Muscle and Tendon Injuries

Introduction

Muscle and tendon injuries collectively represent a substantial portion of musculoskeletal practice, both in the acute trauma setting and in chronic overuse presentations. The spectrum runs from the common muscle strain that resolves spontaneously with relative rest to the dramatic acute tendon rupture (Achilles, biceps, quadriceps, patellar) that requires recognition and prompt management to restore function. The classical concept of the “musculotendinous unit” links muscle and tendon as a single functional entity, with failure typically occurring at the weakest point of the unit — most commonly the myotendinous junction in muscle strains, the tendon midsubstance in degenerative ruptures, and the bony insertion in avulsion injuries. The principles of management share several recurring themes: distinguishing partial from complete injury, weighing operative versus non-operative management based on patient-specific factors, the role of imaging (with MRI as the principal modality), and the importance of structured rehabilitation in recovery. This chapter, drawing on Rockwood and Green’s Fractures in Adults, Apley & Solomon’s, Miller’s Review of Orthopaedics, and Dutton’s Orthopaedic Examination, addresses the principal muscle and tendon injuries encountered in orthopedic practice.

Muscle Injuries — Strains and Contusions

Classification of Muscle Strains Muscle strains are graded by the magnitude of the injury: Grade I (mild): Minor stretching of muscle fibers without macroscopic tear. Pain at rest or with use, but normal strength and range of motion. Resolution typically within 1 to 2 weeks. Grade II (moderate): Partial tear of the muscle with macroscopic disruption of some fibers. Significant pain, weakness, and reduced range of motion; palpable defect may be present. Recovery typically 4 to 8 weeks. Grade III (complete rupture): Complete tear of the muscle, often at the myotendinous junction. Inability to contract the muscle; palpable defect; substantial weakness. Recovery may be incomplete without surgical intervention in some sites. The classification by Mueller-Wohlfahrt et al. (2013) provides more sophisticated grading for elite athletes, distinguishing fatigue-induced injury, delayed-onset muscle soreness, functional muscle disorders, structural injury (minor partial muscle tear, moderate partial muscle tear, subtotal or complete muscle tear), and contusions. Common Sites and Mechanisms Hamstring strain is the most common muscle injury in sports, particularly in sprinting and high-speed running activities. The biceps femoris is the most commonly affected of the three hamstring muscles, with the proximal hamstring origin avulsion (at the ischial

tuberosity) being a distinct entity that may require operative repair. Recovery from hamstring strains is notoriously variable, with high recurrence rates if return to sport is rushed. Quadriceps strain typically affects the rectus femoris (the only quadriceps muscle to cross both the hip and knee joints, making it the most vulnerable to strain). The injury is common in kicking sports. Gastrocnemius strain (“tennis leg”) affects the medial head of the gastrocnemius at the myotendinous junction. The clinical presentation is sudden severe calf pain during athletic activity, with bruising and swelling of the calf. The injury must be distinguished from acute Achilles rupture and deep vein thrombosis. Adductor strain (“groin pull”) affects the adductor longus most commonly, with chronic adductor enthesopathy at the pubic insertion being a separate entity in athletes. Pectoralis major rupture is uncommon but occurs most often during eccentric loading in bench-press exercise. Operative repair is preferred in active patients to restore strength and cosmesis. Muscle Contusions Muscle contusions result from direct blunt trauma to the muscle, producing intramuscular bleeding and inflammation. The classical site is the anterior thigh (“charley horse”), produced by direct trauma during contact sports. The treatment is the RICE / POLICE protocol (with the principal modification being early protected loading rather than complete rest). Severe contusions may produce myositis ossificans — heterotopic ossification within the muscle, particularly in the quadriceps — recognized by progressive heterotopic ossification 2 to 6 weeks after injury. Management is rest, NSAIDs, and gentle range of motion; excision is reserved for mature heterotopic ossification (typically 12 to 18 months after injury) producing persistent functional limitation, with attention to the risk of recurrence.

Compartment Syndrome After Muscle Injury Compartment syndrome can follow muscle injury, particularly in patients on anticoagulation, in those with severe contusion of a closed compartment (anterior thigh, posterior compartment of leg), and after eccentric loading injuries. The same principles of recognition and treatment apply as discussed for compartment syndrome in fracture care (Topic Trauma-32 for vascular injuries and compartment syndrome in detail).

Achilles Tendon Rupture

Anatomy and Mechanism The Achilles tendon is the largest tendon in the body, formed by the convergence of the gastrocnemius (medial and lateral heads) and soleus muscles to a single tendon inserting on the posterior calcaneal tuberosity. The tendon has a relative avascular zone

approximately 2 to 6 cm proximal to the insertion, which is the site of most degenerative ruptures. The classical mechanism of Achilles rupture is sudden eccentric loading of a dorsiflexed foot — typically during athletic activity (sprinting, pivoting) or descending stairs. The patient is typically a male recreational athlete in the third to fifth decade, with a strong association between Achilles rupture and degenerative changes in the tendon related to age, repetitive microtrauma, and possibly underlying tendinopathy. Specific risk factors include fluoroquinolone antibiotic exposure (a well-recognized association), corticosteroid injection into or around the tendon, systemic corticosteroid use, and chronic Achilles tendinopathy. Clinical Assessment The classical presentation is sudden sharp pain in the posterior calf during athletic activity, often described as feeling “kicked” or “struck” in the leg. Inability to push off the affected leg is common. The clinical examination findings include: Palpable gap in the tendon (specific but not always present, particularly with thick patients or with proximal ruptures). Thompson test (Simmonds-Thompson sign): With the patient prone and the foot hanging off the table, squeezing the calf normally produces plantar flexion of the foot; absence of plantar flexion indicates Achilles rupture. The test has very high sensitivity and specificity for complete rupture. Matles test: With the patient prone and the knees flexed to 90 degrees, the affected foot will appear dorsiflexed compared with the contralateral side because of loss of resting tension in the Achilles tendon. Weakness or inability to perform single-leg heel raise: A useful functional test. Imaging is generally not required for diagnosis when the clinical examination is unequivocal. Ultrasound is the most cost-effective imaging modality and shows the gap and tendon discontinuity; MRI provides more detailed assessment of the tendon and the gap and is useful for chronic ruptures or for surgical planning. Treatment The management of acute Achilles rupture has been one of the most actively debated topics in orthopedic sports medicine. The principal options are: Operative repair: Direct end-to-end suture repair of the tendon through a posterior or paramedian approach, with various reinforcement techniques (Krackow stitch, Bunnell- type stitch). The historical advantage of operative repair has been a lower re-rupture rate (approximately 2 to 5 percent with operative versus 10 to 15 percent with conservative management in older series). The disadvantages include wound complications (5 to 10 percent), infection, sural nerve injury, and the morbidity of surgery.

Conservative (non-operative) management: Functional immobilization in a brace or boot with the foot in plantar flexion, progressing through reduced plantar flexion over 8 to 12 weeks with early controlled motion. Re-rupture rates have approached operative rates in modern protocols with early functional loading. The Wallace and other functional protocols have transformed conservative management from prolonged casting to early functional treatment. The contemporary evidence — multiple randomized trials and the Cochrane review — shows that with appropriate functional protocols, conservative management produces re- rupture rates similar to operative management (approximately 5 to 8 percent), with substantially lower complication rates. The current management trend is therefore toward non-operative functional management for most patients, with operative repair reserved for elite athletes (where slightly lower re-rupture rate may justify the operative risks), patients presenting late (more than 4 to 6 weeks after injury, where tendon retraction may preclude direct repair without augmentation), and patients with specific contraindications to functional treatment. Percutaneous repair has emerged as a middle-ground option, with smaller incisions and lower wound complication rates than open repair while maintaining the strength of operative repair. The technique uses jamshidi-style passers or specialized devices (Achillon, PARS) to deliver suture through small percutaneous incisions, achieving end-to- end repair with minimal soft-tissue dissection. Outcomes are reported as comparable to open repair with substantially lower wound complications and similar re-rupture rates. Chronic Achilles Rupture The chronic Achilles rupture (>4 to 6 weeks after injury) typically presents with weakness and inability to push off rather than acute pain. Direct end-to-end repair is often not feasible because of tendon retraction and gap formation; reconstructive options include V-Y advancement of the proximal Achilles, turn-down flap from the proximal Achilles, flexor hallucis longus (FHL) transfer (most commonly used because of the proximity of the FHL tendon to the Achilles and the strength of the FHL), and gastrocnemius or fascia lata allograft reconstruction.

Patellar Tendon and Quadriceps Tendon Rupture

Patellar Tendon Rupture The patellar tendon connects the inferior pole of the patella to the tibial tubercle, providing the final pathway of the extensor mechanism. Patellar tendon rupture typically occurs in patients under 40 years, often during sports activities, with the typical pattern being avulsion from the inferior pole of the patella rather than midsubstance rupture. Risk factors include systemic disease (renal failure, diabetes), corticosteroid use (systemic or local injection), and prior tendinopathy. The clinical presentation is sudden anterior knee pain during a quadriceps contraction (jumping, landing, slipping), with inability to extend the knee against gravity, a palpable defect at the inferior pole of the patella, and patella alta (high-riding patella) on

lateral radiograph. The Insall-Salvati ratio (the ratio of patellar tendon length to patella length) is increased; the normal ratio is 0.8 to 1.2, with the ruptured side typically greater than 1.2. Treatment is urgent operative repair through a midline anterior approach. The technique uses transosseous sutures or suture anchors to reattach the patellar tendon to the inferior pole of the patella. Augmentation with cerclage wire or bioabsorbable cable may be added in selected cases to protect the repair. Postoperative immobilization in extension for 2 to 6 weeks followed by progressive range of motion produces good outcomes in most patients. Chronic patellar tendon rupture (>3 to 6 weeks) is more challenging because of quadriceps contracture and tendon retraction. Reconstruction options include hamstring autograft, allograft, or local soft-tissue augmentation; outcomes are inferior to those of acute repair.

Quadriceps Tendon Rupture The quadriceps tendon is the convergence of the four quadriceps muscles (rectus femoris, vastus lateralis, vastus medialis, vastus intermedius) just proximal to the patella. Quadriceps tendon rupture typically occurs in older patients (over 40 years), often with degenerative changes or systemic risk factors (corticosteroids, renal failure, diabetes, gout). The mechanism is forceful eccentric quadriceps contraction. The clinical presentation is similar to patellar tendon rupture but with the palpable defect superior to the patella, and patella baja (low-riding patella) on lateral radiograph (with reduced Insall-Salvati ratio). Inability to extend the knee against gravity is the key functional sign. Treatment is urgent operative repair through an anterior approach. The technique uses transosseous sutures through the patella to reattach the quadriceps tendon. Acute repair within 2 to 6 weeks produces good outcomes; chronic ruptures require reconstruction with hamstring autograft, V-Y plasty, or allograft.

Biceps Tendon Rupture

Distal Biceps Tendon Rupture The distal biceps tendon rupture is most commonly seen in middle-aged men with sudden eccentric loading of the elbow in a flexed and supinated position. The clinical presentation is sudden pain in the antecubital fossa, ecchymosis tracking distally along the forearm, palpable defect in the distal biceps, and reduced supination strength (the principal functional deficit, since pronation strength is preserved through the pronator teres and quadratus). The hook test (Ruland, 2005) is the standard clinical test: with the patient’s elbow flexed to 90 degrees and the forearm fully supinated, the examiner attempts to “hook” the finger under the distal biceps tendon from the lateral side. A normal biceps tendon allows the

finger to hook under it; in distal biceps rupture, the finger encounters no tendinous structure. The test has high sensitivity and specificity for complete rupture. Treatment is urgent operative repair in patients valuing supination strength (most patients with active occupations or sporting interests). The traditional two-incision Boyd- Anderson approach (anterior and posterior incisions) and the modern single-incision anterior approach with cortical button fixation through the radial tuberosity are the principal techniques. The posterior interosseous nerve is at risk in either approach but particularly in the single-incision technique; meticulous identification and protection are essential. Non-operative management results in approximately 30 to 50 percent loss of supination strength but is acceptable in low-demand patients. Proximal (Long Head) Biceps Tendon Rupture The proximal long head of the biceps tendon rupture produces the classical “Popeye sign” — distal migration of the muscle belly producing a prominent bulge in the lower arm with apparent loss of the proximal arm contour. The rupture is typically degenerative and is often associated with rotator cuff pathology. Most proximal long head biceps ruptures are treated non-operatively, with no significant functional consequences (the short head of biceps preserves most of the biceps function, and supination strength is largely maintained). The cosmetic Popeye deformity may be a concern for some patients. Operative management (tenodesis or tenotomy) is reserved for symptomatic patients or those with associated rotator cuff pathology requiring surgery.

Rotator Cuff Tears

Anatomy and Classification The rotator cuff comprises four muscles (supraspinatus, infraspinatus, subscapularis, teres minor) and their tendons converging on the proximal humerus. The supraspinatus is the most commonly torn cuff component, particularly at its insertion on the greater tuberosity. The tears are classified by: Mechanism: Acute (traumatic) versus chronic (degenerative). Size: Small (less than 1 cm), medium (1 to 3 cm), large (3 to 5 cm), and massive (greater than 5 cm or involving two or more tendons). Depth: Partial thickness (articular-sided, bursal-sided, or intratendinous) or full thickness. Pattern: U-shaped, L-shaped, crescent-shaped, longitudinal, or massive irreparable. The Goutallier classification of muscle quality on CT or MRI organizes fatty infiltration on a scale from 0 (normal) to 4 (more fat than muscle); higher Goutallier grades correlate with worse outcomes of operative repair and increasing irreparability.

Clinical Assessment Clinical assessment of suspected rotator cuff tear includes: Empty can test (Jobe test): Assessment of supraspinatus by resisted elevation in scapular plane with thumb down. Pain or weakness is a positive test. External rotation lag sign: With the elbow at the side and flexed 90 degrees, the patient’s externally rotated position is held by the examiner and then released; inability to maintain external rotation indicates infraspinatus or teres minor weakness. Hornblower’s sign: Inability to externally rotate with the arm abducted 90 degrees indicates posterior cuff (teres minor) weakness. Belly press test, lift-off test, bear hug test: Assessment of subscapularis function. Drop arm test: Inability to slowly lower the arm from full abduction indicates supraspinatus tear. Imaging includes plain radiographs (with attention to acromiohumeral interval — reduced in chronic massive tears, suggesting proximal migration of the humeral head from loss of cuff function — and bony spurring or os acromiale), ultrasound (operator- dependent but cost-effective for cuff evaluation), and MRI (the principal imaging modality, providing detailed assessment of tear morphology, muscle quality, and associated pathology).

Treatment of Rotator Cuff Tears Asymptomatic rotator cuff tears are common in the older population (incidence approximately 30 percent in patients over 60) and do not necessarily require treatment. Symptomatic partial thickness tears are typically treated with physical therapy, NSAIDs, and selective subacromial corticosteroid injection for 6 to 12 weeks before consideration of operative intervention. Symptomatic full thickness tears in patients with good muscle quality (Goutallier 0- 2) are candidates for arthroscopic repair. The technique uses suture anchors placed in the greater tuberosity bony footprint, with sutures passing through the tendon. Single-row versus double-row repair has been debated, with the double-row technique providing more anatomical footprint coverage but at greater complexity and cost; outcomes are broadly similar. Massive rotator cuff tears with reasonable muscle quality may be repairable with techniques including margin convergence (side-to-side suturing to reduce the tear size before footprint repair), superior capsule reconstruction (with fascia lata or allograft to reconstruct the cuff’s superior stabilizing effect on the humeral head), or tendon transfers (lower trapezius transfer for posterosuperior tears, latissimus dorsi for posterosuperior, pectoralis major for subscapularis tears).

Massive irreparable tears with poor muscle quality (Goutallier 3-4), particularly with cuff tear arthropathy (advanced glenohumeral arthritis with proximal humeral migration), are typically managed with reverse total shoulder arthroplasty (Grammont design), which provides reliable restoration of elevation through deltoid leverage independent of the rotator cuff (see Topic Trauma-13 for the reverse arthroplasty discussion).

Other Important Tendon Injuries

Tibialis Posterior Dysfunction Posterior tibial tendon dysfunction (PTTD) is the most common cause of acquired adult flatfoot, with progressive failure of the tibialis posterior tendon producing loss of medial longitudinal arch support and progressive valgus and abduction deformity of the foot. The classification by Johnson and Strom (1989) has been expanded by Bluman and others: Stage I: Tendinitis without deformity. Conservative management with orthotics and physiotherapy. Stage II: Flexible flatfoot deformity with intact subtalar motion. Subdivided IIA (no forefoot abduction) and IIB (forefoot abduction). Treatment with tendon transfer (FDL to navicular), medial column reconstruction, and selective osteotomies (calcaneal medial slide for hindfoot valgus, lateral column lengthening for forefoot abduction). Stage III: Rigid flatfoot deformity with subtalar joint involvement. Treatment with subtalar fusion or triple arthrodesis. Stage IV: Stage III with ankle joint involvement and deltoid attenuation. Treatment with pantalar arthrodesis or, in selected cases, total ankle arthroplasty with deltoid reconstruction. Peroneal Tendon Injuries Peroneal tendon injuries include tendinosis, tendon tears (most commonly of peroneus brevis, with longitudinal split tears), and dislocation/subluxation (typically from forced dorsiflexion with eversion, with disruption of the superior peroneal retinaculum). Treatment is generally non-operative for tendinosis and selected partial tears; operative for symptomatic tears (debridement and repair, or in severe cases, tenodesis to the FHL or transfer) and recurrent dislocation (superior peroneal retinaculum reconstruction). Flexor Hallucis Longus Injuries FHL tendinopathy (“dancer’s tendinitis”) affects ballet dancers and others performing repetitive plantar flexion. Treatment is generally non-operative with relative rest and graded return to activity; operative tenolysis is reserved for refractory cases.

Tendinopathy and Tendinosis

The terms tendinitis (acute inflammatory pathology), tendinosis (chronic degenerative pathology), and tendinopathy (the broader term encompassing both) describe the

spectrum of overuse tendon pathology. The classical concept of “tendinitis” as an inflammatory entity has been largely supplanted by recognition that most chronic tendon pathology represents failed healing response with degeneration rather than inflammation — hence the preferred term tendinosis for the chronic form. The principles of management of tendinopathy include: Relative rest and modification of provocative activities. Eccentric exercise programs (the Alfredson protocol for Achilles tendinopathy is the prototype, with eccentric calf raises producing improvement in approximately 80 percent of patients with chronic Achilles tendinopathy through the proposed mechanism of stimulating tendon remodeling). Adjunctive modalities including extracorporeal shock wave therapy (with reasonable evidence in selected tendinopathies), platelet-rich plasma injections (with mixed evidence), and laser therapy. Avoidance of corticosteroid injection within or adjacent to load-bearing tendons (Achilles, patellar) because of the increased rupture risk; corticosteroid injection retains a role in some upper extremity tendinopathies (lateral epicondylitis, de Quervain’s) but with cautious patient selection. Surgical intervention is reserved for chronic refractory cases failing 6 to 12 months of structured non-operative management. Techniques include open or arthroscopic debridement, percutaneous tenotomy, and tendon repair where structural pathology is identified. Common tendinopathies include Achilles tendinopathy (insertional and non-insertional), patellar tendinopathy (“jumper’s knee”), lateral epicondylitis (“tennis elbow”), medial epicondylitis (“golfer’s elbow”), de Quervain’s tenosynovitis (first dorsal extensor compartment), and trigger finger (A1 pulley stenosing tenosynovitis).

Sports-Specific Injuries

The groin pain in athletes, the shoulder injuries in throwing athletes (anterior internal impingement, SLAP lesions, partial thickness articular cuff tears in throwers), the knee injuries in cutting sports (ACL injuries, meniscal tears, MCL injuries, patellar instability), and the ankle injuries in jumping athletes form sport-specific patterns of injury that are extensively addressed in the sports medicine literature. The principles of management — accurate diagnosis, structured rehabilitation, return-to-play criteria — extend across all these settings.

Summary and Take-Home Points

Muscle injuries span the spectrum from minor strain to complete rupture, with the myotendinous junction being the typical site of failure. Grade I and II strains respond to relative rest, ice, gentle progressive loading, and structured return to activity; grade III ruptures may require operative repair depending on the muscle and the patient’s

functional demands. Muscle contusions require attention to compartment syndrome risk and the potential development of myositis ossificans. Achilles tendon rupture is recognized by the Thompson test and is increasingly managed by non-operative functional protocols that produce re-rupture rates comparable to operative repair (5 to 8 percent) with substantially lower complication rates. Percutaneous repair is a middle ground with reduced wound complications. Patellar and quadriceps tendon ruptures are recognized by inability to extend the knee against gravity, palpable defect, and patella alta or baja on lateral radiograph. Both require urgent operative repair with transosseous sutures to restore extensor mechanism function. Distal biceps tendon rupture is recognized by the hook test and is generally repaired operatively to preserve supination strength. Proximal long head biceps rupture is usually managed non-operatively unless associated rotator cuff pathology requires surgery. Rotator cuff tears are classified by mechanism, size, depth, and Goutallier muscle quality grade. Symptomatic full-thickness tears with good muscle quality are repaired arthroscopically; massive tears with poor muscle quality and associated cuff tear arthropathy are managed with reverse total shoulder arthroplasty. Posterior tibial tendon dysfunction is the most common cause of adult acquired flatfoot, with the Johnson-Strom classification guiding management from conservative treatment in early stages to tendon transfer and osteotomies in intermediate stages and arthrodesis in advanced rigid deformity. Tendinopathy is now understood as a primarily degenerative rather than inflammatory entity, with eccentric exercise programs (the Alfredson protocol) being the cornerstone of management. Corticosteroid injection should be avoided within load-bearing tendons because of rupture risk. The chapter that follows turns to peripheral nerve injuries — the closely related soft-tissue injuries that often accompany the orthopedic trauma considered throughout this section.