Patten and Pun (2) and Jerome et al (5) reported histologic findings of chalky
Financial Disclosure: None reported. Conflict of Interest: Lawrence Fallat reports a consultancy with Depuy-Synthes. Address correspondence to: Lawrence Fallat, DPM, FACFAS, Podiatric Surgery Residency, Beaumont Hospital Wayne, 20555 Ecourse Road, Taylor, MI 48180. E-mail address: [email protected] (L. Fallat).
white deposits within the substance of a ruptured TAT. When examined microscopically, gouty tophi were noted to have displaced the normal fibers of the tendon. The deposition of the uric acid crystals had completely compromised the structural integrity of the TAT tendon. Polarized light microscopy revealed pathognomonic findings of negatively birefringence needle-shaped crystals. Localized steroid injections in the area of tendon insertion or along its course increase the risk of tendon rupture. The steroid causes tenocyte death, which reduces the tensile strength of the tendon. The most commonly documented cause of local steroid-associated TAT rupture is injections into the first tarsometatarsal joint (6). The mechanism of failure for spontaneous rupture is an eccentric load of a degenerated, weakened TAT against a plantarflexed ankle (2). Although injury from blunt trauma and laceration is easily diagnosed, spontaneous rupture of the TAT is often associated with vague symptoms, such as mild pain, that subside shortly after the initial injury (7). After rupture of the TAT, the long extensors are recruited to assist in dorsiflexion (8), and this, along with no clear traumatic event, makes it difficult for patients to notice any acute pathologic features after injury. Often, the vague symptoms can lead to the patient presenting past the acute stage of the tendon rupture. It is important to carefully evaluate the extremity and make an accurate diagnosis. On visual examination, a pseudocyst will commonly be noted along the anterior aspect of the ankle (i.e., the distal aspect of the ruptured tendon after it has retracted along its sheath). Extensor substitution can be seen when the patient attempts to dorsiflex the ankle. A marked weakness in dorsiflexion at the ankle joint on manual muscle testing is usually
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noted compared with the contralateral limb. Pain is not a reliable marker in the subacute stage of the injury owing to the slow resolution of the symptoms as time passes. On gait examination, the patient will be seen to have a mild “foot slap,” and firing of the long extensors will be seen during the swing phase to help compensate for the loss of dorsiflexion. The common differential diagnoses for a TAT rupture include a common peroneal nerve lesion causing foot drop or L5 radiculopathy. A combination of imagining modalities and a careful physical examination will easily lead to the exclusion of these causes in a spontaneous TAT rupture. The medical imaging findings can provide a quick and accurate confirmation of the diagnosis once a thorough physical examination has been performed. Although ultrasonography can be used, magnetic resonance imaging (MRI) is considered the reference standard because of its diagnostic ability to evaluate the TAT and the anatomic structures surrounding it (9). The TAT is the primary dorsiflexor of the foot (10). During the swing phase of gait, contraction of the TAT prevents stumbling or tripping by clearing the foot over the ground. In the contact phase at heel strike, it aids in balancing plantarflexion of the foot by eccentric contraction and preventing foot slap (2). A prompt diagnosis and appropriate treatment of a rupture can prevent long-term sequela such as lost dorsiflexion, which can result in drop foot and Achilles tendon contracture (11). Drop foot alters the normal gait and can lead to abnormal ambulation and increase the risk of future injury. The most common anatomic area of rupture correlates directly with the zone of hypovascularity within the TAT. The vascularity of the tendon is nonhomogeneous, with the anterior half avascular between the superior and inferior extensor retinaculum. This area measures 45 to 67 mm long (12). Appropriate management of these injuries will differs according to each patient’s case. Markarian et al (8) found no significant differences in the outcomes between operative and nonoperative treatment of patients with a TAT rupture. However, in their study, the average age of the operative group was 19 years younger than that of the nonoperative group. Also, a predominance of acute ruptures was present in the operative group. Operative treatment of a TAT rupture for young and active patients for both acute traumatic and subacute spontaneous ruptures remains favored for long-term functionality (13). The mechanism and acuity of the injury are important factors to consider in preoperative planning. A direct surgical approach with end-to-end repair of the tendon with nonabsorbable suture is common for acute traumatic injuries. Alternatively, if the distal portion of the ruptured tendon is nonviable, the tendon can be directly attached to the proximal aspect of the medial cuneiform using a screw and washer, pull-out wire, interference screws, or suture anchors (14). Chronic injuries that present >1 month after injury require more complex surgical management. Often, end-to-end repair of the tendon will no longer be possible because the tendon has retracted proximally along its sheath. Numerous techniques can be used to overcome the deficit left by tendon retraction and to aid in the overall strength of the tendon, including slide lengthening, tendon turndown, interposition or tendon grafting, and augmentation (13,15,16).
was used for hemostasis. The patients underwent the procedure under general anesthesia. Cefazolin 2 g intravenously was administered for surgical prophylaxis. Postoperatively, both patients were placed in a well-padded below-the-knee fiberglass cast, with the foot positioned at 90 . They were instructed to be non-weightbearing on the surgical extremity. Crutches were used for ambulation. Oral deep vein thrombosis prophylaxis and pain medication was prescribed for both patients. Patient 1 The first patient was a 50-year-old female with a medical history of type 2 diabetes and social history of smoking. Her diabetes was rather poorly controlled. Her medications included glipizide (Glucotrol) 10 mg, metformin 1000 mg, and sitagliptin (Januvia) 100 mg. Her hemoglobin A1c was 8.3, with a mean plasma glucose of 216 mg/dL on the day of surgery. She presented to the clinic with a chief complaint of mild pain and weakness along the anteromedial aspect of the right ankle. The patient stated that she remembered the pain beginning about 8 weeks before her presentation to our clinic. She stated that she had “felt a pop,” followed by instant severe pain to the anterior aspect of the right ankle while getting out of bed 1 night. Soon after, the pain had subsided, but the weakness in her ankle remained. On examination in our clinic, we noted a distinct weakness in dorsiflexion of the right ankle. Absence of contracture of the TAT when dorsiflexing was also noted (Fig. 1). During the gait examination, her toes dragged on the ground, and a mild foot slap was noted. An MRI scan was obtained to confirm the working diagnosis of a TAT rupture. The MRI study showed complete rupture of the TAT, with a deficit of 7.8 cm between the proximal and distal stumps (Fig. 2). The large deficit had resulted from the subacute nature of the presentation of the patient, which had allowed the ruptured tendon to retract
Case Reports We present 2 cases, each outlining an atraumatic, spontaneous rupture of the TAT and the appropriate treatment method, with a focus on technique. A different surgical technique was used to repair the tendon in each case. To the best of our knowledge, the combination of differing acuity, method of injury, and surgical technique is unique. Both patients in our reported cases were placed in the supine position on the operating table. A thigh tourniquet set at 325 mm Hg
Fig. 1. View of right foot of patient 1 showing significant loss of dorsiflexion at the ankle joint with hyperextension of the hallux. Note the absence of contracture along the course of the tibialis anterior tendon on the right foot.
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Fig. 2. Magnetic resonance image showing a full-thickness superiorly retracted tear of the tibialis anterior tendon. The torn tendon stump had retracted approximately 7.8 cm and was 2.3 cm superior to the tibiotalar joint.
proximally along its sheath. Pronounced unilateral equinus on the injured side was also noted at the physical examination, which could be attributed to a muscle imbalance created owing to the period from injury to presentation. Given the patient’s functional status and relatively young age, surgical repair of the deformity was warranted. Owing to the large defect and chronicity of the injury, a graft (autograft or allograft) was though likely to be necessary to bridge the deficit created by tendon retraction. An 18-cm-long linear incision was made over the anteromedial aspect of the right foot and ankle, just medial to the TAT. After superficial dissection was completed, the tendon sheath to the TAT was identified and opened. The TAT had retracted significantly, as suggested by the MRI findings (Fig. 3). Owing to the severe tendon retraction, the extensor hallucis longus (EHL) tendon was used to augment the deficit. A small incision was made at the distal aspect of the right hallux at the level of the interphalangeal joint. The EHL and extensor hallucis brevis tendons were identified and sutured together (Fig. 4). The EHL tendon was sectioned just proximal to the tenodesis site. A tendon harvesting instrument was used to release the EHL tendon from its sheath to the level above the ankle joint. Using a tendon stripper, the EHL tendon was slid out of its sheath proximally and sutured to the proximal portion of the TAT using 2-0 braided nonabsorbable polyester suture (Fig. 5). No residual portion of tendon was seen when inspecting the insertion site of the TAT. Thus, a 3.2-mm drill bit was used to create a hole in the medial cuneiform, extending from dorsally to plantarly, where the TAT had attached previously (Fig. 6). The EHL tendon was then inserted through the drill hole and appropriately tensioned before being sutured onto itself with 2-0 braided nonabsorbable polyester suture (Fig. 7). A Strayer type gastrocnemius recession was also performed to correct the gastrocnemius equinus deformity. Before closure, all surgical wounds were irrigated. The tendon sheath and extensor retinaculum were repaired using 3-0 synthetic absorbable suture; 4-0 synthetic absorbable suture was used for subcutaneous closure and 3-0 nylon suture for skin closure.
Fig. 3. Retracted stump of tibialis anterior tendon.
Postoperatively, the patient was placed in a well-padded belowthe-knee fiberglass cast with the foot positioned at 90 . The patient was instructed to be non-weightbearing on the surgical extremity.
Fig. 4. Extensor hallucis longus and extensor hallucis brevis tendons were isolated and tenodesis performed before transection of the extensor hallucis longus tendon in preparation for harvesting.
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Fig. 7. View of completed repair with extensor hallucis longus graft seen spanning the original defect and proximally anchored to the tibialis anterior tendon stump and distally through the medial cuneiform. Fig. 5. Harvesting of the extensor hallucis longus tendon using a tendon stripper.
Crutches were used for ambulation. Apixaban 2.5 mg twice daily was given for 21 days for deep vein thrombosis prophylaxis and ibuprofen 800 mg for pain control. The patient was seen in our clinic every 2 weeks until all surgical wounds had healed. The patient developed a superficial localized infection to the surgical site, which was treated successfully with local wound care and a 10-day course of cephalexin after a culture of the wound grew Staphylococcus aureus. The patient was transitioned to partial weightbearing in a controlled ankle motion walker at 6 weeks
Fig. 6. Drill hole in medial cuneiform through which the extensor hallucis longus graft will pass.
postoperatively. A 1-month long course of physical therapy was prescribed for the patient to regain dorsiflexion strength to the ankle joint. Within 4 months postoperatively, the patient had no complaints and had a manual muscle testing result of 4 of 5 for the right ankle with dorsiflexion (Fig. 8). The patient was able to return to wearing normal shoe gear and her normal activities. The patient was followed up for 1 year and also followed up for diabetic foot care. Patient 2 Our second patient was a 71-year-old male with a significant history of previous ankle pain. The patient presented to clinic after noticing mild pain to the anterior aspect of his left foot and ankle. He was unable to recall a specific event but stated that the pain had been present for a few months. He reported that the pain had progressively increased with time. He rated his pain at 4 of 10 at presentation. The physical examination revealed mild swelling to the left anterior ankle along, with a subcutaneous prominence along the usual course of the TAT. A pronounced equinus deformity was noted on the injured side. The extensor complex could be seen firing for active dorsiflexion of the left foot. Pain along the course of the TAT was noted, along with a distinct absence of TAT tenting. With ambulation, he had a mild foot slap gait with the injured limb. The tentative diagnosis was of a TAT rupture, MRI confirmed the diagnosis (Fig. 9). Preoperative planning was performed, and because the patient did not recall how old the injury was, we anticipated that a graft would be necessary to bridge the defect. A 14-cm-long incision was made over the course of the TAT and extending to its insertion site. The incision was then deepened to the level of the extensor retinaculum, with care taken to identify and retract all vital neurovascular structures out of the way until the extensor retinaculum was identified. The TAT stump was identified, freed up proximally for approximately 4 cm using blunt dissection,
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Fig. 8. View at 5 months postoperatively showing (A) plantarflexion and (B) dorsiflexion.
and the fibrotic stump of the tendon was debrided (Fig. 10). When applying tension to the stump of the TAT, it was evident that the tendon itself would no longer be able to be attached to its insertion site without a graft. Preoperative planning had included a review of the patient’s MRI scan, on which the plantaris tendon had been visualized. The plantaris tendon was deemed appropriate to use as an autograft to bridge the gap, which was approximately 6 cm. The plantaris tendon was chosen owing to its minimal effect on normal function. A 2-cm incision was made at the posteromedial aspect of the Achilles tendon. Adequate dissection was performed, and the plantaris tendon was identified. A tendon stripper was then inserted proximally about 12 cm along the tendon to strip any soft tissue attachments (Fig. 11). Another 2-cm-long incision was made at the proximal aspect of the tendon stripper at the level of the mid-calf. After dissecting down to the plantaris tendon, the tendon was cut
and sutured to the gastrocnemius. This allowed approximately 12 cm of the plantaris tendon to be harvested. The plantaris tendon was then doubled on itself and reinforced using a whip stitch (Fig. 12). A 4.0-mm drill bit was drilled into the medial cuneiform, and a 4.75-mm interference screw was inserted with the harvested plantaris into the medial cuneiform (Fig. 13). The distal stump of the TAT was debrided of all unhealthy tissue, and the proximal end of the plantaris graft was attached to the distal end of the TAT with 2-0 braided nonabsorbable polyester suture after appropriate tensioning of the tendon with the foot slightly dorsiflexed while suturing the 2 ends together. Because of the equinus deformity after the TAT repair, gastrocnemius recession was deemed necessary. An approximately 3-cm incision was made at the distal one third of the leg, and the gastrocnemius was released with a Strayer type recession. The wounds were then flushed with copious amounts of antibiotic solution. The extensor retinaculum was reapproximated with 3-0 synthetic absorbable suture. Subcutaneous closure was completed with 4-0 synthetic absorbable suture, and 3-0 nylon suture was used for skin closure. The patient was seen in our clinic every 2 weeks postoperatively visits and healed uneventfully. He made a full recovery to his previous functional level within 5 months without the need for any physical therapy. His final manual muscle strength was rated at 4 of 5 in dorsiflexion. The final range of motion was 10 of dorsiflexion and 20 of plantarflexion. The patient was followed up for 17 months.
Fig. 9. Magnetic resonance image showing rupture and retraction of tibialis anterior tendon in patient 2.
Fig. 10. Dissection and exposure of tibialis anterior tendon. Note, distal aspect of tendon requires debridement of avascular and fibrotic tissue.
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Fig. 13. Intraoperative view showing fixation of distal stump of graft to insertion site of tibialis anterior tendon. Fig. 11. Harvesting of the plantaris tendon using a tendon stripper.
Discussion Atraumatic TAT ruptures are an infrequent clinical encounter. Detailed physical examination and accurate and early diagnosis are key factors to reducing long-term morbidity. Often, this is difficult because the patients experience vague symptoms and lack a focal defect owing to the compensatory aid of the extensor complex. Markarian et al (8) noted an average delay of 71 days from the initial symptoms to the final diagnosis of a rupture. Previously, it was preferred that patients with a delayed presentation or diagnosis of a TAT rupture be treated conservatively with bracing and activity modification. However, recent data have shown that good outcomes are possible with delayed surgical intervention, even with delayed presentation of the patient (8,17). The patient’s age and functional status are important factors when determining the appropriate treatment options. Conservative treatment should be reserved for patients with minimal ambulatory status and for patients for whom the risk of surgery outweighs the potential benefits. The common conservative treatment options include bracing, splinting, and activity modification. Surgical treatment is preferred for younger patients and patients who require a certain level of functional for their everyday activities.
Fig. 12. Plantaris tendon graft tagged and ready to use to bridge defect.
Surgical treatment was indicated for both patients included in our study. Atraumatic ruptures of the TAT have been confined mostly to case reports or series owing to the uncommon nature of the injury. Numerous surgical techniques have been described in the published data, with good outcomes using those techniques. However, no consensus has been reached regarding which procedure should be used in any given situation. A small treatment algorithm for surgical intervention has been reported, stating that deficits of 4 cm can be successfully treated with a turndown procedure or tendon slide lengthening (18). In patient 1, not only was the patient relatively young and active, but she also had a history of diabetes. Although our patient did not have significant neuropathy, pursuing a surgical option in patients with diabetes is important to decrease the long-term morbidity and restore normal gait function and plantar pressures to prevent ulceration. In her case, a tendon transfer augmentation procedure was chosen. This was determined after consideration of the large 7.8-cm deficit . With a history of diabetes, we sought to give the patient the strongest complex possible to allow for low long-term morbidity. The EHL tendon was chosen as the donor site for multiple reasons. The anatomic location of the tendon aids in dissection, and the size of the EHL tendon provides a strong construct without the need to fold the tendon onto itself to achieve the desired width. Finally, the functional loss of the donor site could be minimized and the full function of the hallux retained by tenodesis of the EHL to the extensor hallucis brevis tendon. In patient 2, surgical treatment was deemed necessary owing to the patient’s functional level. Although the patient was 71 years old, he complained of a foot slap when ambulating. This had limited his activities, and conservative treatment was not the best option for long-term ambulation. The patient’s symptoms had been present for months, indicating that a graft might be necessary to bridge the deficit that is often present in chronic ruptures. A plantaris autograft was chosen for this particular patient to minimize donor site morbidity and provide enough graft material for successful repair. Both cases in our study differed in the presentation and functional needs of the patients. No clear consensus or treatment algorithm for all TAT ruptures exists. Our case series has demonstrated that consideration of multiple factors, such as the acuity of the injury, the size of the deficit, and the functional needs of the patient, can result in successful outcomes with multiple techniques when used appropriately.
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In conclusion, the purpose of our case series was to offer insight into the sometimes subtle nature of the clinical presentation after a TAT rupture, information for a quick and accurate diagnosis using the physical examination and imaging studies, and possible surgical techniques for successful outcomes. References 1. Anzel SH, Covey KW, Weiner AD, Lipscomb PR. Disruption of muscles and tendons: an analysis of 1,014 cases. J Foot Ankle Surg 45:406–414, 1959. 2. Patten A, Pun WK. Spontaneous rupture of the tibialis anterior tendon: a case report and literature review. Foot Ankle Int 21:697–700, 2000. 3. DiDomenico LA, Williams K, Petrolla AF. Spontaneous rupture of the anterior tibial tendon in a diabetic patient: results of operative treatment. J Foot Ankle Surg 47:463–467, 2008. 4. Ramirez LC, Raskin P. Diabetic foot tendinopathy: abnormalities in the flexor plantar tendons in patients with diabetes mellitus. J Diabetes Complications 12:337–339, 1998. 5. Jerome JT, Varghese M, Sankaran B, Thomas S, Thirumagal SK. Tibialis anterior tendon rupture in gout–case report and literature review. Foot Ankle Surg 14:166– 169, 2008. 6. Jain K, Asad M, Joshi Y, Syed A. Tibialis anterior tendon rupture as a complication of first tarsometatarsal joint steroid injection: a case report and review of literature. Foot (Edinb) 3:179–181, 2015. 7. Bernstein RM. Spontaneous rupture of the tibialis anterior tendon. Am J Orthop (Belle Mead NJ) 24:354–356, 1995.
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8. Markarian GG, Kelikian AS, Brage M, Trainor T, Dias L. Anterior tibialis tendon ruptures: an outcome analysis of operative versus nonoperative treatment. Foot Ankle Int 19:792–802, 1998. 9. Lee MH, Chung CB, Cho JH, Mohana-Borges AV, Pretterklieber ML, Trudell DJ, Resnick D. Tibialis anterior tendon and extensor retinaculum: imaging in cadavers and patients with tendon tear. AJR Am J Roentgenol 187:W161–W168, 2006. 10. Scheller AD, Kasser JR, Quigley TB. Tendon injuries about the ankle. Orthop Clin North Am 11:801–811, 1980. 11. Cohen DA, Gordon DH. The long-term effects of an untreated tibialis anterior tendon rupture. J Am Podiatr Med Assoc 89:149–152, 1999. 12. Petersen W, Stein V, Tillmann B. Blood supply of the tibialis anterior tendon. Arch Orthop Trauma Surg 119:371–375, 1999. 13. Ellington JK, McCormick J, Marion C, Cohen BE, Anderson RB, Davis WH, Jones CP. Surgical outcome following tibialis anterior tendon repair. Foot Ankle Int 31:412– 417, 2010. 14. Negrine JP. Tibialis anterior rupture: acute and chronic. Foot Ankle Clin 12:569– 572, 2007. 15. Sapkas GS, Tzoutzopoulos A, Tsoukas FC, Triantafillopoulos IK. Spontaneous tibialis anterior tendon rupture: delayed repair with free-sliding tibialis anterior tendon graft. Am J Orthop (Belle Mead NJ) 37:E213–E216, 2008. 16. Sammarco VJ, Sammarco GJ, Henning C, Chaim S. Surgical repair of acute and chronic tibialis anterior tendon ruptures. J Bone Joint Surg Am 91:325–332, 2009. 17. Michels F, Van Der Bauwhede J, Oosterlinck D, Thomas S, Guillo S. Minimally invasive repair of the tibialis anterior tendon using a semitendinosus autograft. Foot Ankle Int 35:264–271, 2014. € rst OA, Kelm J. Rupture of the anterior tibial 18. Anagnostakos K, Bachelier F, Fu tendon: three clinical cases, anatomical study, and literature review. Foot Ankle Int 27:330–339, 2006.
Contents lists available at ScienceDirect
The Journal of Foot & Ankle Surgery journal homepage: www.jfas.org
Surgical Techniques for Repair of Atraumatic Tibialis Anterior Tendon Ruptures: A Report of Two Cases Romy Patel, DPM 1, Lawrence Fallat, DPM, FACFAS 2 1 2
Second-Year Resident, Podiatric Surgical Residency, Beaumont Hospital Wayne, Podiatric Surgery, Wayne, MI Director, Podiatric Surgical Residency, Beaumont Hospital Wayne, Podiatric Surgery, Wayne, MI
a r t i c l e i n f o
a b s t r a c t
Level of Clinical Evidence: 4
Tendon ruptures of the foot and ankle are overwhelmingly due to direct or blunt force trauma; however, spontaneous tendon ruptures have been less commonly documented in the published data. Surgical techniques for the repair of atraumatic ruptures differ from those for acute traumatic ruptures owing to the delayed patient presentation. Spontaneous tendon ruptures usually result from predisposing factors that have compromised the structural integrity of the tendon before the rupture occurs. We present 2 cases of atraumatic rupture of the tibialis anterior tendon, each repaired using a different surgical technique. A unique surgical procedure was selected after preoperative planning and individual patient considerations. Each patient had a minimum follow-up period of 12 months after surgery. Both patients returned to their previous functional status with no long-term sequela. Ó 2017 by the American College of Foot and Ankle Surgeons. All rights reserved.
Keywords: spontaneous tendon injury tendon reconstruction tendon rupture tibialis anterior
Ruptures of the tibialis anterior tendon (TAT) are quite rare, accounting for only 10 of 1014 foot and ankle tendon ruptures, as reported by Anzel et al (1). Most commonly, they are noted in males aged 50 to 70 years (2). Injuries to the TAT can occur from both traumatic and atraumatic mechanisms. Traumatic mechanisms usually involve direct injury such as an acute laceration or blunt trauma. These types of ruptures have frequently been reported. Spontaneous nontraumatic ruptures of the TAT have been sparingly reported, with the published data limited mostly to isolated cases. Often, spontaneous ruptures occur with concomitant factors that predispose the tendon to failure. These factors include diabetes mellitus, inflammatory arthropathy, a history of steroid injections, or the use of fluoroquinolones (3). A history of diabetes with poor glycemic control has also been associated with increased tendon glycation. The end products of tendon glycosylation contribute to changes in collagen crosslinking within the tendon, which increases the risk of spontaneous rupture from tendon contracture and rigidity. Patients with diabetic-induced neuropathy are also known to have an increased risk of rupture of the flexor tendons (4). Gout and other inflammatory arthropathies have been documented as a potential cause of a spontaneous TAT rupture. Patten and Pun (2) and Jerome et al (5) reported histologic findings of chalky
Financial Disclosure: None reported. Conflict of Interest: Lawrence Fallat reports a consultancy with Depuy-Synthes. Address correspondence to: Lawrence Fallat, DPM, FACFAS, Podiatric Surgery Residency, Beaumont Hospital Wayne, 20555 Ecourse Road, Taylor, MI 48180. E-mail address: [email protected] (L. Fallat).
white deposits within the substance of a ruptured TAT. When examined microscopically, gouty tophi were noted to have displaced the normal fibers of the tendon. The deposition of the uric acid crystals had completely compromised the structural integrity of the TAT tendon. Polarized light microscopy revealed pathognomonic findings of negatively birefringence needle-shaped crystals. Localized steroid injections in the area of tendon insertion or along its course increase the risk of tendon rupture. The steroid causes tenocyte death, which reduces the tensile strength of the tendon. The most commonly documented cause of local steroid-associated TAT rupture is injections into the first tarsometatarsal joint (6). The mechanism of failure for spontaneous rupture is an eccentric load of a degenerated, weakened TAT against a plantarflexed ankle (2). Although injury from blunt trauma and laceration is easily diagnosed, spontaneous rupture of the TAT is often associated with vague symptoms, such as mild pain, that subside shortly after the initial injury (7). After rupture of the TAT, the long extensors are recruited to assist in dorsiflexion (8), and this, along with no clear traumatic event, makes it difficult for patients to notice any acute pathologic features after injury. Often, the vague symptoms can lead to the patient presenting past the acute stage of the tendon rupture. It is important to carefully evaluate the extremity and make an accurate diagnosis. On visual examination, a pseudocyst will commonly be noted along the anterior aspect of the ankle (i.e., the distal aspect of the ruptured tendon after it has retracted along its sheath). Extensor substitution can be seen when the patient attempts to dorsiflex the ankle. A marked weakness in dorsiflexion at the ankle joint on manual muscle testing is usually
1067-2516/$ - see front matter Ó 2017 by the American College of Foot and Ankle Surgeons. All rights reserved. http://dx.doi.org/10.1053/j.jfas.2017.06.024
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noted compared with the contralateral limb. Pain is not a reliable marker in the subacute stage of the injury owing to the slow resolution of the symptoms as time passes. On gait examination, the patient will be seen to have a mild “foot slap,” and firing of the long extensors will be seen during the swing phase to help compensate for the loss of dorsiflexion. The common differential diagnoses for a TAT rupture include a common peroneal nerve lesion causing foot drop or L5 radiculopathy. A combination of imagining modalities and a careful physical examination will easily lead to the exclusion of these causes in a spontaneous TAT rupture. The medical imaging findings can provide a quick and accurate confirmation of the diagnosis once a thorough physical examination has been performed. Although ultrasonography can be used, magnetic resonance imaging (MRI) is considered the reference standard because of its diagnostic ability to evaluate the TAT and the anatomic structures surrounding it (9). The TAT is the primary dorsiflexor of the foot (10). During the swing phase of gait, contraction of the TAT prevents stumbling or tripping by clearing the foot over the ground. In the contact phase at heel strike, it aids in balancing plantarflexion of the foot by eccentric contraction and preventing foot slap (2). A prompt diagnosis and appropriate treatment of a rupture can prevent long-term sequela such as lost dorsiflexion, which can result in drop foot and Achilles tendon contracture (11). Drop foot alters the normal gait and can lead to abnormal ambulation and increase the risk of future injury. The most common anatomic area of rupture correlates directly with the zone of hypovascularity within the TAT. The vascularity of the tendon is nonhomogeneous, with the anterior half avascular between the superior and inferior extensor retinaculum. This area measures 45 to 67 mm long (12). Appropriate management of these injuries will differs according to each patient’s case. Markarian et al (8) found no significant differences in the outcomes between operative and nonoperative treatment of patients with a TAT rupture. However, in their study, the average age of the operative group was 19 years younger than that of the nonoperative group. Also, a predominance of acute ruptures was present in the operative group. Operative treatment of a TAT rupture for young and active patients for both acute traumatic and subacute spontaneous ruptures remains favored for long-term functionality (13). The mechanism and acuity of the injury are important factors to consider in preoperative planning. A direct surgical approach with end-to-end repair of the tendon with nonabsorbable suture is common for acute traumatic injuries. Alternatively, if the distal portion of the ruptured tendon is nonviable, the tendon can be directly attached to the proximal aspect of the medial cuneiform using a screw and washer, pull-out wire, interference screws, or suture anchors (14). Chronic injuries that present >1 month after injury require more complex surgical management. Often, end-to-end repair of the tendon will no longer be possible because the tendon has retracted proximally along its sheath. Numerous techniques can be used to overcome the deficit left by tendon retraction and to aid in the overall strength of the tendon, including slide lengthening, tendon turndown, interposition or tendon grafting, and augmentation (13,15,16).
was used for hemostasis. The patients underwent the procedure under general anesthesia. Cefazolin 2 g intravenously was administered for surgical prophylaxis. Postoperatively, both patients were placed in a well-padded below-the-knee fiberglass cast, with the foot positioned at 90 . They were instructed to be non-weightbearing on the surgical extremity. Crutches were used for ambulation. Oral deep vein thrombosis prophylaxis and pain medication was prescribed for both patients. Patient 1 The first patient was a 50-year-old female with a medical history of type 2 diabetes and social history of smoking. Her diabetes was rather poorly controlled. Her medications included glipizide (Glucotrol) 10 mg, metformin 1000 mg, and sitagliptin (Januvia) 100 mg. Her hemoglobin A1c was 8.3, with a mean plasma glucose of 216 mg/dL on the day of surgery. She presented to the clinic with a chief complaint of mild pain and weakness along the anteromedial aspect of the right ankle. The patient stated that she remembered the pain beginning about 8 weeks before her presentation to our clinic. She stated that she had “felt a pop,” followed by instant severe pain to the anterior aspect of the right ankle while getting out of bed 1 night. Soon after, the pain had subsided, but the weakness in her ankle remained. On examination in our clinic, we noted a distinct weakness in dorsiflexion of the right ankle. Absence of contracture of the TAT when dorsiflexing was also noted (Fig. 1). During the gait examination, her toes dragged on the ground, and a mild foot slap was noted. An MRI scan was obtained to confirm the working diagnosis of a TAT rupture. The MRI study showed complete rupture of the TAT, with a deficit of 7.8 cm between the proximal and distal stumps (Fig. 2). The large deficit had resulted from the subacute nature of the presentation of the patient, which had allowed the ruptured tendon to retract
Case Reports We present 2 cases, each outlining an atraumatic, spontaneous rupture of the TAT and the appropriate treatment method, with a focus on technique. A different surgical technique was used to repair the tendon in each case. To the best of our knowledge, the combination of differing acuity, method of injury, and surgical technique is unique. Both patients in our reported cases were placed in the supine position on the operating table. A thigh tourniquet set at 325 mm Hg
Fig. 1. View of right foot of patient 1 showing significant loss of dorsiflexion at the ankle joint with hyperextension of the hallux. Note the absence of contracture along the course of the tibialis anterior tendon on the right foot.
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Fig. 2. Magnetic resonance image showing a full-thickness superiorly retracted tear of the tibialis anterior tendon. The torn tendon stump had retracted approximately 7.8 cm and was 2.3 cm superior to the tibiotalar joint.
proximally along its sheath. Pronounced unilateral equinus on the injured side was also noted at the physical examination, which could be attributed to a muscle imbalance created owing to the period from injury to presentation. Given the patient’s functional status and relatively young age, surgical repair of the deformity was warranted. Owing to the large defect and chronicity of the injury, a graft (autograft or allograft) was though likely to be necessary to bridge the deficit created by tendon retraction. An 18-cm-long linear incision was made over the anteromedial aspect of the right foot and ankle, just medial to the TAT. After superficial dissection was completed, the tendon sheath to the TAT was identified and opened. The TAT had retracted significantly, as suggested by the MRI findings (Fig. 3). Owing to the severe tendon retraction, the extensor hallucis longus (EHL) tendon was used to augment the deficit. A small incision was made at the distal aspect of the right hallux at the level of the interphalangeal joint. The EHL and extensor hallucis brevis tendons were identified and sutured together (Fig. 4). The EHL tendon was sectioned just proximal to the tenodesis site. A tendon harvesting instrument was used to release the EHL tendon from its sheath to the level above the ankle joint. Using a tendon stripper, the EHL tendon was slid out of its sheath proximally and sutured to the proximal portion of the TAT using 2-0 braided nonabsorbable polyester suture (Fig. 5). No residual portion of tendon was seen when inspecting the insertion site of the TAT. Thus, a 3.2-mm drill bit was used to create a hole in the medial cuneiform, extending from dorsally to plantarly, where the TAT had attached previously (Fig. 6). The EHL tendon was then inserted through the drill hole and appropriately tensioned before being sutured onto itself with 2-0 braided nonabsorbable polyester suture (Fig. 7). A Strayer type gastrocnemius recession was also performed to correct the gastrocnemius equinus deformity. Before closure, all surgical wounds were irrigated. The tendon sheath and extensor retinaculum were repaired using 3-0 synthetic absorbable suture; 4-0 synthetic absorbable suture was used for subcutaneous closure and 3-0 nylon suture for skin closure.
Fig. 3. Retracted stump of tibialis anterior tendon.
Postoperatively, the patient was placed in a well-padded belowthe-knee fiberglass cast with the foot positioned at 90 . The patient was instructed to be non-weightbearing on the surgical extremity.
Fig. 4. Extensor hallucis longus and extensor hallucis brevis tendons were isolated and tenodesis performed before transection of the extensor hallucis longus tendon in preparation for harvesting.
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Fig. 7. View of completed repair with extensor hallucis longus graft seen spanning the original defect and proximally anchored to the tibialis anterior tendon stump and distally through the medial cuneiform. Fig. 5. Harvesting of the extensor hallucis longus tendon using a tendon stripper.
Crutches were used for ambulation. Apixaban 2.5 mg twice daily was given for 21 days for deep vein thrombosis prophylaxis and ibuprofen 800 mg for pain control. The patient was seen in our clinic every 2 weeks until all surgical wounds had healed. The patient developed a superficial localized infection to the surgical site, which was treated successfully with local wound care and a 10-day course of cephalexin after a culture of the wound grew Staphylococcus aureus. The patient was transitioned to partial weightbearing in a controlled ankle motion walker at 6 weeks
Fig. 6. Drill hole in medial cuneiform through which the extensor hallucis longus graft will pass.
postoperatively. A 1-month long course of physical therapy was prescribed for the patient to regain dorsiflexion strength to the ankle joint. Within 4 months postoperatively, the patient had no complaints and had a manual muscle testing result of 4 of 5 for the right ankle with dorsiflexion (Fig. 8). The patient was able to return to wearing normal shoe gear and her normal activities. The patient was followed up for 1 year and also followed up for diabetic foot care. Patient 2 Our second patient was a 71-year-old male with a significant history of previous ankle pain. The patient presented to clinic after noticing mild pain to the anterior aspect of his left foot and ankle. He was unable to recall a specific event but stated that the pain had been present for a few months. He reported that the pain had progressively increased with time. He rated his pain at 4 of 10 at presentation. The physical examination revealed mild swelling to the left anterior ankle along, with a subcutaneous prominence along the usual course of the TAT. A pronounced equinus deformity was noted on the injured side. The extensor complex could be seen firing for active dorsiflexion of the left foot. Pain along the course of the TAT was noted, along with a distinct absence of TAT tenting. With ambulation, he had a mild foot slap gait with the injured limb. The tentative diagnosis was of a TAT rupture, MRI confirmed the diagnosis (Fig. 9). Preoperative planning was performed, and because the patient did not recall how old the injury was, we anticipated that a graft would be necessary to bridge the defect. A 14-cm-long incision was made over the course of the TAT and extending to its insertion site. The incision was then deepened to the level of the extensor retinaculum, with care taken to identify and retract all vital neurovascular structures out of the way until the extensor retinaculum was identified. The TAT stump was identified, freed up proximally for approximately 4 cm using blunt dissection,
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Fig. 8. View at 5 months postoperatively showing (A) plantarflexion and (B) dorsiflexion.
and the fibrotic stump of the tendon was debrided (Fig. 10). When applying tension to the stump of the TAT, it was evident that the tendon itself would no longer be able to be attached to its insertion site without a graft. Preoperative planning had included a review of the patient’s MRI scan, on which the plantaris tendon had been visualized. The plantaris tendon was deemed appropriate to use as an autograft to bridge the gap, which was approximately 6 cm. The plantaris tendon was chosen owing to its minimal effect on normal function. A 2-cm incision was made at the posteromedial aspect of the Achilles tendon. Adequate dissection was performed, and the plantaris tendon was identified. A tendon stripper was then inserted proximally about 12 cm along the tendon to strip any soft tissue attachments (Fig. 11). Another 2-cm-long incision was made at the proximal aspect of the tendon stripper at the level of the mid-calf. After dissecting down to the plantaris tendon, the tendon was cut
and sutured to the gastrocnemius. This allowed approximately 12 cm of the plantaris tendon to be harvested. The plantaris tendon was then doubled on itself and reinforced using a whip stitch (Fig. 12). A 4.0-mm drill bit was drilled into the medial cuneiform, and a 4.75-mm interference screw was inserted with the harvested plantaris into the medial cuneiform (Fig. 13). The distal stump of the TAT was debrided of all unhealthy tissue, and the proximal end of the plantaris graft was attached to the distal end of the TAT with 2-0 braided nonabsorbable polyester suture after appropriate tensioning of the tendon with the foot slightly dorsiflexed while suturing the 2 ends together. Because of the equinus deformity after the TAT repair, gastrocnemius recession was deemed necessary. An approximately 3-cm incision was made at the distal one third of the leg, and the gastrocnemius was released with a Strayer type recession. The wounds were then flushed with copious amounts of antibiotic solution. The extensor retinaculum was reapproximated with 3-0 synthetic absorbable suture. Subcutaneous closure was completed with 4-0 synthetic absorbable suture, and 3-0 nylon suture was used for skin closure. The patient was seen in our clinic every 2 weeks postoperatively visits and healed uneventfully. He made a full recovery to his previous functional level within 5 months without the need for any physical therapy. His final manual muscle strength was rated at 4 of 5 in dorsiflexion. The final range of motion was 10 of dorsiflexion and 20 of plantarflexion. The patient was followed up for 17 months.
Fig. 9. Magnetic resonance image showing rupture and retraction of tibialis anterior tendon in patient 2.
Fig. 10. Dissection and exposure of tibialis anterior tendon. Note, distal aspect of tendon requires debridement of avascular and fibrotic tissue.
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Fig. 13. Intraoperative view showing fixation of distal stump of graft to insertion site of tibialis anterior tendon. Fig. 11. Harvesting of the plantaris tendon using a tendon stripper.
Discussion Atraumatic TAT ruptures are an infrequent clinical encounter. Detailed physical examination and accurate and early diagnosis are key factors to reducing long-term morbidity. Often, this is difficult because the patients experience vague symptoms and lack a focal defect owing to the compensatory aid of the extensor complex. Markarian et al (8) noted an average delay of 71 days from the initial symptoms to the final diagnosis of a rupture. Previously, it was preferred that patients with a delayed presentation or diagnosis of a TAT rupture be treated conservatively with bracing and activity modification. However, recent data have shown that good outcomes are possible with delayed surgical intervention, even with delayed presentation of the patient (8,17). The patient’s age and functional status are important factors when determining the appropriate treatment options. Conservative treatment should be reserved for patients with minimal ambulatory status and for patients for whom the risk of surgery outweighs the potential benefits. The common conservative treatment options include bracing, splinting, and activity modification. Surgical treatment is preferred for younger patients and patients who require a certain level of functional for their everyday activities.
Fig. 12. Plantaris tendon graft tagged and ready to use to bridge defect.
Surgical treatment was indicated for both patients included in our study. Atraumatic ruptures of the TAT have been confined mostly to case reports or series owing to the uncommon nature of the injury. Numerous surgical techniques have been described in the published data, with good outcomes using those techniques. However, no consensus has been reached regarding which procedure should be used in any given situation. A small treatment algorithm for surgical intervention has been reported, stating that deficits of 4 cm can be successfully treated with a turndown procedure or tendon slide lengthening (18). In patient 1, not only was the patient relatively young and active, but she also had a history of diabetes. Although our patient did not have significant neuropathy, pursuing a surgical option in patients with diabetes is important to decrease the long-term morbidity and restore normal gait function and plantar pressures to prevent ulceration. In her case, a tendon transfer augmentation procedure was chosen. This was determined after consideration of the large 7.8-cm deficit . With a history of diabetes, we sought to give the patient the strongest complex possible to allow for low long-term morbidity. The EHL tendon was chosen as the donor site for multiple reasons. The anatomic location of the tendon aids in dissection, and the size of the EHL tendon provides a strong construct without the need to fold the tendon onto itself to achieve the desired width. Finally, the functional loss of the donor site could be minimized and the full function of the hallux retained by tenodesis of the EHL to the extensor hallucis brevis tendon. In patient 2, surgical treatment was deemed necessary owing to the patient’s functional level. Although the patient was 71 years old, he complained of a foot slap when ambulating. This had limited his activities, and conservative treatment was not the best option for long-term ambulation. The patient’s symptoms had been present for months, indicating that a graft might be necessary to bridge the deficit that is often present in chronic ruptures. A plantaris autograft was chosen for this particular patient to minimize donor site morbidity and provide enough graft material for successful repair. Both cases in our study differed in the presentation and functional needs of the patients. No clear consensus or treatment algorithm for all TAT ruptures exists. Our case series has demonstrated that consideration of multiple factors, such as the acuity of the injury, the size of the deficit, and the functional needs of the patient, can result in successful outcomes with multiple techniques when used appropriately.
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In conclusion, the purpose of our case series was to offer insight into the sometimes subtle nature of the clinical presentation after a TAT rupture, information for a quick and accurate diagnosis using the physical examination and imaging studies, and possible surgical techniques for successful outcomes. References 1. Anzel SH, Covey KW, Weiner AD, Lipscomb PR. Disruption of muscles and tendons: an analysis of 1,014 cases. J Foot Ankle Surg 45:406–414, 1959. 2. Patten A, Pun WK. Spontaneous rupture of the tibialis anterior tendon: a case report and literature review. Foot Ankle Int 21:697–700, 2000. 3. DiDomenico LA, Williams K, Petrolla AF. Spontaneous rupture of the anterior tibial tendon in a diabetic patient: results of operative treatment. J Foot Ankle Surg 47:463–467, 2008. 4. Ramirez LC, Raskin P. Diabetic foot tendinopathy: abnormalities in the flexor plantar tendons in patients with diabetes mellitus. J Diabetes Complications 12:337–339, 1998. 5. Jerome JT, Varghese M, Sankaran B, Thomas S, Thirumagal SK. Tibialis anterior tendon rupture in gout–case report and literature review. Foot Ankle Surg 14:166– 169, 2008. 6. Jain K, Asad M, Joshi Y, Syed A. Tibialis anterior tendon rupture as a complication of first tarsometatarsal joint steroid injection: a case report and review of literature. Foot (Edinb) 3:179–181, 2015. 7. Bernstein RM. Spontaneous rupture of the tibialis anterior tendon. Am J Orthop (Belle Mead NJ) 24:354–356, 1995.
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