Rupture of the Triceps Tendon

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CHAPTER 35 Rupture of the Triceps Tendon

Bernard F. Morrey

INTRODUCTION

Rupture of the triceps tendon is rare.^1,^2,³ Anzel and colleagues² reported that 85% of the 1015 tendon injuries treated at the Mayo Clinic involved the upper extremity. Of this group of 856, only 8 instances of triceps tendon injury were reported, and 4 of these were due to laceration. Since the first report of Partridge in 1868 as cited by Bennett,⁵ as of 2000, fewer than 50 instances have been recorded in the English literature.^6,^9,^10,¹¹ Unlike ruptures of the distal biceps tendon, this may occur both in men and women, with a female to male ratio of 2:3. The mean age of occurrence is about 33 years, but rupture has been observed in a broader spectrum of ages including children (aged 7) to adolescents in whom the olecranon physes has just closed,¹⁴ to individuals in the eighth decade.¹⁵

MECHANISM OF INJURY

Rupture of the triceps tendon may occur either spontaneously, after trauma, or after surgical release and reattachment. Two types of traumatic episodes may be implicated. The most common event is a deceleration force imparted to the arm during extension as the triceps muscle is contracting. This usually occurs during a fall, but avulsion has been reported due to simple, uncoordinated triceps muscle contraction against a flexing elbow.^4,²⁶ The association of triceps tendon avulsion³⁹ or tear¹⁹ associated with body builders is consistent with the observation of muscle unit damage associated with eccentric contractures in the unconditioned muscle.^24,³¹ The possibility of anabolic steroid usage must also be considered in this type of patient. A direct blow to the posterior aspect of the triceps at its insertion in varying positions also has been reported in several instances^1,^33,⁴⁵ but is probably an uncommon mechanism of injury.

PREDISPOSING CONDITIONS

An association of olecranon bursitis has been noted to predispose to triceps tendon rupture.¹⁰ Disruption of the triceps also may occur spontaneously with minimal trauma in individuals who are compromised by a systemic disease process,³⁵ such as renal osteodystrophy and secondary hyperparathyroidism.^9,¹⁵ Although the pathophysiology of this association has not been completely explained, an increased amount of elastic fibers in the tendons of patients with renal osteodystrophy undergoing dialysis has been reported.²⁹ Calcification due to the chronic hypercalcemia of secondary hyperparathyroidism may be yet another explanation for the associated tendon ruptures in this group of patients.³⁵ Ruptures also have been reported in association with steroid treatment for lupus erythematosus⁴⁵ and chronic acidosis,²⁹ and in individuals with osteogenesis imperfecta tarda²⁵ or Marfan’s syndrome.³⁸ Diabetes has been recently implicated in a patient with triceps rupture at the musculotendinous junction.⁴⁴

In spite of the association with debilitating states and conditions, this injury is well recognized in the athletic population as well. Such diverse activities as power weightlifting and handball have been implicated.^13,^19,^24,³⁹ It should be noted that the injury can be associated with localized hematoma, and there are reports of ulnar nerve compression as a result of hematoma compression after triceps rupture in power lifters.^13,¹⁹ Triceps deficiency occurring after total elbow replacement is obviously a problem of exposure, and repair and is discussed elsewhere.⁷

DIAGNOSIS

Without question, a history of acute pain and weakness in extension or an eccentric loading in flexion against forcible triceps contracture, such as a fall on the outstretched hand, is the most reliable method of making this diagnosis. A palpable defect is present in some instances, depending on the extent of triceps retraction (Fig. 35-1). Injury to the muscular tendinous junction results in pain proximal to the olecranon.^3,³⁰ Some loss of extension power is universally observed. Some active elbow extension may be present, but extension against gravity is not possible with a complete rupture. The length/tension relationship of the triceps has been studied by Hughes and associates,²⁰ who found that as little as 2 cm shortening between origin and insertion causes a marked (40%) loss of strength.

FIGURE 35-1 On gross examination of the lateral aspect of the elbow, a depression just proximal to the olecranon is noted (arrow) that demonstrates proximal retraction of the triceps.

(From Farrar, E. L., and Lippert, F. G.: Avulsion of the triceps tendon. Clin. Orthop. Rel Res. 161:240, 1981.)

IMAGING

Today, imaging is a most reliable means of making a definitive diagnosis that more precisely defines the location and nature of the tear. A plain radiograph is extremely useful in that uncommon instance in which the triceps rupture occurs with a fleck of bone readilyidentified in the lateral film ^15,^35,³⁸ (Fig. 35-2). Without question, however, the advent of the magnetic resonant imaging has provided an accurate and reliable means of not only diagnosing this injury but also localizing the site and the extent of the pathology (Fig. 35-3).^16,³⁴ Ultrasonic diagnosis is also emerging as a reliable and less expensive imaging modality.^31,³⁴

FIGURE 35-2 Radiograph of a patient with triceps rupture. The fragment is readily viewed on the lateral film.

FIGURE 35-3 A magnetic resonance imaging scan, revealing triceps rupture from its insertion, is more accurate in making the diagnosis if the bone is not involved.

(With permission, Mayo Foundation.)

PATHOLOGY

Theoretically, three sites of failure may occur and these have also been observed clinically: the muscle belly, the musculotendinous junction, and the osseous tendon insertion.²⁷ For this particular injury, the failure has occurred almost universally at the site of insertion, although failure at the musculotendinous junction has occasionally been reported.^18,^28,⁴⁴

Associated injuries also have been reported. Several instances of concurrent fracture of the radial head have been noted,^35,⁴² and a recent report of six such injuries suggests that the association may be more common than is appreciated.²³ I have not diagnosed this combination in my practice. A single report of fracture of the wrist²² along with fracture of the radial head supports the case for the mechanism of injury being a fall on the outstretched hand.

PHYSICAL EXAMINATION

The diagnosis of a partial rupture may be difficult. Pain is not dysfunctional; thus, a number of patients present several weeks after the acute event.²¹ Furthermore, some weak residual extension power may be provided by the anconeus/triceps expansion. This effect can be negated by observing the inability to extend overhead against gravity. The radiograph is of considerable benefit for diagnosis of this injury in some patients, because flecks of avulsed bone are apparent on the lateral film (see Fig. 35-2).^14,⁴¹

TREATMENT

Treatment may be simply categorized according to partial or complete and acute or chronic presentations.

PARTIAL RUPTURES

Incomplete tendon rupture should be initially treated nonoperatively.¹ However, a distinction must be made between a true partial insertional rupture and one occurring at the musculotendinous junction. Improved imaging modalities are helpful to make this distinction.^16,³⁴ A true partial detachment from the olecranon does not reliably heal. With an acute injury, we do favor protecting the extremity and observing the amount of progress over a 6- to 8-week period. A strain of the attachment or of the musculotendinous junction will improve. Although appearing to heal, partial ruptures will continue to be symptomatic with increased activity. In the event that there is no clinical contraindication, surgical intervention is indicated. If there is evidence of healing by progressive resolution of symptoms, then in our judgment this represents a strain and not a rupture and nonoperative management is recommended.

COMPLETE RUPTURE

For complete rupture, immediate surgery is the treatment of choice. At the time of exploration, the tendinous portion of the triceps is usually involved and retracted within the muscle.^22,³⁵ However, complete disruption of the entire extension mechanism is uncommon. More than 90% of these injuries occur at the olecranon, with injury of the other sites being reported only occasionally.^17,²⁵ In our experience, the tendinous central third is most typically detached both with complete and partial injury.⁴² Lateral continuity with the anconeus is thus a common finding.

ACUTE

Direct attachment with a nonabsorbable suture through drill holes placed in the olecranon or through a subperiosteal flap is effective treatment for the acute injury. We employ a heavy No. 5 nonabsorbable suture and place two parallel rows of running locked stitches in the tendinous portion of the triceps mechanism (Fig. 35-4). The suture is then brought through cruciate drill holes in the olecranon. With the elbow extended to 30 degrees, the sutures are tied. To further ensure that the tendon is firmly approximated to its origin and to avoid poor healing from synovial fluid, a second transverse suture may be placed which more securely applies the tendon to its site of attachment. If there has been any delay in the treatment, the adventitial bursa tissue should be removed and the area scarified to ensure healing. Concurrent reconstructive options are not necessary in the acute (i.e., less than 2-week-old) injury.

FIGURE 35-4 For acute triceps tendon avulsion, No. 5 nonabsorbable suture is passed through crossed bone tunnels (A) and into the avulsed tendon with a running locked stitch (B).

(With permission from the Mayo Foundation.)

DELAYED RECONSTRUCTION

Several reconstructive procedures have been reported for individual cases. Bennett ⁵ and Farrar and Lippert¹⁴ describe a forearm fascial flap to reconstruct the triceps mechanism. The classic triceps fascial turndown procedure is not reliable, in our opinion,¹⁰ for those with soft tissue deficiency at the point of attachment.

We use two reconstructive procedures: anconeus slide and achilles tendon allograft reconstruction.³⁷ The slide is used for minor defects when the anconeus is intact.

Technique

The patient is supine and the arm brought across the chest. Kocher’s interval between the anconeus and the extensor carpi ulnaris is entered. The anconeus is mobilized from its humeral and ulnar attachments in continuity with the triceps (Fig. 35-5). The triceps/anconeal sleeve is left attached distally and mobilized sufficiently medial to fully cover the site of triceps attachment (Fig. 35-6). The sleeve of extensor musculature is secured in a manner described earlier with a criss-cross No. 5 nonabsorbable suture. The suture is tied with the elbow at 30 degrees of extension. The tendinous fibers that are displaced medially are rotated under the tendon and sewn to themselves.

FIGURE 35-5 The attachment of the anconeus to the lateral margin of the the triceps allows the anconeus to serve as a reconstructive option for triceps deficiency (A). For modest defects (B) the anconeus may be mobilized and oriented over the tip of the olecranon (C). The tear or deficiency is repaired or re-enforced with a No. 5 nonabsorbable suture (D).

(With permission, Mayo Foundation.)

FIGURE 35-6 When a gap occurs between the triceps tendon and the attachment at the olecranon, as is seen in A, the deficiency is most effectively managed with allograft tissue. The authors prefer an Achilles tendon allograft. The calcaneus can serve as an osseous graft to olecranon if it were deficient (B).

Achilles Tendon Allograft.

The allograft Achilles tendon has recently proven to be particularly attractive in those with marked deficiency (see Fig. 35-6).

The position of patient is the same as that noted earlier. The incision begins distal to the olecranon approximately 4 cm and extends proximally to the extent necessary to identify the distal third of the triceps musculature. The ulnar nerve is identified and protected. The defect is dèbrided, and the triceps musculature is mobilized and its flexibility is tested.

In most instances, a trough is made in the subcutaneous border of the proximal ulna and the tendinous portion of the Achilles graft is inserted into the tendinous trough and secured with a No. 5 nonabsorbable suture placed through two drill holes in the proximal ulna (Fig. 35-7). The elbow is placed in 30 degrees of extension. The triceps musculature is mobilized as far distally as possible. The fascia is brought as far proximal as possible under tension and secured with a No. 5 suture. Once the No. 5 nonabsorbablesuture has been placed and secured, the elbow is brought into full extension relaxing the graft. The triceps tendon is brought distally, and the tendon is secured to the muscle and fascia of the triceps with running absorbable suture.

FIGURE 35-7 If the triceps attachment is deficient of tendinous tissue (A), a trough is made in the proximal ulna (B) and the tendinous portion of the Achilles graft is laid in the trough (C) and secured to the proximal ulna with sutures passing through bone. The remainder of the reconstruction consists of attaching the aponeurosis to the remnants of the triceps tendon and muscle (D).

If osseous union is desired, a Chevron resection of the proximal olecranon is performed. A matching preparation of the calcaneal bone allows an osseous union of the distal site. The calcaneus is fashioned in a way to match the preparation of the proximal ulna (Fig. 35-8). The calcaneus is secured as an allograft to the olecranon with a cancellous screw, and the remainder of the repair is performed as described earlier.

FIGURE 35-8 An Achilles tendon allograft with calcaneal bone provides an effective reconstructive unit. The calcaneus attachment is fashioned (A) and screwed to the olecranon and prepared to receive the calcaneal allograft (B). With the elbow at 20 to 30 degrees of flexion, the remnant of the triceps is brought distally and the Achilles fascia is brought proximally and secured. The proximal aspect of the graft is secured with multiple No. 1 interrupted and running sutures (C).

In all reconstructive options, the construct is secured toward extension, such as about 40 to 60 degrees of flexion. After surgery, the arm is protected at 90 degrees of flexion for 3 weeks. Gentle active motion is begun. We have been impressed that recovery, even for acute repair, is slow, possibly taking 6 months to gain 80% of normal strength. Full function is often not realized for a year.

Results and The Mayo Experience

The results of immediate or delayed repair have ultimately been universally good. In most instances, marked improvement in strength and full motion have been restored. A loss of approximately 5 degrees of terminal extension strength has been regularly noted. Suprisingly, good results have been observed with repair or reconstruction that has been delayed for up to 1 year.⁴⁵ However, as noted earlier, it should be emphasized that recovery may be slow and may take a year for full improvement.

Two comprehensive assessments of Mayo’s 20-year experience with 23 triceps deficiencies have been reported by van Riet et al.⁴² and 14 after total elbow by Celli et al.⁷ Of the 23 not related to joint replacement, there were 8 partial and 15 complete ruptures. Only 2 (8%) had osseous avulsions. Of these 23, 14 were primary repairs and 9 were reconstructions followed on average of 88 months. At final follow-up, the average arc of motion was 10 to 135 degrees. Isokinetic and dynamic testing in 10 patients showed peak strength of approximately 82% of the uninvolved extremity. The endurance, however, was almost 99% of normal. Of interest, results from repair and reconstruction were comparable but the recovery period was prolonged in those undergoing reconstruction. Overall, 90% were considered to have had a subjective satisfactory outcome and all patients were able to extend against gravity. In the group with deficiencies after total elbow, all but one was allowed to extend against gravity.

COMPLICATIONS AND RESIDUA

Few complications have been reported other than delayed recovery, variable loss of extension strength, and olecranon bursitis.³²

AUTHOR’S PREFERRED TREATMENT METHOD

Immediate repair with a posterior incision just lateral to the midline is the treatment of choice. No. 5 nonabsorbable suture is placed in Bunnell fashion in the torn tendon and then through criss-crossed holes in the proximal ulna (see Fig. 35-4). If the avulsion has occurred with a sufficiently large fleck of bone, however, reattachment with the AO tension band technique is preferred.⁴³ If the lesion has been overlooked or treatment delayed by several weeks or months, one of the two reconstructive procedures described earlier is carried out.

SNAPPING TRICEPS TENDON

The perception of a posterior snapping elbow is usually localized posteriorly and medially. The cause of such symptoms may be a subluxating ulnar nerve ⁸ or dislocation of a portion of the triceps mechanism.⁴¹ Furthermore, an anomalous slip of the triceps tendon may cause these symptoms, but the most common etiology is subluxation of the medial head of the triceps over the medial epicondyle, usually occurring spontaneously in the second decade of life.^12,^36,⁴⁰

A common associated finding with this condition is chronic irritation of the ulnar nerve, causing an ulnar neuritis.^12,³⁶ Other than this feature, however, the snapping is generally well tolerated. It is very important to recognize this relationship and be suspicious of a snapping triceps concurrent with a subluxating ulnar nerve.

Treatment consists of simply detaching or releasing and rerouting the offending portion from the medial attachment under the triceps mechanism to its lateral attachment (Fig. 35-9). Management of the ulnar nerve is based on its degree of involvement, especially on the stability of the nerve.