Triceps rupture

1. High-Yield Summary

• Rarity and Mechanism: Distal triceps tendon rupture is the least common of all major tendon injuries, representing less than 1% to 2% of all upper extremity tendon ruptures. It typically results from eccentric overload on an actively contracting triceps against forced elbow flexion, commonly seen in contact athletes, powerlifters, or following a fall onto an outstretched hand.
• Predisposing Systemic and Local Risk Factors: High-risk profiles include patients with chronic kidney disease (secondary hyperparathyroidism and enthesopathy), anabolic-androgenic steroid abuse, systemic lupus erythematosus, diabetes mellitus, fluoroquinolone exposure, or prior local intratendinous corticosteroid injections.
• Anatomic Footprint: The triceps footprint is a crescentic insertion on the dorsal olecranon spanning approximately 466 mm², centered 1.5 cm to 2.0 cm distal to the proximal tip. The deep medial muscular head inserts distally blending with the capsule, while the superficial long and lateral heads form a stout aponeurosis. An intact lateral expansion (continuous with the anconeus fascia) often masks complete tendon ruptures by preserving partial active extension in gravity-eliminated positions.
• Diagnostic Cardinal Signs: Palpable sulcus superior to the olecranon tip, loss of active extension against gravity (modified Campbell / triceps squeeze test), and the radiographic “flake” or “fleck” sign representing an avulsed cortical bone fragment in 60% to 80% of cases. Non-contrast MRI is the definitive imaging modality of choice to quantify tear thickness, retraction distance, and tissue quality.
• Treatment Algorithm: Partial tears (50% detachment or functional extensor deficit) mandate primary anatomical surgical repair using transosseous bone tunnels (cruciate configuration) or suture anchor constructs. Chronic retracted ruptures (>3 to 6 weeks) require reconstructive tendon lengthening, local tissue transposition (anconeus flap), or allograft reconstruction (Achilles tendon bone block or hamstring autograft).

2. Anatomy

The triceps brachii represents the principal extensor engine of the human elbow joint, functioning as a three-headed muscle complex in the posterior compartment of the arm innervated by multiple branches of the radial nerve (C6, C7, C8):

• Long Head: Originates from the infraglenoid tubercle of the scapula. As a biarticular muscle, it bridges both the glenohumeral and elbow joints, contributing to humeral adduction and retroversion in addition to elbow extension.
• Lateral Head: Originates from the posterior humeral shaft superior to the radial (spiral) groove. It represents the strongest head during high-resistance elbow extension.
• Medial Head: Originates broadly from the posterior humerus inferior to the radial groove. It is the deepest head, remaining tonically active across all ranges and velocities of elbow extension regardless of resistance.

Distally, the lateral and long heads coalesce into a stout superficial tendinous aponeurosis approximately 1.5 cm proximal to the joint line, whereas the deep medial head remains predominantly muscular until inserting directly into the deep articular capsule and the anterior margin of the olecranon footprint. The osseous insertion footprint on the proximal olecranon forms a dome-shaped surface averaging 466 mm² (mean length 13.5 mm, mean width 23.0 mm). The center of the footprint lies 1.5 cm to 2.0 cm distal to the proximal olecranon tip, separated from the tip by a retro-olecranon bursa and a bare osseous area.

A clinically vital anatomical feature is the lateral triceps expansion. This aponeurotic expansion extends laterally over the anconeus muscle and blends imperceptibly into the antebrachial deep fascia of the dorsal forearm. When the central triceps tendon completely detaches from the olecranon, this lateral expansion frequently remains intact. Contraction of the muscle belly pulls through this continuous fascial sleeve, allowing the patient to weakly extend the elbow when hanging at the side or in a horizontal plane, thereby masking a complete central rupture.

Internervous Plane and Surgical Approach: There is no true internervous plane within the posterior arm, as all heads are innervated by the radial nerve. Posterior surgical exposure typically utilizes a midline longitudinal skin incision curving gently lateral to the olecranon tip to avoid direct scarring over the bony prominence. Exposure proceeds via a direct posterior triceps-splitting approach, a triceps-reflecting approach (Bryan-Morrey), or a lateral paratricipital interval utilizing the Kocher interval distally.

Neurovascular Danger Zones:

• Ulnar Nerve: Runs in close proximity along the medial border of the distal triceps before entering the cubital tunnel posterior to the medial epicondyle. It is highly susceptible to traction injury during medial retraction, transosseous tunnel drilling through the medial olecranon cortex, and extensive tissue mobilization during chronic reconstructions. Routine identification and mobilization of the ulnar nerve is mandatory in complex or revision cases.
• Radial Nerve: Exits the spiral groove on the posterior humerus between the lateral and medial heads of the triceps, traveling approximately 10 cm to 12 cm proximal to the radiocapitellar joint. Aggressive proximal retraction or deep subperiosteal dissection along the posterior humeral shaft risks direct neuropraxia or transection.
• Posterior Cutaneous Nerve of Forearm: Arises from the radial nerve and traverses the lateral intermuscular septum. Vulnerable during lateral exposures and anconeus flap elevations.

3. Pathogenesis

Distal triceps ruptures are generated by biomechanical failure at the osteotendinous junction under extreme tensile loads, frequently superimposed upon pre-existing microvascular and structural tendon degeneration.

Biomechanical Mechanism of Injury: The primary injury vector is an intense eccentric contraction where an actively firing triceps muscle is violently forced into elbow flexion. Classic clinical scenarios include an athlete attempting to break a fall onto an outstretched hand (FOOSH) with the elbow slightly flexed, a weightlifter decelerating during a heavy bench press or overhead press, or a direct traumatic blow against a flexed arm in contact sports (football, rugby). The eccentric tensile stress generated exceeds the ultimate failure load of the tendon-bone interface, causing sudden structural rupture.

Microstructural and Biological Degeneration: Tendon rupture in healthy young tissue without pre-existing pathology is exceptionally rare. Histopathologic studies demonstrate a relative hypovascular zone within the distal triceps tendon located 1.0 cm to 2.0 cm proximal to its osseous insertion on the olecranon. Repetitive microtrauma and eccentric strain provoke microvascular ischemia, collagen disorganization, mucoid degeneration, and tenocyte apoptosis within this critical zone.

Systemic and Iatrogenic Risk Factors:

• Chronic Kidney Disease (CKD / ESRD): Patients on long-term hemodialysis with secondary hyperparathyroidism exhibit osteoclastic resorption at tendon entheses, coupled with metastatic dystrophic calcification. This weakens the osseous anchor point, leading to spontaneous or low-energy avulsions.
• Anabolic-Androgenic Steroids: Chronic steroid abuse alters collagen cross-linking, increases muscle hypertrophy disproportionately to tendon tensile strength, and causes collagen dysplasia, predisposing young powerlifters to catastrophic rupture.
• Local Corticosteroid Injections: Infiltration of corticosteroids for olecranon bursitis or triceps tendinopathy inhibits tenocyte proliferation, degrades extracellular matrix ground substance, and drastically elevates rupture risk.
• Fluoroquinolone Antibiotics: Exposure to fluoroquinolones (e.g., ciprofloxacin, levofloxacin) upregulates matrix metalloproteinases (MMPs), leading to acute collagen degradation across multiple tendons.

4. Natural History

The natural history of distal triceps tendon rupture is characterized by substantial functional impairment when complete tears remain untreated, contrasted with acceptable outcomes in select low-grade partial injuries.

Epidemiology: Distal triceps tendon rupture accounts for less than 1% to 2% of all major tendon disruptions, with an annual incidence of approximately 1.2 per 100,000 individuals. There is a strong male predilection (male-to-female ratio of 2:1 to 3:1), with two distinct demographic peaks: athletic young males (20 to 40 years old) sustaining sports-related eccentric overload injuries, and older individuals (50 to 75 years old) suffering low-energy falls in the setting of chronic systemic disease or local corticosteroid exposure.

Prognosis of Untreated Complete Tears: Complete tears that are unrecognized or managed expectantly fail to reconstitute an anatomical osteotendinous footprint. Progressive proximal retraction of the tendon stump occurs, accompanied by severe muscle fatty atrophy (Goutallier stage 3 or 4) and extensive interstitial fibrosis within 4 to 8 weeks. Patients develop permanent extensor lag, marked weakness in active extension against gravity (loss of 50% to 80% of peak torque), and severe functional disability in overhead tasks, pushing doors, rising from a seated position, or operating hand-held equipment. Secondary joint instability and early secondary cubital tunnel syndrome due to tethering of the ulnar nerve by retracted fibrous scar have also been documented.

Prognosis of Partial Tears: Stable partial-thickness tears involving less than 50% of the tendon footprint with intact continuity of the lateral expansion and preserved active extension against resistance typically heal with conservative immobilization. However, high-grade partial tears (>50% thickness) subjected to early uninhibited loading frequently propagate to complete rupture, culminating in chronic retraction.

5. Clinical Presentation

History

Patients typically recount an acute, high-energy deceleration event or a direct fall onto an outstretched, slightly flexed upper limb, immediately accompanied by an audible “pop” or tearing sensation in the posterior elbow. This is followed by immediate localized pain, swelling, and an inability to forcefully extend the arm. A detailed medical history must actively investigate:

• Mechanism of injury: Eccentric load (e.g., bench press bar dropping, blocking in football) vs low-energy trip and fall.
• Functional deficits: Difficulty pushing open heavy doors, inability to perform push-ups, or struggling to push out of an armchair.
• Prior systemic or local exposures: History of chronic kidney disease, hemodialysis, inflammatory arthropathy, anabolic steroid use, recent fluoroquinolone therapy, or prior local steroid injections into the olecranon bursa.

Physical Examination

Physical examination begins with bilateral inspection and comparative palpation. Marked ecchymosis and edema develop rapidly across the posterior elbow and distal arm, tracking down the dorsal forearm. The clinician must perform targeted maneuvers to avoid diagnostic delay:

• Palpable Sulcus / Defect: A distinct depression or soft gap is palpable immediately proximal to the olecranon process where the avulsed tendon has retracted. In acute settings (first 24 to 48 hours), this gap may be temporarily masked by a tense hematoma.
• Active Extension Against Gravity: The single most reliable functional discriminator. The patient is placed in the seated or standing position with the shoulder forward flexed to 90° or overhead. The patient is asked to extend the elbow against gravity. In complete tears, active extension against gravity is completely absent, yielding a terminal extensor lag. In gravity-eliminated positions (e.g., shoulder abducted 90° with the forearm resting on a horizontal examination table), patients with intact lateral expansions may weakly extend the joint, leading to frequent diagnostic errors.
• Modified Campbell / Triceps Squeeze Test: Analogous to the Thompson test for the Achilles tendon. The patient is positioned prone with the upper arm supported on the examination table and the forearm hanging freely in 90° of flexion over the edge. Squeezing the triceps muscle belly in the middle third of the arm normally elicits subtle passive extension of the forearm. Absence of forearm motion indicates complete rupture of the triceps tendon.
• Neurological Assessment: Comprehensive sensorimotor examination of the radial and ulnar nerves is mandatory, documenting sensation in the dorsal first web space and small finger, as well as motor function of the first dorsal interosseous and extensor pollicis longus.

6. Imaging and Diagnostic Studies

A structured diagnostic imaging algorithm starting with plain radiography and progressing to advanced imaging is essential for accurate staging and surgical planning.

• Plain Radiographs: Standard series consists of anteroposterior (AP), true lateral, and radiocapitellar views. On the true lateral projection, the pathognomonic “flake” or “fleck” sign (small avulsion fracture fragment of cortical bone displaced from the dorsal olecranon) is identified in 60% to 80% of complete ruptures. Radiographs also rule out concurrent radial head fractures, coronoid fractures, posterior elbow dislocations, or olecranon stress fractures, while demonstrating soft tissue edema and obliteration of the posterior olecranon fat pad.
• Diagnostic Ultrasonography: High-resolution musculoskeletal ultrasound provides a rapid, cost-effective point-of-care modality. It demonstrates interruption of the fibrillar tendon architecture, anechoic hematoma filling the gap, and allows dynamic assessment of tendon continuity and gap excursion during passive elbow flexion and extension. Limitations include operator dependence and difficulty evaluating retracted tears in obese patients.
• Magnetic Resonance Imaging (MRI): Non-contrast MRI of the elbow represents the definitive gold standard. Sagittal T2-weighted and STIR sequences delineate fluid-signal discontinuity across the footprint, quantify retraction distance from the olecranon stump in millimeters, and confirm bony flake displacement. Axial proton density and T2 sequences differentiate partial tears (distinguishing deep medial head avulsion from superficial tendon disruption) and assess the lateral expansion and anconeus. Coronal views and muscle belly architecture assess chronic retraction, fatty infiltration, and muscular atrophy using Goutallier staging.

7. Classification

Several validated classification schemes guide the clinical and surgical management of distal triceps injuries, categorizing tears by anatomic thickness, chronicity, and anatomical location.

8. Treatment

Nonoperative Management

Nonoperative management is strictly reserved for patients with stable, low-grade partial tears (<50% footprint detachment on MRI) who demonstrate preserved active terminal elbow extension against gravity, as well as elderly, non-ambulatory, or medically fragile individuals with prohibitive surgical risk.

• Immobilization Phase (0 to 3 Weeks): The elbow is immobilized in a posterior splint or long-arm cast in approximately 30° of flexion. Extreme flexion is avoided to minimize peak tensile strain across the healing tendon-bone interface. Immediate active motion of the wrist and fingers is encouraged.
• Protected Mobilization Phase (3 to 6 Weeks): The patient transitions into a hinged elbow brace. Passive and active-assisted flexion is permitted within restricted blocks: 0° to 60° during weeks 3 and 4, progressing to 0° to 90° during weeks 5 and 6. Active extension against resistance remains strictly prohibited.
• Strengthening Phase (6 to 12 Weeks): Full active range of motion is achieved out of the brace by 8 weeks. Light isometric strengthening begins at 8 weeks, progressing to concentric resistive strengthening at 10 to 12 weeks. High-demand eccentric loading (e.g., bench press, heavy dips) is restricted until 5 to 6 months post-injury.
• Objective Failure Criteria: Progressive extensor lag exceeding 15° to 20°, worsening subjective instability, persistent grade 3/5 extension weakness, or interval MRI demonstrating tear propagation beyond 50% constitutes nonoperative failure and mandates surgical conversion.

Operative Management

The fundamental goals of operative treatment are anatomical restoration of the broad triceps footprint on the dorsal olecranon, rigid biomechanical fixation with minimal gap formation under cyclic load, early protected functional range of motion, and complete recovery of active extensor power.

Surgical Approaches and Patient Positioning: The patient is positioned lateral decubitus with the operative arm supported over a padded post, or supine with the arm draped across the chest. A sterile pneumatic tourniquet is applied to the upper arm. A posterior longitudinal midline incision is made, curving gently lateral to the olecranon tip to minimize direct scar contact during elbow resting. Full-thickness fasciocutaneous flaps are elevated directly off the deep fascia to avoid skin margin devascularization. The ulnar nerve is identified medially and mobilized if extensive exposure or chronic reconstruction is planned.

Primary Repair Techniques

• Transosseous Cruciate Bone Tunnel Repair (Classic Gold Standard): The olecranon footprint is prepared by debriding soft tissue and decorticating the sclerotic cortex down to bleeding cancellous bone. Two or three longitudinal transosseous tunnels (2.0 mm to 2.5 mm diameter) are drilled from the articular margin of the olecranon footprint exiting 2.5 cm to 3.0 cm distally on the dorsal ulnar shaft, maintaining a minimum 1.0 cm bone bridge between tunnels. Heavy non-absorbable high-tensile sutures (#2 FiberWire) are placed into the tendon in locking Krackow configurations, passed through tunnels in a crossed (cruciate) orientation, tensioned at 30° to 45° of flexion, and tied over the dorsal bony bridges.
• Anatomical Suture Anchor Repair (Double-Row / Transosseous-Equivalent): Utilizes two proximal suture anchors placed at the articular margin of the olecranon footprint and two distal knotless anchors placed in the dorsal ulna cortex. Suture tapes from the proximal anchors are woven through the triceps tendon and secured into the distal knotless anchors, broadly compressing the tendon across the entire 466 mm² footprint. Biomechanical testing demonstrates superior ultimate load to failure, higher stiffness, and lower cyclic gap formation compared to traditional bone tunnels, while eliminating the risk of bone bridge cut-through.

Chronic Reconstruction Techniques

In chronic or neglected ruptures presenting beyond 3 to 6 weeks, tendon retraction, shortening, and scar contracture prevent direct apposition of the tendon stump to the olecranon footprint without excessive joint flexion. Depending on the size of the structural defect, reconstructive options include:

• V-Y Tendon Lengthening: Indicated for retracted tears with mild to moderate gap (2 cm to 3 cm). An inverted V-shaped incision is made through the proximal triceps aponeurosis, the tendon is advanced distally, and repaired in a Y-configuration.
• Anconeus Muscle Transposition Flap: Indicated for moderate gaps. The anconeus is detached from its lateral epicondyle origin, elevated on its neurovascular pedicle, rotated 90° proximally and medially, and sutured into the triceps defect to bridge the gap and provide vascularized soft tissue coverage.
• Autograft Augmentation: Semitendinosus or gracilis autograft is harvested, looped through transosseous bone tunnels in the olecranon, and woven through the retracted triceps muscle belly using a Pulvertaft weave.
• Allograft Reconstruction: Achilles tendon allograft with an attached calcaneal bone block represents the gold standard for massive chronic defects (>4 cm gap). The calcaneal bone block is contoured and secured to the olecranon with cortical screws or an olecranon plate, and the broad tendinous portion is interdigitated into the triceps tendon and fascia.

Indications & Contraindications

Indications for Primary Surgical Repair:

• Acute complete triceps tendon rupture (Type III) in any functionally active individual.
• High-grade partial-thickness tear involving >50% of the tendon footprint with clinical extensor lag >15° to 20° or failed conservative trial.
• Acute bony avulsion fracture (“flake” sign) with articular displacement >2 mm or tendon gap >1 cm.
• High-demand athlete or heavy manual laborer requiring overhead pushing power.

Contraindications:

• Active local infection, extensive cellulitis, or ulceration over the posterior elbow.
• Severe peripheral vascular disease or compromised local soft tissue envelope precluding healing.
• Low-demand, non-ambulatory patient with minimal functional complaints and high surgical risk.
• Pre-existing fixed elbow flexion contracture or severe end-stage tricompartmental arthrosis.

Postoperative Rehabilitation

• Phase I (Weeks 0 to 2): Posterior splint immobilization at 30° of flexion. Cryotherapy and hand/wrist active motion. Full-thickness wound inspection at 10 to 14 days with suture removal.
• Phase II (Weeks 2 to 6): Transition into a hinged elbow brace. Passive and active-assisted flexion allowed with incremental limits: 0° to 30° at week 2, 0° to 60° at week 3, 0° to 90° at week 4, and progressive advance to full passive flexion by week 6. Active extension against gravity is strictly avoided.
• Phase III (Weeks 6 to 12): Brace discontinued. Active unresisted elbow extension and flexion initiated. Progressive isometric strengthening begins at week 8, advancing to light resistive band exercises at week 10.
• Phase IV (Months 3 to 6): Progressive resistance training, plyometrics, and sport-specific drills. Return to unrestricted athletics and heavy manual labor cleared at 6 months, provided extensor strength exceeds 85% of the contralateral limb.

9. Outcome

Surgical repair of acute distal triceps tendon ruptures consistently yields predictable, high-level functional outcomes with high patient satisfaction rates across validated outcome metrics:

• Patient-Reported Outcome Measures (PROMs): Mean postoperative Mayo Elbow Performance Scores (MEPS) range from 90 to 98 points (out of 100), reflecting 85% to 92% good-to-excellent clinical results. American Shoulder and Elbow Surgeons (ASES) elbow scores consistently exceed 90 points, and Disabilities of the Arm, Shoulder and Hand (DASH) scores decrease from preoperative levels >50 to postoperative scores <10.
• Range of Motion: Most patients recover a functional arc of motion exceeding 100° of flexion and extension (mean extension loss 3° to 7°, mean flexion 135° to 140°). Terminal extension loss is significantly lower in patients mobilized early in functional hinged braces compared to prolonged rigid casting.
• Strength Restoration: Objective isokinetic and isometric dynamometry demonstrates restoration of 80% to 90% of peak extension strength and endurance compared to the uninjured contralateral extremity following acute primary repair. In contrast, chronic reconstructions (grafts or flap advancement) recover approximately 65% to 75% of baseline power.
• Return to Play and Work: More than 85% of competitive and recreational athletes successfully return to their previous level of sports competition at a mean of 5.5 to 7.0 months postoperatively. Heavy manual laborers return to full duty at an average of 6 months.

10. Complications

Complications following distal triceps tendon repair range from minor wound healing challenges to catastrophic re-ruptures requiring revision reconstruction.

11. Pearls and Pitfalls

• Avoid the Direct Midline Bone Scar (Pearl): Curve the skin incision 1 cm to 1.5 cm laterally around the olecranon tip. This prevents painful scar adherence directly over the bony prominence when resting the elbow on hard surfaces.
• Maintain Full-Thickness Fasciocutaneous Flaps (Pearl): The soft tissue envelope over the posterior elbow is remarkably thin. Always elevate the skin and subcutaneous tissue together off the deep fascia as a single thick layer to avoid marginal skin necrosis.
• Light Decortication Without Deep Troughing (Pearl): Decorticate the sclerotic olecranon footprint with a high-speed burr or curette to open bleeding cancellous vascular channels, but avoid deep troughing into the olecranon, which weakens the cortical bridges and increases fracture risk.
• Tension the Construct in 30° to 45° of Flexion (Pearl): Tying transosseous sutures or securing knotless anchors with the elbow flexed at 30° to 45° ensures sufficient anatomical tension while preventing overtightening that could compromise postoperative terminal flexion.
• The Gravity-Eliminated Diagnostic Trap (Pitfall): Never evaluate active elbow extension solely with the arm resting horizontally on a desk. Intact lateral expansions and the anconeus muscle can generate 20° to 30° of horizontal extension, falsely reassuring the clinician and causing diagnostic delay in a complete central rupture. Always examine active extension against gravity overhead.
• Narrow Bone Bridges Leading to Cut-Through (Pitfall): When drilling transosseous bone tunnels, placing the drill exit holes less than 10 mm apart or drilling too close to the dorsal cortex invites suture cut-through under cyclic load. Maintain robust bone bridges and use broad suture tape when available.
• Neglecting Ulnar Nerve Mobilization in Chronic Cases (Pitfall): In chronic reconstructions requiring extensive proximal mobilization or graft weaving, failure to identify and gently mobilize the ulnar nerve medially carries a severe risk of traction neuropraxia or accidental transection.

12. Controversy

1. Transosseous Cruciate Bone Tunnels vs Suture Anchor Constructs: A longstanding debate centers on the optimal fixation construct for acute primary repair. Biomechanical investigations have demonstrated that modern knotless double-row suture anchor (transosseous-equivalent) constructs provide greater contact area across the 466 mm² footprint, higher ultimate load to failure, and less displacement under cyclic loading compared to transosseous cruciate tunnels. However, large clinical comparative cohorts and systematic reviews (Mirzayan et al., 2018; Dunn et al., 2017) reveal no statistically significant difference between the two techniques in terms of clinical re-rupture rates (~5% to 6%) or patient-reported outcome scores. Suture anchors introduce higher implant costs and the risk of anchor pullout or hardware prominence in thin subcutaneous tissues, whereas transosseous tunnels require no foreign metal/biocomposite implants but risk cortical cut-through in osteopenic bone.

2. Early Protected Motion vs Rigid Immobilization: Traditional postoperative regimens mandated 4 to 6 weeks of rigid cast immobilization in 30° of flexion to protect the healing enthesis. Modern rehabilitation protocols favor early protected motion within a hinged elbow brace starting at 10 to 14 days postoperatively. Advocates of early motion highlight accelerated soft tissue healing, decreased flexion contractures, and improved terminal extension arcs without an increased rate of construct failure or re-rupture. Nonetheless, some surgeons still advocate rigid protection for patients with compromised bone quality, chronic reconstructions, or poor patient compliance.

3. Graft Selection for Massive Chronic Retracted Defects: In chronic ruptures where the tendon cannot be mobilized to the footprint, controversy persists regarding the superior reconstructive material. Local tissue transposition (anconeus muscle flap or V-Y advancement) eliminates donor site morbidity and allograft costs, but may lack sufficient mechanical tensile strength for heavy labor or athletics. Semitendinosus autograft provides robust biological incorporation and high tensile strength but requires a secondary harvest incision. Achilles tendon allograft with a calcaneal bone block offers anatomical structural reconstruction with rigid bone-to-bone fixation, but carries concerns regarding disease transmission, slower biological remodeling, and substantial graft costs.

13. Evidence-Based Synthesis

Modern clinical decision-making is grounded in high-quality randomized controlled trials and prospective registry analyses, corroborated by seminal biomechanical and anatomical descriptions.

14. References

• Dunn JC, Kusnezov N, Fares A et al. Triceps Tendon Ruptures: A Systematic Review. Hand (N Y). 2017. doi:10.1177/1558944716677338 [Level I: Systematic Review / Meta-Analysis]
• van Riet RP, Morrey BF, Ho E et al. Surgical treatment of distal triceps ruptures. J Bone Joint Surg Am. 2003. doi:10.2106/00004623-200310000-00015 [Level IV: Clinical Case Series / Cohort Study]
• Yeh PC, Dodds SD, Smart LR et al. Distal triceps rupture. J Am Acad Orthop Surg. 2010. doi:10.5435/00124635-201001000-00005 [Level IV: Clinical Review & Diagnostic Algorithm]
• Demirhan M, Ersen A. Distal triceps ruptures. EFORT Open Rev. 2016. doi:10.1302/2058-5241.1.000038 [Level IV: Clinical Review & Technique Analysis]
• Mirzayan R, Acevedo DC, Sodl JF et al. Operative Management of Acute Triceps Tendon Ruptures: Review of 184 Cases. Am J Sports Med. 2018. doi:10.1177/0363546518757426 [Level II: Comparative Study / Decision Analysis]

15. Master Class Pro-Tip

When repairing an acute distal triceps rupture, do not settle for a simple single-line transosseous suture repair. The anatomical footprint on the dorsal olecranon is surprisingly expansive, averaging over 450 mm² and extending well distal to the olecranon tip. Prepare the footprint by lightly decorticating the sclerotic dorsal cortex to bleeding cancellous bone. Utilizing an anatomical double-row or crossed transosseous construct—placing the deep medial muscular fibers down to the articular margin and tensioning the stout superficial aponeurosis broadly across the distal footprint in 30° to 45° of flexion—maximizes contact surface area, minimizes micromotion, and creates an exceptionally stable biomechanical construct that permits safe, early protected passive motion within the second postoperative week.

Master Class Surgical Pearl: Distal Triceps Footprint Restoration