Injuries to the triceps tendon are uncommon. Anzel et al1 published the largest series of tendon injuries involving 781 patients with 1014 tendon ruptures; fewer than 1% involved the triceps. Triceps tendon rupture is 2 to 3 times more common in men than in women, with a mean age of occurrence between 30 and 50 years.2–5 Kibuule and Fehringer6 described an injury in a skeletally immature individual, indicating that patients with incompletely or recently fused physes may be at risk.7 Sports involving elbow extension against extreme loads, such as weightlifting and football, may place patients at higher risk, especially with the use of anabolic steroids.8,9 Comorbidities such as diabetes mellitus, hyperparathyroidism, and chronic renal disease have been linked to triceps tendon weakening and injury.2,5,10–12
The most frequently reported causes of injury in patients without total elbow arthroplasty (anatomic elbows) are fall on an outstretched hand, direct trauma to the elbow, or weightlifting.2–4,6,8,10,13–17 The most common site of rupture is the tendon–osseous junction and often includes bony avulsion.2,6,10,11,18,19 Although radiographs help diagnose complete ruptures, ultrasound and magnetic resonance imaging (MRI) may be needed to diagnose partial tears.3,20 Pain and swelling may limit the value of physical examination.21
Previous discussions on triceps tendon rupture have reviewed outcomes after nonoperative treatment for partial injuries and after primary repair for complete injuries, particularly for athletes.2,3,18,20,22 Further discussion regarding outcomes, including for operative repair of partial injury, newer primary repair techniques, and reconstructive procedures, may provide the clinician with a general treatment guideline. Discussion regarding rehabilitation protocols and return to sports may assist in the treatment of athletes. To aid the orthopedic sports physician in the evaluation and treatment of triceps tendon injuries, this general review examines the anatomy, etiology, clinical presentation, diagnostic protocols, conservative and operative treatments, and outcomes for partial and complete injuries.
The PubMed and OVID databases were searched for English, full-text, peer-reviewed literature pertaining to partial and complete triceps tendon injuries in anatomic elbows (Figure). Of the 90 studies discovered, 59 met these criteria. Literature reviews, case series, and case reports were included; no controlled trials were found. All included literature, regardless of publication year, was considered, although more weight was placed on studies published within the past 10 years. Studies with larger sample sizes were given greater consideration than case reports. Our recommendations are based on the available evidence and deduced from outcomes analyzed across all literature reviewed. Because this review includes case reports, the evidence is assigned a level IV.
The triceps originates from the dorsal aspect of the arm and is composed of the lateral, long, and medial heads. The lateral and medial heads arise posteriorly from the humerus proximal and distal, respectively, to the radial groove. The long head originates from the infraglenoid tuberosity. A variant fourth head, the dorsoepitrochlear, constitutes a muscle between the triceps and latissimus dorsi.23 The triceps tendon is a bilaminated aponeurotic structure beginning at the middle portion of the muscle and inserts onto the surface of the olecranon. The triceps tendon footprint is dome-shaped, widest distally, and longest centrally.24 Width of the central tendon insertion is 78% the width of the olecranon.24 The tendon and a band of muscle fibers extend laterally, approximately 70% the width of central tendon, and distally over the anconeus to join with the deep fascia.24,25 Including the medial and lateral tendinous extensions, the total triceps tendon insertional width is >100% the width of the olecranon.24,26
The triceps act in combination with the anconeus to extend the elbow. If the arm is abducted, the long head aids in shoulder adduction. The radial nerve, a branch from the musculospiral nerve, innervates the triceps. Vascular supply is provided by the muscular branches of the profunda brachii.
Most authors believe that the principal mechanism of triceps tendon injury is falling on an outstretched hand.3,4,6,14,16,17 Direct posterior force on the elbow and weightlifting are also common mechanisms.2,10,13–15,17 Other documented causes include swinging a baseball bat,11 motor vehicle accidents,27 seizures,28,29 pitching,30,31 volleyball serving,32 punching,32 and hammering.33 Outside of direct trauma, the biomechanics of injury are similar for each mechanism. Uncoordinated contraction of the triceps against the flexed elbow, combined with a deceleration-type impact, eccentrically overloads the tendon.2,3,5,6,10,11,13,16,17,20,30 Although the tendon can withstand 3 times tetanic contraction,34 various factors can alter its structural integrity and lower the maximum load capacity.10,11 Systemic conditions associated with pathological change of the triceps tendon include diabetes mellitus, osteogenesis imperfecta tarda, rheumatoid arthritis, and systemic lupus erythematosis.2,5,10,11,15 Anabolic steroid use, systemic corticosteroid use, and local steroid injections for olecranon bursitis, which itself can result in tendon injury,35 may cause pathological changes.2,5,6,9–11,15,20,36 Similarly, connective tissue degeneration from ciprofloxacin use can also increase the risk of tendon rupture.5 Chronic renal disease is significantly related to triceps injury through secondary hyperparathyroidism and corticosteroid treatment regimens.12,15 Furthermore, tendon degeneration may be a complication of renal transplantation resulting from a destructive posttransplant autoimmune response.37 Case reports also document a possible familial disposition to triceps injury involving a father and son without a condition known to cause pathological changes to the tendon.5 Most injuries, however, occur spontaneously in patients with healthy tissue and no predisposing condition.15
Rupture of the triceps tendon typically occurs at the insertion point on the olecranon.2,6,10,11,18–20 A majority of full ruptures also include a bony avulsion of the olecranon.3,16 Reports of musculotendinous junction38 and intramuscular tears3,16 are rare. Concomitant injuries with triceps tears include radial head fracture,39 ulnar collateral ligament laxity,40 ulnar nerve compression through hematoma,14 radial nerve compression through compartment syndrome,30 wrist fracture,15 ulnar collateral ligament avulsion with flexor/pronator group injury,13 and distal humerus fracture.34
Clinical Presentation and Diagnosis
Patients with triceps tendon tears often report an acute tearing sensation at the proximal posterior elbow with subsequent pain, swelling, and extensor weakness. History may include a recent fall on an outstretched hand, direct blow, or weight training. Physical examination may demonstrate tenderness, swelling, ecchymosis, or muscle spasms. A diminished or complete absence of arm extension against resistance, depending on whether the tear is partial or complete, is a common finding but is not diagnostic. An intact lateral tendinous extension, attached to the lateral and proximal ulna, may still provide an active extension against gravity despite a complete tear of the central triceps insertion.41,42 A palpable tendon gap at the proximal olecranon is another indicator of complete injury.
Mair et al9 assessed triceps avulsions with the range of motion (ROM), palpation of triceps tendon insertion, and the use of a modified T. Campbell Thompson test described by Viegas.43 This test involves supporting the upper arm with the elbow flexed to 90 degrees and the forearm/hand hanging relaxed. The triceps muscle belly is squeezed, resulting in no elbow motion in a complete rupture. Weistroffer et al4 described a palpable defect with an inability to extend the arm against resistance as diagnostic of triceps tendon avulsion. Unfortunately, pain and swelling complicate ROM, muscle strength, and palpation techniques and may inhibit an adequate examination.21 Peripheral neurovascular status is typically intact; however, cases of neuropathy secondary to hematoma (ulnar)14 and compartment syndrome (radial)30 have been reported.
Difficulty in diagnosis, low clinical suspicion, and underestimation of injury severity are causes for prolonged disability and delayed surgical intervention.10,42 Delayed diagnosis of triceps injury has been reported in patients who were treated conservatively for months or years before a correct diagnosis was made.17,40,44,45
Radiographs should be obtained when triceps tendon injury is suspected. A small avulsion fracture of the olecranon (positive Flake sign) is pathognomonic for triceps tendon avulsion; these fractures are appreciated on lateral radiographs in 80% of cases.3,20 Radiographs can exclude concomitant injuries, such as radial head and distal humerus fractures. Tendon avulsions are differentiated from calcifications or fractured osteophytes by cortical disruption of the olecranon.39,46
Radiographs may not be adequate for partial tendon, musculotendinous junction, and intramuscular injuries. Ultrasound can be a useful and inexpensive tool. Kaempffe and Lerner21 described the ultrasound use for triceps tendon injury, noting that it differentiated completely from partial injury with minimal patient discomfort and correlated with surgical findings. Tagliafico et al47 conducted a radiological review of elbow sonograms; every case diagnosed with triceps tendon injury correlated, in location and severity, with MRI and surgical findings. Harris et al15 described a patient with bilateral partial tendon ruptures who could not fit an MRI machine; ultrasound definitively diagnosed this patient. Sonography may help detect ruptures in the muscle belly or at the musculotendinous junction as well.17,48 Sensitivity and specificity have not yet been reported, and effectiveness may be operator dependent.
Magnetic resonance imaging is the current standard for the definitive diagnosis and differentiation of complete and partial injuries. Axial and sagittal MRIs are best for determining the extent and location of injury, and conclusions correlate well with intraoperative findings.9,10,18,19 Magnetic resonance imaging may detect additional ligament injuries.49 However, MRI may not be necessary for patients whose examination and radiographic findings clearly indicate a complete tear.18
Table 1 summarizes case reports and series describing nonoperative and operative interventions for partial triceps tendon injuries. Nonoperative treatment generally resulted in full ROM and subjective strength within 3 to 9 months. Primary repair typically resulted in full ROM and subjective strength by 3 to 6 months; reconstruction generally required up to 1 year for full recovery.
Partial triceps tendon ruptures have historically been treated nonoperatively, although this is not a consensus opinion. Bos et al50 described a partial injury treated with posterior splinting of the elbow in 30-degree flexion for 6 weeks followed by active movement. Full ROM and normal strength were seen at 3 and 6 months, and MRI at 3 months showed the return of fibrous tissue continuity. Farrar and Lippert27 reported a successful outcome with the elbow splinted at 30-degree flexion for 3 weeks. Full ROM and extensor strength were achieved at 9 months. Harris et al15 described a patient with 70% right-sided rupture and 50% left-sided rupture per MRI. This patient was not immobilized, per patient request, and arm slings were prescribed. The patient began weightlifting 4 weeks after injury and regained normal function by 41 weeks. Follow-up at 55 weeks showed an increased triceps muscle fatigability.
Mair et al9 reported on 10 professional football players with partial triceps tendon injuries. Disruption of the tendon involved 30% to 75% of the tendon width. Initially, all 10 patients were treated conservatively. Six recuperated with no residual symptoms and 3 of these showed complete tendon healing on MRI. Three players needed surgery after the season to resolve residual weakness and pain. One player returned to practice with his elbow braced and suffered a complete rupture 5 days later. Mean playing time missed was just under 5 weeks.
Evidence supporting early operative treatment of partial triceps tears exists as well. van Riet et al10 described operative treatment of 22 patients, 15 of whom had partial ruptures. Of the 9 cases involving tendon reconstruction, 6 were partial injuries where conservative treatment had failed. Failure of healing led to delayed surgical intervention, increasing the likelihood of a tendon-grafting procedure. With reconstruction, patients had greater loss of elbow ROM and peak strength. Also, full recovery was generally not reported until 1 year postoperatively; patients with acutely repaired injuries regained full function within 3 to 4 months. Almost half of the 15 partial injuries required a reconstructive procedure, and these patients had poorer results and increased recovery time. This finding suggests that early surgical intervention may help avoid a future reconstruction procedure.
In other cases of delayed surgery, primary tendon repair has been used. Madsen et al53 described a patient treated with primary repair and immobilization in 60-degree flexion for 10 days after conservative treatment failure. Despite measurable deficits in muscle biomechanics, the patient attained full ROM by 3 months and did not report subjective strength differences at 6 months. Athwal et al52 described 2 cases of arthroscopic repair of the medial head at 9 and 10 months postinjury. The patients underwent passive extension postoperative day 1, active extension at 6 weeks, and strength training at 3 months. Follow-up at 2 years showed ROM of 5 to 145 degrees, disabilities of the arm, shoulder, and hand (DASH) score of 1.7, and MEPS (Mayo Elbow Performance Score) of 100 points.
Initial conservative treatment with elbow immobilization in 30-degree flexion for 4 to 6 weeks has shown positive long-term results. Regular follow-up is recommended to detect delayed complete rupture.27 Regular MRI is not indicated, but follow-up with ultrasound may be an effective cost-sensitive method of tracking patient progress.15,21 Indicators that may increase the risk of delayed complete rupture and risk rates have not yet been studied.
Conservative treatment of triceps tendon injuries must consider several key factors. Nonoperative treatment for ruptures that present after several months may be ineffective and may eventually require surgical intervention.10,17,52,53 Tendon retraction and scarring are expected for such cases, which may complicate surgical options.44 Early operative treatment after delayed presentation may increase the likelihood that primary repair will be successful. However, conservative treatment of acute injuries may be an effective first step, considering that primary repair is an option if treatment fails.6,52,53 Severity of injury must be considered. Although Strauch54 recommended that tears >50% should be repaired surgically, recommendation of Mair et al9 for conservative treatment for tears up to 75% on MRI seems more appropriate considering case evidence. The overall health of the patient must be considered. Comorbidities predisposing the tendon to injury may affect the success of nonoperative treatment. Examination at the time of injury should be considered when determining treatment for partial tears. A significantly impaired triceps examination may signal the need for surgical treatment,17,27 although correlation between examination status and best treatment method has not yet been studied.
Table 2 summarizes case reports and case series describing primary repair and reconstruction for complete triceps tendon tears. Primary repair generally resulted in full ROM by 3 months and baseline subjective strength by 6 months. Reconstruction typically resulted in some loss of ROM and full subjective strength by 2 to 3 years.
Operative repair is indicated for complete triceps tendon tears; the current literature does not provide indications for nonsurgical management and should be reserved for poor surgical candidates. The most commonly reported method of primary repair is the transosseous cruciate technique described by Yeh.5,10,14,27,55,57 A locking stitch is made at the debrided tendon end, passed through crossing drill holes made on the olecranon at the center of the tendon footprint, and tied down. The suture anchor technique57 is less commonly used for primary repair. Here, suture anchors are placed in the middle of the tendon footprint and tied to locking stitches made on each side of the tendon. Yeh et al57 have recently described a modified “anatomic” technique combining suture anchors and olecranon transosseous tunnels. Results indicated greater anatomic footprint coverage, resistance to cyclic loading, and prevention of tendon breakdown when compared with the transosseous or anchor methods alone. The authors noted that 6 patients have undergone anatomic repair, including 1 revision, and have had excellent outcomes so far. Large bony avulsions require reattachment to the olecranon. The use of absorbable sutures,23,58 nonabsorbable sutures,23,46,58 Deknatel tape (TFX Medical OEM, Jaffrey, New Hampshire),56 tension bands,3,10 and wire sutures23,58,59 has been reported. Hardware increases the likelihood of postoperative complications and should be avoided unless necessary.56
Clinical outcomes of the transosseous approach have been good. van Riet et al10 performed 14 primary repairs, 5 for complete rupture and 1 of which required fragment repair. Three of the 14 repairs reruptured, and 2 were treated satisfactorily with a second primary repair. The other required reconstruction after delayed presentation after rerupture of the primary repair. Patients with primary repair had greater mean ROM and mean peak strength compared with patients with reconstruction. van Riet et al10 noted that patients with primary repair recovered most of their preinjury ROM and muscle strength within 3 to 4 months postoperatively. Other authors have reported similar results, with patients treated with the transosseous technique regaining baseline elbow function within 3 to 4 months.14,27,55 Sierra et al56 described 9 complete ruptures with avulsion treated with the transosseous technique, only 1 of which suffered rerupture (traumatic fall). Farrar and Lippert27 described a patient with suture anchor primary repair for bilateral complete ruptures with bony avulsions. At 9 months, the patient had full ROM and muscle strength ratings of 4 of 5 in both the elbows.
Generally, primary repair should occur within 2 weeks of injury, although successful repairs performed several months after injury have been reported.3,10 van Riet et al10 noted that all 8 patients presenting within 3 weeks of injury underwent primary repair. In comparison, primary repair was possible in only 6 of 15 patients presenting beyond 25 days.
When repairs are delayed, soft tissue quality, scarring, and tendon retraction make surgical intervention more complex. Considerable tendon gaps may render reattachment to bone impossible. Reconstruction techniques are then indicated.
Sanchez-Sotelo and Morrey11 described an anconeus rotation flap technique. The proximal anconeus–lateral triceps flap was lifted from the ulna, mobilized over the olecranon, and reattached to the extensor mechanism with the elbow in 30-degree flexion. At 49 months postoperatively, the patient regained full ROM and strength, described painless daily function, and reported a MEPS of 100 points. The authors recommend this method when the anconeus is of good quality and continuous with the lateral triceps. van Riet et al10 used the same technique with satisfactory results.
Large tendon gaps or a devitalized anconeus require other techniques, such as tendon augmentation. Petre et al41 compared the biomechanical properties of uninjured triceps tendons, tendons primarily repaired, and tendons with an FCR autograft augmentation. Although neither technique returned the cadaveric tendon to preinjury performance, augmented tendons were 187% stronger and 195% stiffer and could absorb 264% more energy compared with tendons primarily repaired. Sanchez-Sotelo and Morrey11 described the use of Achilles tendon allograft with a calcaneal bony attachment. Here, the distal calcaneal block is to be secured into a V-shaped osteotomy of the proximal olecranon through screw fixation, and the proximal tendon allograft is stitched to the triceps muscle and tendon. The outcome was similar to anconeus reconstruction, with a satisfactory subjective result and a MEPS score of 100 at 38 months postoperatively. The authors recommended Achilles tendon allograft because it is easily accessible, provides secure fixation proximally and distally, allows earlier postoperative mobilization, and returns normal function more quickly.
Hamstring allograft has also been used. One patient had full ROM by 6 months, 5 of 5 strength by 24 months, and <6% difference in muscle strength between the right and left triceps at 40 months.4 Another patient returned to firefighting duty 6 months postoperatively without pain, although he had 63% loss of peak torque in extension at 30 months.51 Ligament augmentation devices, palmaris longus, and plantaris grafts have been used and have resulted in 4+/5 muscle strength up to 5 years postoperatively, but these procedures may result in ROM limitations.10
If reconstruction is needed, use of the anconeus rotation technique is recommended if the tissue is viable and no large tendon defect exists.11 With tendon gaps, Achilles allograft may provide a better long-term result than hamstring graft, especially with the risk of hamstring weakness and atrophy after graft removal.4,11,51
Postoperative rehabilitation schedules are variable. Blackmore et al18 reviewed the literature and recommended the following regimen:
- Immobilization for 2 weeks at 30-degree elbow flexion with full-extension splint at night if passive extension is difficult.
- Progressive flexion block at 30, 45, 60, and 90 degrees by week 5. Full flexion by week 6.
- Active extension by week 6.
- Extension strengthening by 12 weeks.
- Unrestricted activity at 5 months.
The authors noted that passive ROM difficulties resulted from joint stiffness, tendon shortening, or other surgical complications, not postoperative adhesions. As of 2005, the authors had not found evidence of triceps repair requiring tenolysis, and our search of the current literature found the same. Rehabilitation for reconstruction follows a similar protocol regardless of graft type.11,51 In devising a regimen, tissue quality and conditions that may prolong healing must be considered.
The sports clinician faces the additional question of the appropriateness of return to sport. For athletes with partial triceps tendon injury, several weeks of refraining from competition may be adequate before return to play. Nine professional football players were able to return to full-contact participation with brace support and complete their respective seasons after a mean recovery period of 5 weeks.9 Similarly, a male high-level bodybuilder with bilateral partial triceps tendon tears returned to his normal weightlifting regimen without brace support after 4 weeks of healing.17 Athletes should be aware of the possibility of residual pain and weakness despite a recovery period.9,17 Immediate return to athletics risks progression to complete rupture8,9,14 or chronic extensor dysfunction.17
Evidence to suggest guidelines for return to sport following operative repair of triceps tendon rupture, whether partial or complete, is lacking in the literature. Authors have initiated a gradual weight-lifting program at 3 months postoperatively in athletes.8,18,54 Mair et al9 reported that, although 1 patient returned to full-contact professional football at 7 weeks without rerupture, 10 other patients required a longer rehabilitation period; however, an exact time is not given. The current recommendation is a rehabilitation period of 4 to 6 months before return to full-contact sports10,16 because earlier return may place the athlete at risk of rerupture.8 Further study is needed to recommend a guideline for return to sports after operative triceps tendon repair.
The most apparent deficiency in the literature regarding triceps tendon injuries is the lack of controlled studies. The dependency on case studies makes forming definitive conclusions a difficult task. The significance of various factors, such as medical comorbidities, baseline function, time to treatment, and rehabilitation schedules, to name a few, on patient outcomes is unknown. An examination of case studies may provide the clinician only general guides toward the treatment of triceps tendon tears. Furthermore, a majority of studies relied on subjective outcomes, mainly ROM and subjective strength. The use of outcome scales, such as the MEPS or DASH, may allow the clinician to compare the results across studies on a more objective basis. At this point, more study is needed to determine operative versus nonoperative treatment for partial injuries, best operative repair techniques, or ideal postoperative care.
Triceps tendon insufficiency in an anatomic elbow is an uncommon injury. Patients are typically men between the ages of 30 and 50 years who present with pain and weakness of extension. Examination may reveal a palpable tendon gap, and radiographs may show a pathognomonic Flake sign. Magnetic resonance imaging is the gold standard to determine injury severity.
Injury is typically caused by fall on an outstretched hand, direct trauma on the elbow, or lifting against resistance. Most injuries occur at the tendon–osseous junction. Preexisting medical conditions and drug treatments can predispose the tendon to rupture. Most injuries occur in patients with no such history.
Partial triceps tendon injuries can be managed with immobilization in 30-degree flexion for 4 to 6 weeks, although presentation delay and injury severity should be considered. Delayed presentation may increase the likelihood for surgical intervention. Regular follow-up to detect delayed complete rupture is recommended.
Primary repair for complete triceps injury is typically performed within 2 weeks of injury. Patients often regain normal daily function at 3 to 4 months postoperatively, and risk of rerupture is low. Delayed intervention can make primary repair difficult. Reconstruction with the anconeus rotation procedure may provide full ROM and strength on long-term follow-up. When large tendon gaps exist or the anconeus is devitalized, allograft with the Achilles tendon can be effective.
Most authors immobilize the elbow postoperatively for 2 to 3 weeks at 30- to 40-degree flexion followed by flexion block bracing for an additional 3 weeks. Active extension is usually begun 6 weeks postoperatively. Extension strength physiotherapy is started at 12 weeks, and unrestricted activity is allowed at 6 months. Athletes may return to sports after several weeks of recovery from a partial injury, but return may be delayed if operative repair is performed.
The authors of this article would like to acknowledge the extraordinary contributions of Diana Winters, whose tireless efforts allow us to continue contributing to the database of orthopedic knowledge.
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