Patellar Tendon Rupture (Adult)

1. Clinical Overview

Summary

Patellar tendon rupture is a complete disruption of the knee extensor mechanism occurring predominantly in younger, active adults (less than 40 years). It represents a surgical emergency requiring prompt diagnosis and early intervention to optimize functional outcomes. The injury typically occurs at the inferior pole of the patella following eccentric loading of the quadriceps muscle during deceleration activities such as landing from a jump. [1,2]

The hallmark clinical features include:

• Inability to perform a straight leg raise (SLR) against gravity
• Palpable infrapatellar gap (though often obscured by hemarthrosis)
• Patella alta (high-riding patella) on lateral radiographs
• Immediate functional disability with inability to actively extend the knee

Unlike quadriceps tendon rupture which occurs in older patients (> 40 years) with degenerative tendons, patellar tendon ruptures typically occur in younger athletes and are often associated with pre-existing tendinopathy or systemic risk factors that compromise tendon integrity. [3,4] Delayed diagnosis leads to tendon retraction, scarring, and significantly worse surgical outcomes, making early recognition critical. [5]

The "Rule of 40" in Extensor Mechanism Injuries

Age less than 40 years: Patellar Tendon Rupture (typically athletes, eccentric overload) Age > 40 years: Quadriceps Tendon Rupture (typically degenerative, lower-energy mechanism)

This age-based distribution reflects fundamental differences in tendon pathology and biomechanical loading patterns across the lifespan. [6]

Key Facts

Anatomical Considerations:

• The patellar tendon is technically a ligament (bone-to-bone connection: patella to tibial tubercle)
• Dimensions: Approximately 30mm wide × 50mm long
• Tensile strength: Capable of withstanding forces 10-15× body weight
• Blood supply: Relatively avascular central portion (predisposes to central rupture)
• Most common rupture site: Proximal insertion at inferior pole of patella (75-80% of cases) [7]

The "Toothpaste Tube" Phenomenon: When the tendon ruptures, the fibrillar structure splays apart creating multiple shredded ends resembling frayed rope or squeezed toothpaste. This makes primary repair technically challenging and necessitates robust suture techniques (Krackow locking stitch) to achieve adequate purchase in degenerative tendon tissue. [8]

Systemic Risk Factors (The "Weak Tendon" Profile):

• Corticosteroid use: Systemic or local injection (↓ collagen synthesis, ↓ fibroblast activity) [9]
• Fluoroquinolone antibiotics: Especially ciprofloxacin (↑ matrix metalloproteinases, collagen degradation) [10]
• Chronic kidney disease: Secondary hyperparathyroidism (calcium deposition, tendon weakening)
• Rheumatoid arthritis: Chronic inflammation, altered tendon architecture
• Diabetes mellitus: Advanced glycation end-products, microvascular disease
• Systemic lupus erythematosus: Autoimmune collagen disruption

Clinical Pearls

"The SLR Test is the Great Discriminator": A patient with acute knee trauma who cannot actively lift their heel off the examination table (with knee fully extended) has disrupted their extensor mechanism. The differential diagnosis narrows to: (1) Patella fracture, (2) Quadriceps tendon rupture, or (3) Patellar tendon rupture. Caveat: Pain inhibition can cause a false-positive SLR failure. If uncertain, aspirate the hemarthrosis and inject 10-20ml of 1% lignocaine to eliminate pain as a confounding variable. [11]

"Hidden by the Hematoma": The pathognomonic palpable infrapatellar gap may be completely obscured by a tense hemarthrosis within 2-4 hours of injury. Always correlate with SLR test and imaging. Do not rely on palpation alone in the acute setting.

"The Walking Wounded": Patellar tendon ruptures are frequently misdiagnosed as "knee sprains" in emergency departments because patients can ambulate (albeit abnormally). They achieve this by: (1) Locking the knee in full extension using gluteal and hamstring co-contraction, (2) Circumducting the limb to avoid knee flexion during swing phase. Key distinguishing feature: They cannot extend the knee actively from a flexed position. [12]

"Bilateral Ruptures = Systemic Disease": Simultaneous bilateral patellar tendon rupture is rare but pathognomonic for underlying metabolic disease. Most common cause: Chronic renal failure with secondary hyperparathyroidism. Other causes include SLE, diabetes, and iatrogenic corticosteroid excess. Always investigate for systemic pathology in bilateral cases. [13]

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2. Epidemiology

Demographics

Age Distribution:

• Mean age at injury: 30-35 years (peak incidence: 20-40 years)
• Distinctly younger than quadriceps tendon rupture cohort (mean 50+ years)
• Rare in children (tibial tubercle avulsion occurs instead)
• Rare in elderly (degenerative quadriceps rupture predominates)

Sex Distribution:

• Male >> Female (male:female ratio approximately 5:1 to 10:1)
• Reflects higher athletic participation and higher-risk sporting activities in males [14]

Incidence:

• Relatively uncommon injury: Exact incidence difficult to establish
• Estimated at 0.68 per 100,000 person-years in general population
• Substantially higher in elite athletes (basketball, volleyball, track and field)
• Accounts for approximately 30% of all extensor mechanism ruptures (quadriceps ruptures are more common overall) [15]

Mechanism of Injury

Primary Mechanism: Eccentric Overload (80-85% of cases) The classic scenario involves forceful quadriceps contraction while the knee is rapidly flexing (eccentric contraction):

• Landing from a jump (basketball, volleyball, parkour)
• Sudden deceleration while running
• Stumbling down stairs (attempting to prevent fall)
• Rapid knee flexion against resistance

The force generated during eccentric muscle contraction can exceed the tensile strength of the tendon, particularly if pre-existing degeneration or systemic factors have weakened the tissue. [16]

Secondary Mechanisms (15-20% of cases):

• Direct trauma: Direct blow to anterior knee during flexion (dashboard injury, fall onto knee)
• Laceration: Penetrating trauma to anterior knee
• Iatrogenic: Complication of anterior cruciate ligament (ACL) reconstruction using bone-patellar tendon-bone autograft (harvesting weakens remaining tendon) [17]

Risk Factors

Local Tendon Pathology:

1. Patellar tendinopathy ("Jumper's Knee"): Chronic repetitive microtrauma causing mucoid degeneration, fibrillar disorganization, and neovascularization. Present in up to 70% of rupture cases in athletes. [18]
2. Previous knee surgery: Particularly ACL reconstruction with patellar tendon autograft, total knee arthroplasty
3. Prior corticosteroid injection: Into or around patellar tendon

Systemic/Metabolic Factors:

1. Chronic kidney disease: Especially if on dialysis (secondary hyperparathyroidism, beta-2 microglobulin amyloidosis)
2. Diabetes mellitus: Non-enzymatic glycation of collagen, reduced tensile strength
3. Rheumatoid arthritis: Inflammatory arthropathy with synovitis affecting tendon
4. Systemic lupus erythematosus: Autoimmune collagen disease
5. Hyperparathyroidism: Calcium deposition within tendon substance
6. Gout: Urate crystal deposition causing tendon inflammation

Pharmacological:

1. Corticosteroids (systemic or local): Impaired collagen synthesis, reduced fibroblast proliferation, direct catabolic effect on tendon [9]
2. Fluoroquinolones: FDA black-box warning for tendon rupture risk (mechanism: upregulation of matrix metalloproteinases) [10]
3. Anabolic steroids: Used by athletes; paradoxically weaken tendons despite strengthening muscle
4. Statins: Proposed association (conflicting evidence)

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3. Pathophysiology

Functional Anatomy of the Extensor Mechanism

The knee extensor mechanism is a complex biomechanical system consisting of:

1. Quadriceps muscle group (rectus femoris, vastus medialis, vastus lateralis, vastus intermedius)
2. Quadriceps tendon (convergence of four muscle bellies)
3. Patella (largest sesamoid bone; increases mechanical advantage by lengthening moment arm)
4. Patellar tendon/ligament (connects inferior pole of patella to tibial tubercle)
5. Medial and lateral retinacula (expansions from vasti providing dynamic stabilization)

Patellar Tendon Detailed Anatomy:

• Origin: Inferior pole of patella (30mm wide insertion)
• Insertion: Tibial tubercle (25mm wide insertion)
• Length: Approximately 50mm (varies with patient height; Insall-Salvati ratio maintained)
• Thickness: 4-6mm
• Blood supply: Branches from inferior genicular arteries; relatively avascular central zone (predisposes to degeneration and rupture)
• Innervation: Sensory from infrapatellar branch of saphenous nerve

Biomechanical Function:

• Transmits quadriceps muscle force to tibia to extend knee
• Normal tensile forces during activities:
  • "Walking: 2-3× body weight"
  • "Stair climbing: 4-5× body weight "
  • "Jumping/landing: 10-15× body weight"
• Peak stress occurs during eccentric loading (muscle lengthening while contracting)

Mechanism of Rupture

Biomechanical Failure: Rupture occurs when applied tensile force exceeds the ultimate tensile strength of the tendon. In healthy tendon, this requires force > 15× body weight (rarely achieved). However, pre-existing tendon degeneration reduces tensile strength by 50-75%, making rupture possible during routine athletic activities. [7]

The Eccentric Overload Paradigm: During landing from a jump:

1. Quadriceps contracts maximally (attempting to decelerate body)
2. Simultaneously, knee rapidly flexes (body weight driving knee into flexion)
3. Tendon subjected to eccentric tensile load (stretching while under tension)
4. If force exceeds tendon strength → catastrophic failure at weakest point

Sites of Rupture (in order of frequency):

1. Proximal insertion (inferior pole of patella): 75-80% of cases [7]
2. Mid-substance: 15-20% (often associated with pre-existing tendinopathy)
3. Distal insertion (tibial tubercle): 5% (more common as avulsion fracture in adolescents)

Partial vs. Complete Rupture:

• Complete rupture: Both central tendon substance AND medial/lateral retinacula disrupted → complete loss of active extension
• Partial rupture: Central substance torn but retinacula intact → weak but present active extension (can perform SLR with extensor lag)

Tendon Degeneration: The "Failed Healing Response"

Chronic tendinopathy preceding rupture is characterized by:

• Mucoid degeneration: Accumulation of glycosaminoglycans
• Fibrillar disorganization: Loss of parallel collagen alignment
• Neovascularization: Abnormal vessel ingrowth
• Cellular changes: Increased cellularity, chondrocyte-like cells
• Calcification: Dystrophic calcium deposition
• Absence of inflammatory cells: This is a failed healing response, not inflammation [18]

The "Degenerative Cascade": Repetitive microtrauma → collagen microtears → attempted healing → abnormal collagen deposition → further mechanical weakening → macroscopic failure

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4. Clinical Presentation

History

Mechanism:

• Sudden onset during athletic activity (landing from jump, cutting maneuver, deceleration)
• Often history of preceding knee pain (chronic patellar tendinopathy) in 40-70% of cases
• May report previous episodes of tendon pain (prodromal symptoms)

Symptoms at Time of Injury:

• Audible "pop" or "snap": Frequently reported (though not universal)
• Immediate severe pain: Localized to anterior knee, infrapatellar region
• Immediate giving way: Inability to bear weight or knee buckles
• Sensation of "something tearing": Patient may describe feeling tendon separate
• Rapid swelling: Hemarthrosis develops within minutes to hours

Functional Deficit:

• Cannot extend knee from flexed position
• Cannot perform straight leg raise
• Cannot walk normally: If ambulatory, uses compensatory "stiff-leg" gait
• Cannot ascend/descend stairs

Examination Findings

Inspection:

• Patella alta: High-riding patella (best appreciated by comparing to contralateral side)
• Visible swelling: Anterior knee effusion/hemarthrosis
• Ecchymosis: May develop over 24-48 hours (infrapatellar region)
• Altered knee contour: Loss of normal patellar tendon prominence
• Suprapatellar bulge: Quadriceps remains contracted, pulling patella proximally

Palpation:

• Palpable gap: Defect in infrapatellar region (PATHOGNOMONIC if present)
  • "Timing critical: Gap may be palpable acutely (first 1-2 hours) but obscured once hemarthrosis develops"
  • Best palpated with knee in extension and quadriceps relaxed
• Tenderness: Marked tenderness at rupture site
• Patella mobility: Abnormally increased superior mobility of patella

Functional Testing:

Straight Leg Raise (SLR) Test ⭐ MOST IMPORTANT CLINICAL TEST:

• Patient supine, knee fully extended
• Instruct to lift heel off bed while keeping knee straight
• Complete rupture: Cannot perform SLR (patella moves proximally, tibia does not move)
• Partial rupture: Can perform SLR with extensor lag (weak, painful, incomplete extension)

Important Caveat: Pain inhibition from hemarthrosis can cause false-positive (inability to SLR despite intact extensor mechanism). If diagnostic uncertainty:

1. Aspirate hemarthrosis
2. Inject 10-20ml local anesthetic (1% lignocaine)
3. Repeat SLR test

Active Extension Test:

• Patient seated, knee flexed to 90°
• Attempt active knee extension against gravity
• Complete rupture: Cannot extend at all (or minimal extension from intact retinacula)
• Partial rupture: Weak extension with extensor lag

Modified Active Extension Test (gravity eliminated):

• Patient supine, examiner passively flexes knee
• Attempt active extension in horizontal plane (gravity eliminated)
• May demonstrate small degree of active extension from intact medial/lateral retinacula even with complete central tendon rupture

Special Considerations

Bilateral Ruptures:

• Rare (5% of all patellar tendon ruptures) but important
• Always investigate for systemic disease: renal failure, hyperparathyroidism, SLE, corticosteroid use
• Often occur with minimal trauma (e.g., rising from chair) due to severe underlying tendon pathology [13]

Open Ruptures:

• Associated laceration or penetrating trauma
• Risk of infection
• Surgical emergency: Requires urgent irrigation, debridement, repair

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5. Investigations

Plain Radiography

Lateral Knee X-ray (MOST IMPORTANT INITIAL IMAGING):

Primary Sign: Patella Alta

• Superior displacement of patella relative to femoral trochlea
• Best assessed using Insall-Salvati Ratio: [19]

Insall-Salvati Ratio Calculation:

• Ratio = Length of Patellar Tendon (LT) ÷ Length of Patella (LP)
• LT: Distance from inferior pole of patella to tibial tubercle insertion
• LP: Maximum diagonal length of patella

Interpretation:

• Normal: 0.8 - 1.2 (mean = 1.0)
• Patella Alta (patellar tendon rupture): > 1.2
• Patella Baja (quadriceps rupture or scarring): less than 0.8

Alternative Methods:

• Modified Insall-Salvati: Uses articular surface of patella (more reliable in partial tears)
• Caton-Deschamps Index: Patellar articular surface to tibial plateau
• Blackburne-Peel Ratio: Articular surface to tibial plateau line

Secondary Signs:

• Avulsion fracture: Small bone fragment from inferior pole of patella
• Soft tissue swelling: Anterior knee effusion
• Obliteration of infrapatellar fat pad: Secondary to hematoma

AP X-ray:

• Typically normal (rupture is anteroposterior injury)
• May show associated injuries (patella fracture, tibial plateau fracture)

Skyline/Sunrise View:

• Generally not helpful for diagnosing patellar tendon rupture
• May show associated patellofemoral pathology

Ultrasound

Advantages:

• Rapid, bedside/point-of-care imaging
• No radiation
• Dynamic assessment: Can assess gap with knee flexion/extension
• Cost-effective
• Useful in emergency department for rapid diagnosis

Findings:

• Complete rupture: Complete fiber discontinuity, gap filled with hematoma
• Partial rupture: Partial fiber disruption, thinning, increased echogenicity
• Tendon retraction: Proximal stump retracted superiorly
• Hematoma: Anechoic or hypoechoic fluid collection

Limitations:

• Operator-dependent (requires experienced sonographer)
• Limited soft tissue detail compared to MRI
• Difficult to assess retinacular integrity (medial/lateral extent of tear)

Magnetic Resonance Imaging (MRI)

Gold Standard for Detailed Assessment [20]

Indications:

• Confirmation of diagnosis if uncertainty on clinical examination and X-ray
• Differentiate complete vs. partial tear
• Pre-operative planning (assess tendon quality, retraction distance, retinacular involvement)
• Chronic presentations (assess degree of degeneration, scarring, feasibility of primary repair)
• Assess associated injuries (meniscal tears, cruciate ligament injuries, bone bruising)

MRI Protocol:

• T1-weighted: Anatomical detail, distinguish tendon from surrounding fat
• T2-weighted/STIR: Fluid-sensitive; highlights tendon discontinuity, edema, hematoma
• Proton density: Best for tendon internal architecture

Findings:

Complete Rupture:

• Complete fiber discontinuity on sagittal images
• Tendon gap filled with high T2 signal (hematoma/edema)
• Proximal tendon stump retraction
• Wavy tendon morphology (loss of normal taut appearance)
• Patella alta
• Disruption of medial and lateral retinacula

Partial Rupture:

• Partial fiber disruption (some intact fibers)
• Tendon thickening and increased T2 signal (edema/hemorrhage)
• Maintained tendon continuity (even if attenuated)
• Intact retinacula

Chronic Tendinopathy (Pre-rupture Degeneration):

• Thickened tendon (> 7mm)
• Increased intratendinous signal on T1 and T2 (mucoid degeneration)
• Loss of normal hypointense signal (fibrillar disorganization)

Associated Findings:

• Bone marrow edema: Inferior pole of patella, tibial tubercle
• Quadriceps muscle atrophy: May develop rapidly post-injury
• Intra-articular pathology: Meniscal tears, ACL injury (if associated trauma)

Laboratory Investigations

Not routinely required for diagnosis of patellar tendon rupture.

Consider in specific scenarios:

Bilateral Ruptures or Atraumatic Rupture:

• Renal function: Urea, creatinine, eGFR (chronic kidney disease)
• Parathyroid hormone (PTH): Secondary hyperparathyroidism
• Calcium and phosphate: Hyperparathyroidism, renal osteodystrophy
• Autoimmune screen: ANA, ENA, anti-dsDNA (SLE), RF, anti-CCP (rheumatoid arthritis)
• HbA1c: Diabetes mellitus
• Serum urate: Gout

Pre-operative Workup:

• Routine pre-anesthetic assessment as per institutional protocol
• Particularly if patient has known comorbidities

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6. Management

Initial Emergency Department Management

Assessment:

1. History and examination (confirm diagnosis clinically)
2. Neurovascular examination (document distal pulses, sensation, motor function)
3. Plain radiographs (lateral knee to confirm patella alta)
4. Analgesia (IV or oral opioids as required)

Immediate Management:

1. Knee immobilization: Full-length hinged knee brace or cylinder cast in full extension (prevents further tendon retraction)
2. Ice and elevation: Reduce swelling
3. Analgesia: Multimodal (paracetamol, NSAIDs, opioids)
4. Non-weight bearing: Crutches, avoid weight bearing on affected limb
5. Urgent orthopedic referral: For definitive surgical management

Timeframe: Ideally refer to orthopedic surgery within 24-48 hours for surgical planning.

Definitive Management: Surgical Repair

Indications for Surgery:

• ALL complete patellar tendon ruptures (operative management is standard of care) [1,2]
• Partial ruptures with > 50% tendon involvement or functional deficit

Non-operative management is rarely indicated and limited to:

• Partial tears with intact active extension and minimal extensor lag
• Patients unfit for surgery (severe medical comorbidities)
• Patient declines surgery

Surgical Timing

Acute Repair (less than 2-3 Weeks from Injury): OPTIMAL

• Tendon ends have not yet retracted significantly
• Minimal scar tissue formation
• Direct end-to-end repair feasible
• Best functional outcomes [5]

Subacute (3-6 Weeks): CHALLENGING

• Moderate tendon retraction
• Early scar formation
• May require mobilization of proximal stump (quadriceps recession)
• Primary repair still usually possible

Chronic (> 6 Weeks): DIFFICULT

• Significant tendon retraction (proximal stump may be 5-10cm proximally displaced)
• Dense scar tissue
• Tendon atrophy and degeneration
• Primary end-to-end repair usually impossible
• Requires reconstruction (allograft, autograft, or augmentation techniques) [21]

Surgical Principle: "The Earlier, the Better" — Delay worsens outcomes exponentially.

Surgical Techniques

1. Primary End-to-End Repair (Acute Ruptures)

Approach:

• Midline longitudinal incision over anterior knee (10-12cm)
• Evacuate hematoma
• Identify proximal and distal tendon stumps
• Debride devitalized tissue (minimal debridement to preserve length)

Repair Methods:

A. Transosseous Suture Technique (GOLD STANDARD) [8]

Principle: Drill longitudinal tunnels through patella; pass sutures from tendon through tunnels; tie over superior pole.

Technique:

1. Drill 3 parallel longitudinal tunnels through patella (2-3mm drill bit)
   • 1 central, 1 medial, 1 lateral
   • Entry: Inferior pole; Exit: Superior pole
2. Prepare tendon: Krackow locking stitch configuration using heavy non-absorbable suture (#5 FiberWire or Ethibond)
   • Krackow: Multiple locking loops along medial and lateral borders of tendon providing robust purchase [8]
3. Pass sutures through tunnels: Use suture passer or wire loop
4. Tie sutures over superior pole of patella with knee in full extension (ensure appropriate tendon length — compare to contralateral side)
5. Repair retinaculum: Absorbable suture (medial and lateral expansions)

Advantages: Strong, reliable fixation; no implant removal required; gold standard with extensive literature support

Disadvantages: Technically demanding; risk of patella fracture during drilling; longer operative time

B. Suture Anchor Repair

Principle: Insert bone anchors into inferior pole of patella; pass sutures through tendon; tie to anchor sutures.

Technique:

1. Insert 2-4 suture anchors into inferior pole of patella (follow manufacturer's guidelines)
2. Prepare tendon: Krackow configuration using anchor sutures
3. Tie sutures with knee in extension

Advantages: Faster technique; no transosseous drilling (less risk of patella fracture); biomechanically equivalent to transosseous repair

Disadvantages: Higher cost; potential for anchor pullout; implant remains in situ

C. Augmentation Techniques (Selected Cases)

Indications: Poor tendon quality, chronic tears, revision surgery

Options:

1. Cerclage wire: Protective tension band (historical; rarely used now due to need for removal and complications)
2. Suture augmentation: Figure-of-8 or box stitch using heavy suture passed through quadriceps tendon, around patella, through patellar tendon
3. Synthetic augmentation: Mersilene tape, FiberTape
4. Biological augmentation: Autograft semitendinosus tendon weave

2. Chronic Patellar Tendon Reconstruction

Indications: Ruptures > 6 weeks old with significant retraction where primary repair impossible

Challenges:

• Tendon gap too large for direct repair
• Tendon degeneration and poor tissue quality
• Quadriceps contracture and patella alta
• Scar tissue

Options:

A. Quadriceps Turndown/V-Y Advancement [21]

• Lengthens extensor mechanism by creating V-Y flap in quadriceps tendon
• Allows patella to be advanced distally to bridge gap

B. Achilles Tendon Allograft

• Calcaneal bone block into tibial tubercle (screw fixation)
• Tendon woven through patella (transosseous or anchor fixation)
• Strong reconstruction option

C. Autograft Reconstruction

• Semitendinosus/gracilis harvest
• Hamstring tendons woven through patella and fixed to tibial tubercle

D. Synthetic Scaffolds

• Emerging technology; limited long-term data

Intra-operative Considerations

Tendon Length Restoration:

• Critical to restore normal patellar height
• Use Insall-Salvati ratio or compare to contralateral knee
• Fluoroscopy: Intraoperative lateral X-ray to confirm patella position before final suture tying
• Over-tightening → patella baja, restricted flexion, patellofemoral pain
• Under-tightening → residual patella alta, extensor lag

Retinacular Repair:

• Medial and lateral retinacula must be repaired (absorbable suture)
• Provides secondary stabilization
• Reduces stress on primary tendon repair

Closure:

• Meticulous hemostasis (reduce hematoma formation)
• Layered closure (retinaculum, subcutaneous, skin)
• Drain often used (remove at 24-48 hours)

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7. Rehabilitation

The Rehabilitation Paradox

Competing Goals:

1. Protect the repair: Avoid tensile stress that could cause re-rupture
2. Prevent stiffness: Mobilize early to avoid arthrofibrosis (major complication)

Solution: Protected early motion protocols have replaced historical cast immobilization. Modern evidence supports early passive range of motion with delayed active loading. [22]

Rehabilitation Protocol

Phase 1: Protection (Weeks 0-2)

Goals: Protect repair, control swelling, maintain quadriceps activation

Immobilization:

• Hinged knee brace locked in full extension (0°)
• Remove brace only for wound care and gentle passive motion

Weight Bearing:

• Non-weight bearing (NWB) or touch-toe weight bearing (TTWB)
• Bilateral crutches

Exercises:

• Ankle pumps: Prevent DVT, maintain calf pump
• Quadriceps isometrics: Gentle static quadriceps sets (no resistance)
• Passive knee flexion: 0-30° (therapist-assisted; NO active flexion)
• SLR in brace: Locked in extension

Precautions: NO active knee flexion; NO resisted extension; Brace locked at all times when ambulatory

Phase 2: Early Motion (Weeks 2-6)

Goals: Progressive passive flexion, initiate gentle quadriceps strengthening, prevent arthrofibrosis

Immobilization:

• Hinged brace unlocked for passive ROM, locked in extension for ambulation
• Continue brace 24/7 (can remove for exercise sessions)

Weight Bearing:

• Progress to partial weight bearing (PWB): 25% → 50% → 75% body weight (weeks 2-4-6)

Exercises:

• Passive knee flexion (therapist or patient-assisted):
  • "Weeks 2-4: 0-60°"
  • "Weeks 4-6: 0-90°"
• Active-assisted knee extension: Gravity-assisted, minimal load
• Closed-chain exercises: Mini-squats (0-30° flexion) with support
• Quadriceps strengthening: Isometrics, electrical muscle stimulation (EMS)
• SLR: Progress from brace-assisted to unassisted (as able)

Precautions: NO active knee flexion against resistance (flexion loads tendon); NO deep squats; Avoid resisted terminal extension (high patellofemoral load)

Phase 3: Strengthening (Weeks 6-12)

Goals: Restore full ROM, progressive quadriceps strengthening, wean brace, achieve independent ambulation

Immobilization:

• Wean brace (weeks 8-10): Initially remove for indoor ambulation, progress to brace-free
• Discontinue brace fully by week 10-12 (as tolerated)

Weight Bearing:

• Progress to full weight bearing (FWB) by week 8

Exercises:

• Full passive ROM: Achieve 0-120° flexion by week 12
• Active knee flexion: Now permitted (hamstring curls, stationary bike)
• Progressive resistance training: Leg press, closed-chain exercises
• Proprioception: Balance board, single-leg stance
• Gait re-education: Normalize gait pattern without limp

Functional Milestones:

• Week 6: FWB without aids
• Week 8: Symmetrical gait
• Week 12: Full ROM, 80% quadriceps strength

Phase 4: Return to Activity (Months 3-6)

Goals: Restore full strength, endurance, proprioception; return to sport/work

Exercises:

• Advanced strengthening: Plyometrics (gradual introduction)
• Cardiovascular: Swimming, cycling, elliptical
• Sport-specific training: Gradual progression (month 4+)

Return to Sport Criteria (Minimum 6 months post-op):

1. Full ROM (equal to contralateral)
2. Quadriceps strength ≥90% of contralateral (isokinetic testing)
3. Functional tests: Single-leg hop ≥90% of contralateral; Y-balance test symmetry
4. No pain or effusion with high-level activities
5. Psychological readiness: Confidence in knee stability

Typical Timeline:

• Month 3: Light jogging (straight-line)
• Month 4: Cutting, agility drills (low intensity)
• Month 6: Return to competitive sport (case-by-case)
• Month 9-12: Full unrestricted activity

Accelerated vs. Conservative Protocols

Evidence: Accelerated protocols (earlier motion, earlier weight bearing) show equivalent re-rupture rates with improved ROM and faster functional recovery compared to conservative immobilization. [22] Most modern surgeons favor accelerated rehabilitation.

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8. Complications

1. Re-rupture

Incidence: 2-5% (varies by repair technique, patient compliance, timing of surgery) [1,2]

Risk Factors:

• Poor tissue quality (chronic tendinopathy, systemic disease)
• Delayed surgical repair (> 3 weeks)
• Inadequate surgical technique (weak repair construct)
• Non-compliance with rehabilitation protocol
• Premature return to activity

Timing: Most re-ruptures occur in first 3 months (before tendon healing complete)

Management:

• Revision surgery (usually requires augmentation or reconstruction)
• Worse prognosis than primary repair

2. Arthrofibrosis (Knee Stiffness)

Incidence: 10-30% (most common complication) [23]

Presentation:

• Loss of knee flexion (typically less than 90-100°)
• Anterior knee pain
• Difficulty with stairs, sitting, squatting

Etiology:

• Intra-articular adhesions (scar tissue between quadriceps, patella, femur)
• Infrapatellar contracture syndrome: Scarring of fat pad and patellar tendon
• Prolonged immobilization (historical complication with cast immobilization)

Prevention:

• Early passive ROM (modern protocols)
• Aggressive physical therapy
• Patient education and compliance

Treatment:

• Conservative: Intensive physiotherapy (manual therapy, dynamic splinting)
• Manipulation under anesthesia (MUA): Force knee into flexion under GA (risk of patella fracture, tendon re-rupture)
• Arthroscopic adhesiolysis: Arthroscopic debridement of intra-articular scar tissue
• Open quadricepsplasty: For severe refractory cases (extensive surgical release)

3. Patella Baja (Low-Riding Patella)

Incidence: 5-15%

Etiology:

• Over-tightening during repair: Tendon repaired too short (Insall-Salvati ratio less than 0.8)
• Scar contracture: Tendon heals in shortened position

Consequences:

• Restricted flexion: Patella impinges on femoral trochlea
• Anterior knee pain: Abnormal patellofemoral contact pressures
• Patellofemoral arthritis: Long-term complication

Prevention:

• Intraoperative fluoroscopy: Confirm patellar height before tying sutures
• Compare to contralateral knee

Treatment:

• Proximal patella realignment: Surgical lengthening of patellar tendon (complex reconstructive procedure)

4. Quadriceps Weakness and Atrophy

Incidence: Near-universal (some degree of residual weakness even with successful repair)

Magnitude:

• Persistent 10-20% quadriceps strength deficit compared to contralateral side (even at 1-2 years post-op)
• Visible muscle atrophy (reduced thigh circumference)

Impact:

• Reduced sports performance
• Increased risk of re-injury
• Functional limitation for high-demand activities

Management:

• Aggressive strengthening: Progressive resistance training
• Neuromuscular electrical stimulation (NMES): Augment voluntary activation
• Long-term physical therapy: May continue 12-24 months post-op

5. Infection

Incidence: 1-3% (surgical site infection)

Risk Factors:

• Diabetes
• Immunosuppression
• Open rupture
• Prolonged surgery

Prevention:

• Pre-operative antibiotics (cefazolin or equivalent)
• Sterile technique
• Meticulous hemostasis and closure

Management:

• Superficial infection: Oral antibiotics
• Deep infection: Surgical debridement, IV antibiotics (risk of repair failure)

6. Extensor Lag

Definition: Inability to achieve full active knee extension despite passive full extension achievable

Incidence: 10-25% (usually mild: 5-10° lag)

Etiology:

• Incomplete tendon healing
• Quadriceps weakness/inhibition
• Residual tendon lengthening

Impact:

• Gait abnormality (circumduction, hyperextension thrust)
• Functional limitation (difficulty with stairs, rising from chair)

Management:

• Quadriceps strengthening
• Gait re-education
• Bracing (dynamic extension brace) if persistent

7. Patellofemoral Pain and Arthritis

Long-term complication (years post-injury)

Etiology:

• Altered patellofemoral mechanics: Even with successful repair, biomechanics may not fully normalize
• Patella baja or alta: Abnormal patellar tracking
• Cartilage damage: From initial injury or surgical intervention

Management:

• Activity modification
• Physical therapy (VMO strengthening, patellar taping)
• Analgesia (NSAIDs, intra-articular corticosteroid)
• Surgical options for severe cases (tibial tubercle osteotomy, patellofemoral arthroplasty)

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9. Prognosis

Functional Outcomes

With Acute Surgical Repair (less than 2 weeks):

• 80-90% good to excellent functional outcomes [1,2,5]
• Return to pre-injury activity level: 60-80%
• Return to competitive sport: 50-70% (varies by sport demands)

With Delayed or Chronic Repair (> 6 weeks):

• Significantly worse outcomes
• Return to pre-injury level: 30-50%
• Higher complication rates (stiffness, weakness, re-rupture)

Factors Predicting Better Outcome

Favorable Prognostic Factors:

1. Early surgical repair (less than 2 weeks) [5]
2. Younger age (less than 35 years)
3. Absence of systemic disease (no diabetes, renal disease, rheumatoid arthritis)
4. Acute traumatic rupture (vs. chronic degenerative)
5. Good surgical technique (strong repair, appropriate tendon length)
6. Excellent rehabilitation compliance
7. No smoking

Unfavorable Prognostic Factors:

1. Delayed diagnosis and treatment (> 3 weeks)
2. Poor tissue quality (chronic tendinopathy, systemic disease)
3. Bilateral ruptures
4. Re-rupture
5. Smoking (impairs tendon healing)
6. Older age (> 50 years)

Long-Term Outcomes

At 2 Years Post-Repair:

• ROM: 90-95% of patients achieve full ROM (0-130° flexion)
• Strength: Residual 10-20% quadriceps weakness common
• Patient satisfaction: 75-85% satisfied or very satisfied
• Return to work: > 90% return to pre-injury employment

At 5-10 Years:

• Chronic pain: 20-30% report persistent anterior knee pain
• Patellofemoral arthritis: Radiographic changes in 15-25%
• Activity limitation: 30-40% report some activity limitation compared to pre-injury

Sport-Specific Return to Play

Caveat: Return to sport does NOT necessarily mean return to pre-injury performance level. Many athletes experience reduced explosiveness, jumping ability, and confidence.

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10. Evidence & Guidelines

Key Clinical Studies

Repair Techniques: Multiple biomechanical and clinical studies demonstrate that transosseous suture repair and suture anchor repair have equivalent clinical outcomes and re-rupture rates. Choice depends on surgeon preference, cost considerations, and technical factors. [8]

Krackow Suture Configuration: Biomechanical studies confirm this locking stitch provides superior pullout strength compared to simple running or Bunnell-type stitches, making it the standard suture technique for tendon repairs. [8]

Early Motion Protocols: Systematic reviews and meta-analyses show that early passive motion (starting week 1-2) results in:

• Improved ROM (better flexion at 6-12 months)
• Reduced arthrofibrosis rates
• No increase in re-rupture rate compared to prolonged immobilization [22]

Timing of Surgery: Cohort studies consistently demonstrate that repair performed less than 2 weeks from injury has significantly better outcomes than delayed repair (> 4-6 weeks). Every week of delay worsens prognosis. [5]

Surgical Controversies

Augmentation: No high-quality evidence supports routine use of augmentation (wire cerclage, suture augmentation, mesh) in acute primary repairs. Reserve for high-risk cases (poor tissue quality, chronic tears, revision surgery).

Open vs. Minimally Invasive: Limited data on arthroscopic-assisted or mini-open techniques. Traditional open midline approach remains standard.

Guideline Recommendations

While no formal international guidelines exist specifically for patellar tendon rupture, consensus from orthopedic societies includes:

1. Immediate orthopedic referral for all suspected extensor mechanism ruptures
2. Surgical repair is standard of care for complete ruptures
3. Early surgery (less than 2-3 weeks) whenever medically feasible
4. Protected early motion rehabilitation protocols preferred over prolonged immobilization
5. Minimum 6 months before return to high-demand sports

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11. Differential Diagnosis

Quadriceps Tendon Rupture

Key Differences:

• Age: > 40 years (older population)
• Gap location: Suprapatellar (above patella)
• Patella position: Patella baja (low-riding) on X-ray (Insall-Salvati less than 0.8)
• Otherwise similar: Both have SLR failure, both require surgery

Patella Fracture

Key Differences:

• Mechanism: Direct blow to anterior knee (fall on knee)
• Imaging: Fracture line visible on X-ray
• Palpation: Crepitus, fracture gap (not soft tissue gap)
• SLR: May be intact if retinaculum intact (transverse fracture with undisplaced fragments)

Tibial Tubercle Avulsion

Key Differences:

• Age: Adolescents (open physes)
• Imaging: Avulsion fracture of tibial tubercle visible on X-ray
• Associated condition: Osgood-Schlatter disease background
• Treatment: ORIF (screw fixation of bone fragment) rather than tendon repair

Partial Patellar Tendon Tear

Key Differences:

• SLR: Intact (can perform SLR, though may have extensor lag)
• Imaging: MRI shows partial fiber disruption with intact fibers remaining
• Treatment: Often non-operative (brace, rehabilitation) unless > 50% torn

Acute Patellar Tendinopathy (Jumper's Knee)

Key Differences:

• Onset: Gradual (chronic repetitive microtrauma), NOT acute rupture
• SLR: Normal (full active extension)
• Imaging: MRI shows tendon thickening, signal change, but no discontinuity
• Treatment: Non-operative (activity modification, eccentric exercises, PRP)

Acute Knee Effusion/Hemarthrosis (Other Causes)

ACL rupture, meniscal tear, tibial plateau fracture can all cause acute swelling and pain limiting knee function. However, active knee extension is preserved (can perform SLR). Always assess extensor mechanism integrity in acute knee trauma.

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12. Prevention Strategies

Primary Prevention (Pre-Injury)

Athlete Education:

• Recognize prodromal symptoms of patellar tendinopathy (early intervention before progression to rupture)
• Appropriate training load management (avoid sudden increases in volume/intensity)
• Cross-training to reduce repetitive loading

Treatment of Patellar Tendinopathy:

• Eccentric strengthening programs: Decline squat protocols reduce tendinopathy progression [18]
• Activity modification: Reduce high-impact loading during symptomatic periods
• PRP/orthobiologics: Emerging evidence for chronic tendinopathy (quality of evidence variable)

Medication Awareness:

• Avoid fluoroquinolones in athletes with tendon pathology (use alternative antibiotics)
• Minimize corticosteroid injections: Especially near patellar tendon (systemic corticosteroids also increase risk)
• Educate patients on tendon rupture risk with systemic corticosteroids

Management of Systemic Risk Factors:

• Optimize diabetes control (reduce glycation-related tendon damage)
• Manage chronic kidney disease (parathyroid control, avoid calcium-phosphate dysregulation)
• Treat inflammatory arthropathies (disease-modifying therapy)

Secondary Prevention (Post-Injury)

Prevent Re-rupture:

1. Strict adherence to rehabilitation protocol (patient education critical)
2. Gradual return to sport progression (minimum 6 months; criteria-based clearance)
3. Avoid premature loading (most re-ruptures occur months 2-4)
4. Biomechanical assessment: Address predisposing factors (muscle imbalance, poor landing mechanics)

Prevent Contralateral Rupture:

• Address systemic risk factors (investigate for metabolic disease if initial rupture atraumatic)
• Strengthen contralateral quadriceps (prevent compensatory overload during rehabilitation)
• Avoid fluoroquinolones and minimize corticosteroid use

Long-Term Monitoring:

• Annual follow-up for first 2-3 years (assess for complications, functional deficits)
• Surveillance for patellofemoral arthritis (may develop 5-10 years post-injury)

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13. Special Populations

Chronic Kidney Disease Patients

Epidemiology: CKD patients have 100-fold increased risk of spontaneous tendon ruptures (patellar and quadriceps) [13]

Pathophysiology:

• Secondary hyperparathyroidism (↑ PTH → calcium deposition in tendon)
• Beta-2 microglobulin amyloidosis (dialysis-related amyloidosis)
• Uremic toxins affecting collagen metabolism

Clinical Presentation:

• Often bilateral ruptures
• May occur with minimal trauma (rising from chair, minor stumble)
• Poor tissue quality noted at surgery

Management Considerations:

• Pre-operative optimization (dialysis timing, electrolyte correction)
• Expect difficult repair (poor tendon quality; may require augmentation/reconstruction)
• Higher complication rates (infection, delayed healing, re-rupture)
• Close multidisciplinary management (orthopedics + nephrology)

Patients on Systemic Corticosteroids

Risk: Dose-dependent (higher cumulative dose → higher rupture risk)

Surgical Considerations:

• Poor wound healing: Meticulous closure, consider delayed suture removal
• Infection risk: Prophylactic antibiotics, vigilant wound monitoring
• Tendon quality: Expect degenerative tissue requiring robust repair technique
• Augmentation often needed

Post-operative: Cannot abruptly stop corticosteroids (taper under medical supervision)

Athletes and High-Demand Patients

Expectations Management: Critical to counsel athletes that:

• Return to sport typically 9-12 months minimum
• May NOT return to pre-injury performance level (especially power/explosiveness)
• 30-40% do not return to pre-injury level of competition

Rehabilitation: More aggressive (earlier progression) but MUST still respect tissue healing timelines

Psychosocial Support: Higher rates of anxiety/depression related to prolonged recovery and uncertainty about return to sport

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14. Patient Education and Counseling

What Has Happened?

"The tendon that connects your kneecap to your shin bone has completely torn. This tendon is like a strong rope that transmits the power from your thigh muscles to your lower leg, allowing you to straighten your knee and walk, run, and jump. When it tears, the connection is broken and your leg cannot function properly."

Why Did This Happen?

"In most cases, this happens because the tendon was already weakened by wear and tear (tendinopathy) from repetitive activities. When you [landed from a jump/suddenly changed direction], the force was greater than the weakened tendon could handle. Sometimes medications (like steroids or certain antibiotics) or medical conditions (like kidney disease or diabetes) can weaken tendons. We will investigate if any underlying factors contributed to your injury."

Can It Heal Without Surgery?

"No. The torn ends of the tendon are pulled apart by your strong thigh muscles and will never heal back together on their own. Surgery is required to reconnect the tendon. Without surgery, you would have permanent difficulty walking, inability to climb stairs, and very limited knee function."

What Does the Surgery Involve?

"The surgery involves making an incision on the front of your knee, finding the torn tendon ends, and sewing them back together using very strong sutures. We typically thread the sutures through tunnels drilled in your kneecap to create a solid repair. The procedure takes 1-2 hours and is performed under general or spinal anesthesia. Most patients go home the same day or the next day."

What Is the Recovery Timeline?

Important: This is a slow recovery (6-12 months to return to normal activities).

• Weeks 0-6: Knee brace worn continuously; limited weight bearing; gentle passive movement only
• Weeks 6-12: Brace weaned off; walking without crutches; active exercises begin
• Months 3-6: Progressive strengthening; return to light jogging and daily activities
• Months 6-12: Gradual return to sports and high-demand activities (if cleared by surgeon and physiotherapist)

What Are the Risks?

Surgery Risks (Standard):

• Infection (1-3%)
• Blood clots (DVT/PE) - prevention with blood thinners
• Anesthetic risks
• Nerve or blood vessel injury (rare)

Specific to This Surgery:

• Re-rupture (2-5%): Tendon tears again (usually from falling or not following rehabilitation protocol)
• Stiffness (10-30%): Loss of knee bending (may require further physiotherapy or procedures)
• Persistent weakness (very common): Most patients have some residual thigh muscle weakness even after successful repair
• Chronic pain (20-30%): Ongoing discomfort around the kneecap
• Kneecap too low or too high (if repair too tight or too loose)

What Can I Do to Maximize My Recovery?

1. Follow the rehabilitation protocol strictly: This is THE most important factor in your recovery
2. Attend all physiotherapy appointments: Consistent, supervised therapy prevents complications
3. Do NOT rush: Returning to activities too early is the main cause of re-rupture
4. Stop smoking (if applicable): Smoking significantly impairs tendon healing
5. Optimize your overall health: Control diabetes, maintain healthy weight, eat nutritious diet
6. Be patient: This is a marathon, not a sprint. Most patients continue improving for 12-18 months.

What If I Don't Have Surgery?

Without surgery, you will have permanent severe disability:

• Inability to walk normally (need walking aids)
• Cannot climb stairs
• Cannot drive safely
• Cannot return to work (if job involves walking/standing)
• Cannot participate in sports or recreational activities
• Progressive muscle wasting in your thigh

Surgery is not optional for this injury.

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15. Examination Focus (MRCS/FRCS/FRACS Viva)

Core Knowledge Questions

Q1: How do you clinically differentiate patellar tendon rupture from quadriceps tendon rupture?

A: Both present with inability to perform straight leg raise (SLR), but differ in:

Q2: What is the Insall-Salvati ratio and how is it calculated?

A: A radiographic measurement on lateral knee X-ray to assess patellar height:

Ratio = Patellar Tendon Length (LT) ÷ Patellar Length (LP)

• LT: Distance from inferior pole of patella to tibial tubercle insertion
• LP: Maximum diagonal length of patella
• Normal: 0.8 - 1.2 (mean = 1.0)
• Patella alta (patellar tendon rupture): > 1.2
• Patella baja (quadriceps rupture): less than 0.8

Q3: Describe the surgical technique for acute patellar tendon repair.

A: Transosseous repair technique (gold standard):

1. Approach: Midline longitudinal incision over anterior knee
2. Evacuate hematoma and identify tendon stumps
3. Prepare patella: Drill 3 parallel longitudinal tunnels (2-3mm) through patella from inferior to superior pole
4. Prepare tendon: Place Krackow locking stitches along medial and lateral borders of tendon using #5 non-absorbable suture (FiberWire/Ethibond)
5. Pass sutures through patellar tunnels (inferior to superior)
6. Tie sutures over superior pole of patella with knee in full extension (check patellar height with fluoroscopy; compare to contralateral side)
7. Repair retinacula (medial and lateral) with absorbable sutures
8. Close in layers; consider drain

Alternative: Suture anchor repair (biomechanically equivalent; faster but more expensive)

Q4: What is the Krackow suture technique and why is it used?

A: A locking loop suture configuration for tendon repair that provides superior pullout strength.

Technique:

• Multiple interlocking loops placed along the longitudinal axis of the tendon
• Each loop "locks" by passing through the previous loop before re-entering the tendon
• Creates secure purchase in degenerative or poor-quality tendon tissue
• Distributes tensile load across multiple loops (prevents "cheese-wiring" through tendon)

Why used: Standard of care for tendon repairs because it is biomechanically strongest suture technique for tendon fixation.

Q5: What medications are associated with increased risk of tendon rupture?

A:

1. Fluoroquinolones (ciprofloxacin, levofloxacin):

   • Mechanism: ↑ matrix metalloproteinases → collagen degradation
   • FDA black-box warning for tendon rupture risk
   • Risk persists for months after cessation

2. Corticosteroids (systemic or local injection):

   • Mechanism: ↓ collagen synthesis, ↓ fibroblast proliferation, direct catabolic effect
   • Dose-dependent risk
   • Local injection near tendon particularly high risk

3. Anabolic steroids: Used by athletes; weaken tendons despite strengthening muscle

4. Statins: Proposed association (evidence conflicting; less clear than above)

Q6: What are the key complications following patellar tendon repair and how are they managed?

A:

Q7: Why is early surgical repair critical?

A: Time-dependent deterioration in surgical outcomes:

Acute (less than 2 weeks): OPTIMAL

• Tendon ends have minimal retraction
• Primary end-to-end repair feasible
• Best functional outcomes (80-90% good/excellent)

Chronic (> 6 weeks): POOR

• Significant tendon retraction (5-10cm proximal migration)
• Dense scar formation
• Tendon degeneration and atrophy
• Primary repair usually impossible (requires complex reconstruction)
• Inferior outcomes (30-50% return to pre-injury level)

Principle: "Every week of delay worsens outcome."

Q8: What is the rehabilitation timeline and rationale?

A: Modern approach: Protected early motion (balance protecting repair vs. preventing stiffness)

Evidence: Early motion protocols have equivalent re-rupture rates but better ROM and lower stiffness compared to prolonged immobilization.

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16. Key Clinical Decision Points

Decision Point 1: Emergency Department Assessment

• Is this an extensor mechanism rupture? → Check SLR (cannot perform = ruptured)
• Which component is ruptured? → Age + gap location + X-ray (patella alta vs. baja)
• Is it open? → Urgent surgery if contaminated
• Is it bilateral? → Investigate for systemic disease

Decision Point 2: Surgical Planning

• Timing? → Acute (less than 2 weeks) = primary repair; Chronic (> 6 weeks) = reconstruction
• Repair technique? → Transosseous tunnels (gold standard) vs. suture anchors (faster, equivalent outcomes)
• Augmentation needed? → Yes if poor tissue quality, chronic tear, revision

Decision Point 3: Rehabilitation Progression

• When to unlock brace? → Week 2 (for passive ROM exercises)
• When to wean brace? → Weeks 8-10 (when achieving active extension without lag)
• When to return to sport? → Minimum 6 months + meet functional criteria (strength ≥90%, hop test ≥90%)

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17. References

1. Siwek CW, Rao JP. Ruptures of the extensor mechanism of the knee joint. J Bone Joint Surg Am. 1981;63(6):932-937. [Classic landmark study describing extensor mechanism ruptures]

2. Matava MJ. Patellar tendon ruptures. J Am Acad Orthop Surg. 1996;4(6):287-296. doi:10.5435/00124635-199611000-00001

3. Garner MR, Gausden E, Berger M, et al. Extensor mechanism injuries of the knee: Demographic characteristics and comorbidities from a review of 726 patient records. J Bone Joint Surg Am. 2015;97(19):1592-1596. doi:10.2106/JBJS.N.01318

4. Shah MK. Simultaneous bilateral patellar tendon rupture: Analysis of risk factors and systematic review of the literature. J Orthop Surg Res. 2012;7:35. doi:10.1186/1749-799X-7-35

5. Gilmore JH, Clayton-Smith ZJ, Aguilar M, et al. Traumatic extensor mechanism injuries of the knee: Timing of reconstruction and results. Knee. 2014;21(6):1186-1192. doi:10.1016/j.knee.2014.07.022

6. Clayton RAE, Court-Brown CM. The epidemiology of musculoskeletal tendinous and ligamentous injuries. Injury. 2008;39(12):1338-1344. doi:10.1016/j.injury.2008.06.021

7. Zernicke RF, Garhammer J, Jobe FW. Human patellar-tendon rupture. J Bone Joint Surg Am. 1977;59(2):179-183.

8. Gilmore JH, Clayton-Smith ZJ, Aguilar M, et al. Reconstruction techniques and clinical results of patellar tendon ruptures: Evidence today. Knee. 2015;22(3):148-155. doi:10.1016/j.knee.2014.10.001

9. Wong MW, Tang YN, Fu SC, et al. Triamcinolone suppresses human tenocyte cellular activity and collagen synthesis. Clin Orthop Relat Res. 2004;(421):277-281. doi:10.1097/01.blo.0000118184.83983.65

10. Khaliq Y, Zhanel GG. Fluoroquinolone-associated tendinopathy: A critical review of the literature. Clin Infect Dis. 2003;36(11):1404-1410. doi:10.1086/375078

11. Ramsey ML, Willms K, Rudzki JR, et al. Missed extensor mechanism injuries of the knee. Clin Orthop Relat Res. 2002;(404):197-202. doi:10.1097/00003086-200211000-00033

12. Hak DJ, Sanchez A, Malkani A. Extensor mechanism injuries of the knee. J Am Acad Orthop Surg. 2010;18(2):106-116. doi:10.5435/00124635-201002000-00006

13. Otani T, Saito M, Ito T, et al. Quadriceps and patellar tendon rupture in chronic renal failure. Clin Orthop Relat Res. 1989;(246):199-203.

14. Boudreaux BA, Rosenwasser MP, Lee SK. A review of bilateral tendon ruptures. J Hand Surg Am. 2014;39(11):2256-2259. doi:10.1016/j.jhsa.2014.07.042

15. Hsu H, Siwiec RM. Patellar Tendon Rupture. In: StatPearls. StatPearls Publishing; 2023. [Updated epidemiological data]

16. West JL, Keene JS, Kaplan LD. Early motion after quadriceps and patellar tendon repairs: Outcomes with single-surgeon protocol. Orthop J Sports Med. 2008;36(2):316-323. doi:10.1177/0363546507308192

17. Marder RA, Timmerman LA. Primary repair of patellar tendon rupture without augmentation. Am J Sports Med. 1999;27(3):304-307. doi:10.1177/03635465990270030701

18. Cook JL, Purdam CR. Is tendon pathology a continuum? A pathology model to explain the clinical presentation of load-induced tendinopathy. Br J Sports Med. 2009;43(6):409-416. doi:10.1136/bjsm.2008.051193

19. Insall J, Salvati E. Patella position in the normal knee joint. Radiology. 1971;101(1):101-104. doi:10.1148/101.1.101

20. Kaplan PA, Gehl RH, Dussault RG, et al. Bone contusions of the posterior lip of the medial tibial plateau (contrecoup injury) and associated internal derangements of the knee at MR imaging. Radiology. 1999;211(3):747-753. [MRI assessment principles]

21. Bushnell BD, Whitener GB, Rubright JH, et al. The use of suture anchors to repair the ruptured patellar tendon. J Bone Joint Surg Am. 2008;90(6):1271-1278. doi:10.2106/JBJS.G.00822

22. Erickson BJ, Mascarenhas R, Saltzman BM, et al. Is operative treatment of patellar tendon ruptures superior to nonoperative treatment? A systematic review of overlapping meta-analyses. Orthop J Sports Med. 2017;5(6):2325967117707721. doi:10.1177/2325967117707721

23. Rosso F, Bonasia DE, Cottino U, et al. Patellar tendon: From tendinopathy to rupture. Asia Pac J Sports Med Arthrosc Rehabil Technol. 2015;2(4):99-107. doi:10.1016/j.asmart.2015.07.001

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18. Additional Resources

For Clinicians:

• AAOS Clinical Practice Guidelines on Extensor Mechanism Injuries
• British Orthopaedic Association Standards for Trauma (BOAST)

For Patients:

• OrthoInfo (AAOS Patient Education): Patellar Tendon Tear
• NHS Patient Information: Knee Tendon Injuries

For Rehabilitation Professionals:

• Postoperative rehabilitation protocols (institution-specific)
• Criteria-based return to sport algorithms

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