Anterior Tibial Tendon Rupture
Primary Dorsiflexor Rupture
By Chronicity
Critical Must-Knows
- Anterior ankle mass with palpable gap + preserved toe extension = TA rupture
- Acute (less than 4 weeks) with gap less than 3cm: primary repair
- Chronic or gap greater than 3cm: EHL transfer reconstruction
- Always fuse/tenodese hallux IP joint with EHL transfer
Examiner's Pearls
- "Distinguish from L5 radiculopathy (weak EHL) and peroneal palsy (weak eversion)
- "EDL compensation masks diagnosis - always test heel walking
- "8 weeks immobilization minimum to prevent re-rupture
Clinical Imaging
Imaging Gallery
Exam Warning
The Triple Differential
1. TA Rupture: Anterior mass + Slap foot + Toe Extension Intact. 2. L5 Radiculopathy: Foot drop + EHL Weakness + Sensory changes. 3. Peroneal Nerve: Foot drop + Eversion Weakness + 1st web space numb.
Missed Diagnosis Trap
EDL Compensation: Patients can still dorsiflex using extensors/peroneals, but cannot heel walk. Always test heel walking.
Biomechanics
Loss of Eccentric Control: Leads to 'Slap Foot' at heel strike. Swing Phase: High steppage to clear toes.
Management
Acute (less than 4wk): Repair. Chronic: EHL Transfer (most common).
Anatomy and Biomechanics
Tibialis Anterior Tendon Anatomy
The tibialis anterior is the primary ankle dorsiflexor with critical function during gait cycle.
Origin and Course
- Origin: Lateral tibial condyle, proximal two-thirds lateral tibial shaft, interosseous membrane, deep fascia
- Muscle belly: Largest and most medial of anterior compartment muscles
- Myotendinous junction: Junction occurs 5-7 cm proximal to ankle joint
- Tendon course: Crosses ankle joint beneath extensor retinaculum in medial-most tunnel
- Insertion: Medial and plantar aspect of medial cuneiform and base of first metatarsal
- Tendon width: Approximately 10-15 mm at insertion, thickest of ankle tendons
Vascular Anatomy
- Proximal blood supply: Anterior tibial artery branches to muscle belly
- Intratendinous vascularity: Longitudinal vessels within tendon substance
- Zone of hypovascularity: Beneath extensor retinaculum where rupture typically occurs
- Distal blood supply: Branches from dorsalis pedis near insertion
- Watershed zone: 2-3 cm proximal to insertion with reduced perfusion
Retinacular Anatomy
Superior, inferior, and stem components of extensor retinaculum constrain ankle tendons. Separate compartments for TA, EHL, EDL, and peroneals beneath retinaculum. TA occupies most medial tunnel beneath extensor retinaculum, susceptible to stenosis.
Biomechanical Function
- Primary dorsiflexor: Accounts for 80% of ankle dorsiflexion strength
- Gait importance: Essential for heel strike and toe clearance during swing phase
- Supination force: Secondary function as hindfoot invertor (synergist with TP)
- Arch support: Contributes to medial longitudinal arch stability
- Load tolerance: Can generate forces up to 3-4 times body weight
- Excursion: Approximately 25-30 mm of tendon excursion with full ankle motion
At a Glance
Anterior tibial tendon rupture is a rare injury typically affecting older males with degenerative tendinopathy, occurring at the hypovascular zone beneath the extensor retinaculum. Clinical features include an anterior ankle mass (retracted tendon), palpable gap, and slap foot gait with forefoot-first contact. Diagnosis is often delayed because EDL compensation masks the dorsiflexion weakness. Differential diagnosis includes peroneal nerve palsy and L5 radiculopathy—distinguish by intact toe extension (EHL, EDL) with isolated TA loss. MRI confirms rupture location and tendon quality. Acute complete ruptures (under 4 weeks) are managed with primary end-to-end repair if tension-free. Chronic or large gaps require reconstruction using EHL transfer (most common), EDL transfer, or allograft interposition. Post-operative immobilisation for 6-8 weeks is essential.
DISSTibialis Anterior Functions
Memory Hook:TA tendon function? Don't DISS the dorsiflexor
Overview
Anterior Tibial Tendon Rupture
Anterior tibial tendon (ATT) rupture is an uncommon but significant injury affecting the primary dorsiflexor of the foot. It may be acute (traumatic) or chronic (degenerative), with distinct presentations and management strategies.
Key Features:
- Third most common lower limb tendon rupture (after Achilles and patellar)
- Often misdiagnosed initially (up to 25% delayed diagnosis)
- Typically affects older patients (greater than 45 years) with degenerative ruptures
- Acute ruptures occur in younger, active patients
- Surgical repair generally recommended for active patients
Pathophysiology
Mechanisms of Rupture
Anterior tibial tendon rupture occurs through degenerative and traumatic mechanisms affecting a hypovascular zone.
Degenerative Rupture (Most Common)
- Age-related tendinosis: Collagen degeneration with mucoid changes
- Hypovascular zone: Reduced blood supply beneath extensor retinaculum
- Mechanical wear: Repetitive friction against superior extensor retinaculum
- Tibial osteophytes: Inferior anterior tibial lip spurs causing mechanical attrition
- Systemic factors: Diabetes, inflammatory arthropathy, fluoroquinolone use
- Steroid injections: Previous local corticosteroid may predispose to rupture
Traumatic Rupture
- Laceration: Direct penetrating injury to anterior ankle
- Forced plantarflexion: Eccentric loading during fall or stumble
- Avulsion injury: Sudden forceful dorsiflexion against resistance
- Iatrogenic: Surgical injury during ankle arthroscopy or anterior ankle procedures
- Ankle fracture-dislocation: High-energy trauma with tendon disruption
Chronic Attrition
The combination of intrinsic and extrinsic factors leads to gradual tendon failure:
- Intrinsic factors: Tendon degeneration, age greater than 45 years, hypovascular zone
- Extrinsic factors: Retinacular stenosis, tibial osteophytes, tight footwear
- Inflammatory conditions: Rheumatoid arthritis, seronegative spondyloarthropathy, gout
- Metabolic disorders: Diabetes mellitus, renal failure, hypercholesterolemia
Rupture Classification
Rupture Classification and Characteristics
| type | timing | tendonQuality | gapSize | surgicalOptions |
|---|---|---|---|---|
| Acute Complete | Less than 4 weeks from injury | Usually good quality ends | Variable, often less than 3 cm | Primary repair usually feasible |
| Chronic Complete | Greater than 4 weeks from injury | Degenerated ends, muscle retraction | Often greater than 3 cm | Reconstruction required (transfer or graft) |
| Partial Tear | Variable onset, progressive symptoms | Intact fibers with intratendinous split | Not applicable | Debridement and repair if greater than 50% |
| Insertional Avulsion | Acute traumatic event | Good tendon with bone fragment | Minimal if bone fixation immediate | Bone reattachment with suture anchors |
RUPTUREDRisk Factors for TA Tendon Rupture
Memory Hook:What gets RUPTURED? The TA tendon in these scenarios
Anatomy
Tibialis Anterior Tendon Anatomy
Origin:
- Lateral tibial condyle
- Upper 2/3 lateral tibial surface
- Interosseous membrane
- Deep fascia
Course:
- Most medial tendon in anterior compartment
- Passes under superior extensor retinaculum
- Passes under inferior extensor retinaculum (Y-shaped)
- Crosses ankle joint anteriorly
Insertion:
- Medial cuneiform (plantar and medial surfaces)
- Base of first metatarsal
- Wide footprint: 10-15mm
Relations:
- Lateral: EHL tendon, deep peroneal nerve, anterior tibial artery
- Medial: saphenous vein and nerve (more proximal)
Classification
Classification by Acuity
| Type | Timing | Characteristics |
|---|---|---|
| Acute | less than 6 weeks | Clear injury event, definable tendon ends |
| Subacute | 6-12 weeks | Delayed presentation, some retraction |
| Chronic | greater than 12 weeks | Significant retraction, often degenerative |
Clinical Implications:
- Acute: Primary repair often feasible
- Subacute: Repair possible but may need augmentation
- Chronic: Usually requires reconstruction (graft or transfer)
History and Symptoms
The clinical presentation varies based on acuity and degree of rupture.
Acute Rupture
- Sudden onset pain: Sharp anterior ankle pain during specific event
- Popping sensation: Audible or palpable snap at time of injury
- Immediate weakness: Inability to dorsiflex ankle or walk on heels
- Anterior ankle swelling: Visible mass from rolled-up proximal tendon stump
- Activity recall: Often occurs during plantar flexion against resistance
Chronic Rupture
- Gradual weakness: Progressive difficulty with stairs and inclines
- Slap foot gait: Foot slaps down after heel strike due to loss of eccentric control
- Toe catching: Stumbling over ground irregularities from reduced clearance
- Compensatory fatigue: EDL overuse causing anterior shin discomfort
- Delayed presentation: Often misdiagnosed as sprain or neuropathy
Functional Deficits
- Heel walking impossible: Cannot walk on heels due to absent dorsiflexion strength
- Stair difficulties: Ascending stairs requires hip and knee compensation
- Gait abnormalities: Steppage gait or circumduction to clear foot
- Running impairment: Cannot run due to loss of push-off control
- Footwear problems: Difficulty donning shoes from weak dorsiflexion
Physical Examination
Systematic examination confirms the diagnosis and assesses compensatory mechanisms.
Inspection
- Anterior ankle mass: Bulge from retracted proximal tendon stump
- Palpable gap: Defect palpable distal to extensor retinaculum
- Muscle atrophy: TA muscle wasting in chronic cases (rare due to intramuscular tear pattern)
- Gait observation: Slap foot or steppage pattern
- Toe clawing: Compensatory EDL overactivity causing toe hyperextension
Palpation
- Tendon continuity: Gap palpable 2-4 cm above insertion typically
- Rolled tendon: Proximal stump palpable as firm mass
- Point tenderness: Local pain at rupture site in acute injuries
- Distal stump: Thin or absent tendon palpable distally
Functional Testing
Ankle dorsiflexion strength typically grade 0-1 with complete rupture despite EDL compensation. Partial tears or chronic compensated ruptures may demonstrate grade 2-3 strength from EDL. Normal or increased toe extension from compensatory EDL overactivity.
Specific tests:
- Resisted dorsiflexion: Severe weakness or absent function with resistance
- Heel walking: Inability to walk on heels (pathognomonic for TA dysfunction)
- Toe dorsiflexion: Preserved or enhanced from EDL compensation
- Passive plantarflexion: May reproduce pain at rupture site if acute
- Thompson test analogue: Squeezing TA belly does not produce dorsiflexion
Differential Diagnosis Testing
- L5 radiculopathy: Check EHL strength (should be normal in isolated TA rupture)
- Common peroneal nerve: Assess ankle eversion (should be normal)
- Deep peroneal nerve: Test sensation first web space (should be intact)
- Compartment syndrome: Assess for firmness and pain with passive stretch (absent in isolated rupture)
Exam Pearl
The key clinical finding is a palpable anterior ankle mass with a distal gap, combined with inability to heel walk despite preserved toe dorsiflexion. This triad distinguishes TA rupture from neurological causes of foot drop. The "reverse Thompson test" (squeezing TA muscle belly produces no ankle dorsiflexion) confirms the diagnosis.
Investigations
Imaging Studies
Imaging confirms the clinical diagnosis and guides treatment planning.
Radiographs
Views: Weight-bearing AP, lateral, and oblique foot-ankle
Findings:
- Usually normal in acute ruptures
- Chronic cases may show:
- Anterior distal tibial osteophytes (site of mechanical attrition)
- Soft tissue swelling or calcification anterior ankle
- First ray elevation from loss of plantarflexion force
- Arthritic changes if inflammatory etiology
- Avulsion fracture at cuneiform or first metatarsal base (rare)
Ultrasound
Advantages: Dynamic assessment, real-time evaluation, cost-effective
Technique:
- High-frequency linear probe (10-15 MHz)
- Long-axis and short-axis imaging of entire tendon
- Compare to contralateral side
- Dynamic testing with active dorsiflexion
Findings:
- Complete tendon discontinuity with gap
- Hypoechoic or anechoic rupture site
- Proximal tendon retraction and thickening
- Hematoma or fluid in gap
- Measure gap size (critical for surgical planning)
- Partial tears show incomplete fiber disruption
MRI
Protocol: Ankle-foot protocol with T1, T2, STIR sequences in axial, sagittal, and coronal planes
Indications:
- Uncertain diagnosis
- Pre-operative planning
- Assessment of chronic ruptures
- Evaluation of tendon quality
- Identify associated pathology
Key findings:
MRI Characteristics by Chronicity
| finding | acute | chronic | significance |
|---|---|---|---|
| Tendon Continuity | Complete disruption with wavy retracted ends | Wide gap with muscle retraction and fatty infiltration | Determines feasibility of primary repair |
| Gap Size | Typically 1-3 cm, measured in neutral position | Often greater than 4 cm with maximal plantarflexion | Gap greater than 3 cm requires reconstruction |
| Tendon Quality | Normal signal in proximal/distal stumps | Degenerated stumps with increased T2 signal | Poor quality precludes primary repair |
| Muscle Changes | Normal muscle bulk and signal | Atrophy and fatty infiltration of TA muscle | Severe atrophy indicates poor functional recovery potential |
| Retinaculum | Intact but may show fluid/edema | Thickened with scarring and adhesions | Chronic stenosis contributes to rupture |
Advanced Imaging
- CT scan: Rarely needed, may help identify bony pathology
- Nerve conduction studies: If suspicion of neurological cause for foot drop
- EMG: Distinguish denervation from tendon rupture in unclear cases
GAPSMRI Findings in TA Tendon Rupture
Memory Hook:MRI shows GAPS in ruptured TA tendon
Non-Operative Management
Management Algorithm
Non-operative management is reserved for specific patient populations with acceptable functional compensation.
Indications
- Sedentary elderly patients: Minimal functional demands, acceptable gait with EDL compensation
- Severe medical comorbidities: Prohibitive surgical risk
- Patient preference: Informed decision declining surgery despite deficits
- Partial tears: Less than 50% cross-sectional area involved with good strength
- Chronic ruptures with good compensation: Well-adapted gait with minimal disability
Contraindications to Conservative Care
- Young active patients requiring normal gait mechanics
- Inability to compensate with EDL (weak toe extension)
- Progressive deformity or gait deterioration
- Patient desire for optimal functional restoration
- Occupation requiring normal dorsiflexion (e.g., driving, climbing)
Non-Operative Protocol
Phase 1 (0-6 weeks): Protection and adaptation
- AFO (ankle-foot orthosis): Articulated or fixed AFO to assist dorsiflexion
- Immobilization: Short leg cast or boot if acute and painful
- Weight-bearing: As tolerated with assistive device if needed
- Pain management: NSAIDs, ice, elevation for acute symptoms
Phase 2 (6-12 weeks): Functional adaptation
- Gait training: Compensatory strategies using EDL and hip flexors
- Strengthening: EDL and peroneals to optimize compensation
- Proprioception: Balance training to reduce fall risk
- Orthotic refinement: Adjust AFO for optimal function
Phase 3 (3-6 months): Long-term management
- Permanent AFO: Custom molded articulated AFO for daily use
- Footwear modification: Rocker bottom sole to assist heel-toe transition
- Activity modification: Avoid activities requiring heel walking or dorsiflexion
- Surveillance: Monitor for progressive deformity or gait dysfunction
Outcomes of Conservative Treatment
- Function: Acceptable for low-demand activities, limited for sports
- Gait: Persistent abnormality with slap foot or steppage pattern
- Satisfaction: Variable, depends on functional demands and expectations
- Complications: Chronic ankle pain, ankle stiffness, falls from tripping
- Long-term: May develop secondary issues (back pain from gait asymmetry)
Non-operative management of complete TA tendon rupture results in permanent functional deficit. AFO is required indefinitely for optimal gait. This approach should only be chosen after thorough discussion of limitations and with appropriate patient selection (elderly, sedentary, high surgical risk).
Operative Management
Management Algorithm
Surgical Indications and Timing
Surgery is the preferred treatment for most patients with complete TA tendon rupture.
Indications for Surgery
- Complete acute rupture: Less than 4 weeks old in active patients
- Symptomatic chronic rupture: Functional impairment despite conservative trial
- Young active patients: Desire for optimal functional restoration
- Failed conservative management: Progressive symptoms or inadequate compensation
- Large partial tears: Greater than 50% cross-sectional involvement
- Occupational requirement: Jobs requiring normal ankle dorsiflexion
Timing Considerations
- Acute ruptures (less than 4 weeks): Primary repair often feasible
- Subacute ruptures (4-12 weeks): May require augmentation or short reconstruction
- Chronic ruptures (greater than 12 weeks): Reconstruction with tendon transfer or allograft
- Emergency surgery: Not required unless open injury with contamination
Pre-Operative Planning
- MRI review: Assess gap size, tendon quality, muscle status
- Surgical approach selection: Based on rupture location and chronicity
- Reconstruction strategy: Primary repair vs. augmentation vs. reconstruction
- Graft/transfer planning: Identify donor tendon or arrange allograft
- Patient counseling: Realistic expectations for recovery timeline (6-12 months)
Surgical Techniques
End-to-End Tendon Repair
Indications:
- Acute rupture (less than 4 weeks)
- Gap less than 3 cm with ankle in plantarflexion
- Good quality tendon ends
- No significant muscle retraction
Patient Positioning:
- Supine with bump under ipsilateral hip
- Thigh tourniquet (250-300 mmHg)
- Ensure foot mobile for intraoperative positioning
Surgical Approach:
- Longitudinal incision over anterior ankle (8-12 cm)
- Center over palpable gap or TA tendon course
- Incise skin and subcutaneous tissue
- Identify and protect superficial peroneal nerve branches
- Open extensor retinaculum along medial border
Tendon Preparation:
- Identify proximal and distal tendon stumps
- Debride degenerated or frayed tissue to healthy tendon
- Freshen ends with sharp blade (perpendicular cuts)
- Assess gap with ankle in maximal plantarflexion
- If gap greater than 3 cm, consider augmentation or reconstruction
Repair Technique:
- Krackow suture configuration: Locking stitches in each stump
- Suture material: Non-absorbable braided (FiberWire, Ethibond) size 2 or 0
- Core suture: 4-6 strand repair for optimal strength
- Tensioning: Repair with ankle in 10-15 degrees plantarflexion
- Epitendinous suture: Running 4-0 absorbable to smooth repair site
- Test repair: Ensure intact with passive ankle dorsiflexion to neutral
Augmentation Options (if tension on repair):
- Turndown flap: Proximally based TA tendon flap to bridge gap
- EHL transfer: Add EHL as side-to-side augmentation
- Plantaris graft: Harvest plantaris for interpositional graft
- EDL transfer: Transfer central EDL slip for reinforcement
Retinaculum Management:
- Excise portion of superior retinaculum to decompress repair
- Avoid complete retinaculum excision (prevents bowstringing)
- Ensure tendon glides smoothly beneath retinaculum
Closure:
- Close retinaculum loosely if intact
- Subcutaneous layer with 3-0 absorbable suture
- Skin closure with 4-0 nylon or staples
- Apply soft dressing and posterior splint in 10-15 degrees plantarflexion
Post-Operative Protocol:
- 0-2 weeks: NWB in posterior splint, plantarflexed position
- 2-6 weeks: NWB in cast or boot, gradual bring to neutral by week 6
- 6-8 weeks: Begin PWB in neutral boot, gentle AROM exercises
- 8-12 weeks: Progress to FWB, weaning from boot, start strengthening
- 3-6 months: Gradual return to activities, continue rehabilitation
- 6-12 months: Full recovery expected with return to impact activities
The superficial peroneal nerve crosses the anterior ankle and is at risk during exposure. Identify and protect throughout procedure. Excessive tension on the repair increases failure risk - if gap greater than 3 cm even in plantarflexion, consider augmentation or reconstruction rather than tensioned primary repair.
Outcomes of TA Tendon Reconstruction
- 86% good-to-excellent outcomes at 3.2-year follow-up
- Primary repair: 92% strength recovery but 25% failure in chronic ruptures
- EHL transfer: 76% strength recovery with 89% good-to-excellent results
- Complications: infection 2%, re-rupture 4%, nerve injury 3%
Complications
Surgical Complications
Understanding and preventing complications is essential for optimal outcomes.
Intraoperative Complications
- Neurovascular injury: Superficial peroneal nerve (2-3%), anterior tibial artery (rare)
- Deep peroneal nerve: At risk with deep dissection, causes first web space numbness
- Inadequate gap closure: Excessive tension on repair leading to early failure
- Incorrect tension: Over-tight (equinus contracture) or under-tight (weak dorsiflexion)
- Donor site injury: EHL laceration during harvest, hallux devascularization (rare)
Early Post-Operative Complications
Common Early Complications
| complication | incidence | presentation | management |
|---|---|---|---|
| Wound Complications | 5-8%, higher in diabetics | Delayed healing, dehiscence, superficial infection | Local wound care, oral antibiotics, revision closure if severe |
| Re-Rupture | 4-6% overall, higher with primary repair of chronic ruptures | Acute pain, loss of dorsiflexion, palpable gap recurs | Revision surgery with reconstruction (EHL transfer or allograft) |
| DVT/PE | Less than 1% with prophylaxis | Calf swelling, positive D-dimer, PE symptoms | Anticoagulation, may require admission for PE |
| Compartment Syndrome | Rare (less than 0.5%) | Severe pain, tense leg, pain with passive stretch | Emergency fasciotomy if confirmed by pressure measurement |
Late Complications
- Persistent weakness: Incomplete strength recovery, more common with reconstructions
- Ankle stiffness: Limited dorsiflexion from prolonged immobilization or adhesions
- Hallux deformity: Cock-up hallux after EHL transfer without IP fusion/tenodesis
- Gait abnormalities: Persistent slap foot or steppage despite intact repair
- Chronic pain: Anterior ankle pain from adhesions, nerve injury, or arthrofibrosis
- Tendon adhesions: Scarring to retinaculum limiting gliding
- Equinus contracture: From excessive plantarflexion during immobilization
Specific Complication Management
Re-Rupture:
- Diagnosis: Clinical examination, ultrasound or MRI confirmation
- Timing: Usually within first 3 months post-operatively
- Causes: Excessive tension, premature weight-bearing, poor tendon quality
- Management: Revision surgery with reconstruction (EHL transfer preferred)
- Prevention: Adequate immobilization (8 weeks minimum), appropriate tension, patient compliance
Persistent Weakness:
- Evaluation: Compare to contralateral ankle dorsiflexion strength
- Acceptable: 70-80% strength after EHL transfer, 90%+ after primary repair
- Causes: Muscle atrophy, incomplete healing, adhesions, inadequate rehabilitation
- Management: Prolonged physiotherapy (6-12 months), AFO if severe
- Consider: Revision surgery if less than 50% strength and daily impairment
Nerve Injury:
- Superficial peroneal nerve: Numbness dorsum of foot, usually resolves 3-6 months
- Deep peroneal nerve: First web space numbness, persistent but not functionally limiting
- Painful neuroma: Rare, may require neuroma excision or nerve decompression
- Prevention: Careful dissection, protect nerve branches throughout
The most significant complication is re-rupture, which occurs in 4-6% of cases. Risk factors include chronic ruptures treated with primary repair under tension, inadequate immobilization duration, and premature return to activities. Ensure 8 weeks of strict immobilization and gradual progression through rehabilitation phases to minimize risk.
Complications After TA Tendon Surgery
- 24% complication rate in 67 patients at 2-year follow-up
- Re-rupture 6%, superficial infection 7.5%, nerve injury 6%
- All infections resolved with oral antibiotics
- 85% overall satisfaction despite complications
Return to Activity and Outcomes
Complications
Early Complications (0-6 weeks)
| Complication | Incidence | Management |
|---|---|---|
| Wound infection | 3-8% | Oral/IV antibiotics, debridement if deep |
| Wound dehiscence | 2-5% | Dressings, secondary closure, skin graft |
| Nerve injury | 5-10% | Observation (usually transient) |
| DVT/PE | less than 1% | Prophylaxis, treatment anticoagulation |
| Hematoma | 2-3% | Aspiration or evacuation |
Wound Problems:
- Higher risk in chronic ruptures with poor tissue
- Diabetes and PVD increase risk
- Careful tissue handling essential
Recovery Timeline and Expectations
Understanding the prolonged recovery process is essential for patient counseling.
Rehabilitation Phases
Immobilization in plantarflexion gradually brought to neutral. Non-weight bearing progressing to partial weight bearing.
Active range of motion, progressive weight bearing, gait normalization. Begin gentle strengthening.
Progressive resistance exercises, proprioception training, functional activities. Return to low-impact activities.
Sport-specific training, gradual return to full activities. Complete recovery expected by 12 months.
Functional Outcomes
Expected Functional Recovery
| outcome | primaryRepair | ehlTransfer | nonOperative |
|---|---|---|---|
| Walking | Normal gait by 3-4 months | Normal gait by 4-6 months | Permanent slap foot gait, AFO dependent |
| Stairs/Inclines | Full function by 4-6 months | Near-normal by 6-9 months | Permanent difficulty, uses handrail |
| Running | Return to running 6-9 months | Return to running 9-12 months | Usually not possible |
| Sports/Impact | Full return 9-12 months, 90% performance | Most sports 12+ months, 75-85% performance | High-impact sports not feasible |
Strength Recovery
- Primary repair: 90-100% contralateral strength if successful
- EHL transfer: 70-80% contralateral strength (functionally adequate)
- EDL transfer: 60-70% contralateral strength (may limit high-level sports)
- Allograft: 70-85% strength once fully incorporated (12-18 months)
- Non-operative: 20-30% strength from EDL compensation alone
Patient Satisfaction
Studies report high satisfaction rates across surgical interventions:
- Primary repair: 90-95% satisfied with outcome
- EHL transfer: 85-90% satisfied despite some weakness
- Revision surgery: 70-80% satisfied (lower due to complications/reoperations)
- Non-operative: 40-60% satisfied, limited by persistent functional deficits
Return to Work
- Sedentary work: 6-8 weeks with protected weight-bearing
- Light duty: 12-16 weeks with gradual transition
- Heavy labor: 6-9 months minimum, may require job modification
- Driving: Right foot 3-4 months once off immobilization and adequate strength
Prognostic Factors
Favorable outcomes:
- Acute rupture (less than 4 weeks) treated with primary repair
- Good quality tendon and muscle
- Young patient with good rehabilitation compliance
- Non-smoking, non-diabetic, healthy weight
- Appropriate surgical technique and post-operative protocol
Poor prognostic factors:
- Chronic rupture (greater than 6 months) with muscle atrophy
- Failed prior surgery
- Diabetes, smoking, obesity
- Poor compliance with immobilization or rehabilitation
- Inflammatory arthropathy affecting healing
Long-Term Functional Outcomes
- AOFAS scores improved from 48 to 89 at 5-year follow-up
- Primary repair: 94% strength recovery vs EHL transfer: 77%
- 91% returned to desired activity level
- 93% patient satisfaction overall
Viva Scenarios
Outcomes
Functional Outcomes by Treatment
| Outcome Measure | Primary Repair | EHL Transfer | Non-operative |
|---|---|---|---|
| AOFAS Score | 85-95 | 80-90 | 60-70 |
| Strength recovery | 90-100% | 70-80% | 20-30% |
| Return to normal gait | 95% | 85% | less than 50% |
| Patient satisfaction | 90-95% | 85-90% | 40-60% |
| Return to sport | 85-90% | 70-80% | Limited |
Timeline to Recovery:
- Normal walking: 3-4 months (repair), 4-6 months (transfer)
- Running: 6-9 months (repair), 9-12 months (transfer)
- Full sport: 9-12 months (repair), 12+ months (transfer)
Evidence Base
Key Studies - Surgical Outcomes
| Study | Design | N | Key Finding |
|---|---|---|---|
| Bernhard 2020 | Systematic review | 318 | 90% good/excellent outcomes with surgery |
| Dooley 1980 | Case series | 16 | First major series describing EHL transfer |
| Markarian 1998 | Comparative | 32 | Primary repair superior when possible |
| Elias 2021 | Meta-analysis | 412 | Surgery significantly better than conservative |
Evidence Summary:
- Level IV evidence predominates (case series)
- No RCTs comparing surgical vs non-operative
- Consistent finding: surgery superior for active patients
Exam Viva Scenarios
Practice these scenarios to excel in your viva examination
Scenario 1: Acute TA Tendon Rupture in Active Patient
"A 52-year-old recreational runner presents to your clinic 10 days after acute onset of anterior ankle pain while running downhill. He describes a pop and immediate weakness. Examination reveals a palpable anterior ankle mass, a gap 3 cm above the TA insertion, and inability to heel walk. MRI shows complete TA tendon rupture with 2.5 cm gap in neutral position and good quality tendon ends. He is otherwise healthy and wants to return to running."
Scenario 2: Chronic TA Tendon Rupture with Diagnostic Uncertainty
"A 68-year-old man presents with 9 months of progressive difficulty walking and frequent tripping. He cannot recall a specific injury. He was initially diagnosed with sciatica and had lumbar spine MRI which was unremarkable. On examination, he has weak ankle dorsiflexion (2/5) but normal toe extension (5/5). He can evert the ankle normally. There is a subtle anterior ankle fullness. Ankle sensation is intact. He ambulates with a steppage gait pattern. You order an MRI which shows complete TA tendon rupture with 5 cm gap, degenerated tendon ends, and moderate TA muscle atrophy with early fatty infiltration."
MCQ Practice Points
Exam Pearl
Q: What is the typical patient demographic and mechanism for anterior tibial tendon rupture?
A: Typically affects elderly patients (60-80 years) with spontaneous or low-energy rupture. Risk factors include: diabetes mellitus, inflammatory arthritis, corticosteroid use, and chronic tendinopathy. Often occurs with minor trauma (stumbling, missing a step) in a chronically weakened tendon. The zone of relative hypovascularity at the inferior extensor retinaculum is the most common rupture site.
Exam Pearl
Q: What are the clinical features of anterior tibial tendon rupture?
A: Gait abnormality: Steppage gait (high-stepping to clear foot) or slap gait (foot slaps during heel strike). Weakness: Unable to dorsiflex ankle against resistance. Palpable defect: Gap at the anterior ankle, though swelling may obscure this. Pseudotumor: Mass from retracted tendon stump may be palpable. Foot drop: Inability to clear foot during swing phase. Differential includes common peroneal nerve palsy (sensory changes, different weakness pattern).
Exam Pearl
Q: What are the surgical treatment options for anterior tibial tendon rupture?
A: Acute ruptures (less than 6 weeks): Primary repair with end-to-end suture if possible. Chronic ruptures: Often require augmentation due to tendon degeneration and gap. Options include: EHL transfer (extensor hallucis longus) - most common; Peroneus tertius transfer; Allograft reconstruction; Free gracilis/semitendinosus graft. The tendon is repaired through an anterior ankle incision, often requiring Z-lengthening.
Exam Pearl
Q: Why is EHL (extensor hallucis longus) the preferred tendon transfer for chronic anterior tibial tendon rupture?
A: EHL is preferred because: (1) Similar line of pull to tibialis anterior; (2) Adequate strength (approximately 80% of tibialis anterior); (3) Sufficient length for transfer; (4) Minimal donor morbidity - hallux IP joint extension loss is well-tolerated. Technique involves harvesting EHL distally, weaving through tibialis anterior stump, and anchoring to medial cuneiform/navicular with interference screw or suture anchors.
Exam Pearl
Q: What is the expected functional outcome after anterior tibial tendon repair or reconstruction?
A: Good to excellent outcomes in 80-90% of cases with surgical treatment. Most patients regain independent ambulation without orthotic support. Residual findings may include: Mild weakness of dorsiflexion (grade 4/5 power), altered gait pattern with reduced push-off, and prolonged rehabilitation (3-6 months). Non-operative treatment (AFO) is reserved for sedentary elderly patients with high surgical risk.
Australian Context
Australian Epidemiology
Incidence:
- Rare injury: estimated less than 0.5 per 100,000 person-years
- Higher rates in active elderly population
- Increasing with aging population and activity levels
Demographics:
- Mean age: 60-70 years for degenerative ruptures
- Male predominance (3:1)
- Risk factors: diabetes (higher in Aboriginal communities), corticosteroid use
Regional Considerations:
- Higher rates of delayed presentation in rural/remote areas
- Limited access to foot/ankle subspecialty expertise outside major centres
- Telemedicine increasingly used for initial assessment
TA Tendon Rupture Exam Essentials
High-Yield Exam Summary
Must-Know Anatomy
- •TA: primary dorsiflexor, 80% of ankle dorsiflexion power
- •Origin: lateral tibia, insertion: medial cuneiform and first MT base
- •Hypovascular zone beneath extensor retinaculum - rupture site
- •Superficial peroneal nerve crosses anterior ankle - protect during surgery
- •Three retinacular bands constrain tendons - excise superior portion for decompression
Classic Presentation
- •Elderly male, often spontaneous or minor trauma
- •Anterior ankle mass (rolled-up tendon) with distal gap
- •Unable to heel walk despite preserved toe extension (EHL intact)
- •Slap foot gait - forefoot hits ground before heel
- •Often misdiagnosed as sciatica or peroneal nerve palsy
Key Differentiation
- •TA rupture: weak dorsiflexion, normal toe extension (EHL), palpable mass
- •L5 radiculopathy: weak dorsiflexion AND weak EHL, radicular pain
- •Peroneal nerve palsy: weak dorsiflexion AND eversion, foot numbness
- •Compartment syndrome: tense leg, severe pain, pain with passive stretch
- •Pseudoparalysis: pain limiting function, improves with anesthesia
Imaging Essentials
- •MRI gold standard: confirms rupture, measures gap, assesses muscle/tendon quality
- •Acute: gap less than 3 cm, good tendon quality, no muscle atrophy
- •Chronic: gap greater than 4 cm, degenerated tendon, muscle atrophy/fatty infiltration
- •Ultrasound: dynamic assessment, can diagnose acute ruptures
- •XR: usually normal, may show tibial osteophytes in chronic cases
Treatment Algorithm
- •Acute (less than 4 weeks) + gap less than 3 cm: primary Krackow repair
- •Acute but gap greater than 3 cm: augment with EHL or turndown flap
- •Chronic (greater than 4 weeks) or gap greater than 3 cm: EHL transfer reconstruction
- •Severe muscle atrophy or revision: consider allograft or EDL transfer
- •Non-operative: AFO only for sedentary elderly with high surgical risk
Surgical Pearls
- •Primary repair: Krackow locking sutures, repair in 10-15 degrees plantarflexion
- •EHL transfer: hallux IP fusion/tenodesis mandatory to prevent cock-up deformity
- •Tension with ankle neutral dorsiflexion, slight hindfoot inversion
- •Excise portion of superior retinaculum to decompress repair site
- •Post-op: 8 weeks immobilization essential, NWB initially progressing by weeks
Viva Traps
- •Primary repair under tension will fail - augment or reconstruct if gap greater than 3 cm
- •EHL transfer achieves 70-80% strength NOT 100% - set realistic expectations
- •Muscle atrophy greater than 50% predicts poor recovery even with surgery
- •Return to running needs 6-9 months minimum, full recovery 12 months
- •Re-rupture risk highest with inadequate immobilization or chronic rupture primary repair
Critical Numbers
- •Gap less than 3 cm: primary repair feasible if acute and in plantarflexion
- •8 weeks: minimum immobilization duration to prevent re-rupture
- •70-80%: expected strength recovery with EHL transfer
- •90-95%: good-excellent results with appropriate surgery and patient selection
- •4-6%: re-rupture rate overall, higher with tensioned repairs