Triceps brachii tendon disruption rarely occurs in companion animals, with limited case reports in dogs and cats (1,7-9,14). Triceps tendon disruption often results in significant lameness, including non-weight-bearing, due to the inability to extend the elbow joint (1,7). Surgical intervention is typically necessary to restore normal limb function following triceps tendon disruption. However, tendon healing is inherently slow due to its low metabolic rate and relatively acellular nature (19). Successful tendon repair requires achieving significant tensile strength without excessive scar formation to allow proper gliding during limb movement (2).

Chronic triceps tendon injuries present significant challenges for surgical repair, which often leads to tendon-end retraction, leaving insufficient tissue for reconstruction (1). Excessive scar tissue formation and soft tissue contracture can further complicate the repair, as scar tissue must be excised before tendon repair (10,22). In such cases, primary repair may be inadequate, necessitating the use of autogenous or synthetic materials to bridge the defect or provide additional support (1,4,5,15,20).

This report aims to describe the successful surgical treatment of a chronic triceps tendon disruption with a defect in a dog using an autogenous fascia lata graft. To our knowledge, this is the first report documenting the successful surgical repair of chronic triceps tendon disruption with a defect using an autogenous fascia lata graft in a dog.

A 4-year-old, 1.8 kg, castrated male Yorkshire Terrier was referred to a referral animal hospital for persistent non-weight-bearing lameness in the right forelimb for two months (Supplementary Video 1). The cause of lameness was unknown and had not responded to NSAIDs treatment. One month prior to referral, an open wound developed over the right elbow joint (Fig. 1). On physical examination, the dog was unable to extend the right elbow joint and held the right forelimb up while walking, presenting with grade 4/4 lameness at both walk and trot (13). Severe muscle atrophy of the right forelimb was noted, and palpation around the olecranon revealed a pain response and a defect in the continuity of the triceps tendon. The passive range of motion of the right elbow joint was normal, with no other orthopedic or neurological abnormalities detected. Radiographic examination revealed an osteolytic lesion around the right olecranon and surrounding soft tissue swelling (Fig. 2). Ultrasonography indicated the absence of identifiable triceps tendon structures at the olecranon attachment site, with hypoechoic changes and no distinct inflammatory signs, suggesting potential tendon damage and chronic inflammatory changes (Fig. 3). The diagnosis of chronic triceps tendon disruption was established based on the comprehensive evaluation of all conducted examinations. The open wound was treated with antibiotics, guided by sensitivity testing, and appropriate wound care for 2 weeks.

Figure 1. Chronic open wound located over the right elbow joint (arrow).

Figure 2. Radiographic findings: presence of an osteolytic lesion and surrounding soft tissue swelling in the area of the right olecranon (red arrow).

Figure 3. Ultrasonographic findings: absence of a distinct triceps tendon structure at the olecranon insertion (yellow arrow).

Subsequently, a surgical intervention was planned due to the chronic nature of the triceps tendon disruption. Given the condition, primary repair was not feasible, and an autogenous fascia lata graft was chosen for augmentation. The patient was premedicated with acepromazine (0.03 mg/kg, intravenously [IV]) and fentanyl (2 µg/kg, IV) prior to induction with propofol (6 mg/kg, IV). General anesthesia was maintained with isoflurane, and perioperative analgesia was provided through a constant rate infusion (CRI) of fentanyl (2-6 µg/kg/h). Cefazolin (22 mg/kg, IV) was administered prophylactically. The right forelimb and hind limb were prepared aseptically for surgery.

The dog was positioned in left lateral recumbency, and a C-shaped incision was made on the caudolateral aspect of the olecranon, extending from just distal to the midshaft of the humerus to the proximal ulna (12). The subcutaneous fat and fascia were incised on the same line and retracted.

The triceps brachii tendon was detached from its insertion on the olecranon and retracted, revealing granulation tissue at the tear site. The radial nerve was identified and protected throughout the procedure. To minimize tendon damage, a 23-G needle was inserted through the body of the tendon, away from the tendon ends. Debridement was performed with a scalpel until healthy tissue was identified, and no tendon remnants were attached to the olecranon (Fig. 4A). With the elbow joint fully extended and the triceps tendon under tension by applying full traction toward the olecranon, a 1-cm gap was observed between the distal triceps brachii tendon and olecranon. To bridge this gap, an autogenous fascia lata graft was applied between the distal end of the tendon and the olecranon.

Figure 4. (A) Intraoperative photo following debridement of scar tissue. (B) The fascia lata graft was sutured to the distal triceps brachii tendon (arrow). (C) A lateral-to-medial bone tunnel was created in the proximal olecranon using a 1.2-mm Kirschner wire. (D) The 1-cm defect was bridged by the fascia lata graft secured to the bone tunnel using a modified three-loop pulley suture technique (arrow).

An incision was made along the lateral aspect of the right hind limb, extending proximally from the greater trochanter to the patella to harvest the autogenous facia lata graft. The subcutaneous tissues were dissected, exposing fascia lata. The fascia lata, which was released using two longitudinal parallel incisions, from just distal to the tensor fascia lata muscle to the proximal border of the patella. The fascia strip was sized according to the length of the triceps tendon defect, with an additional 0.5 cm at each end for secure fixation to the remaining portions of the triceps tendon and olecranon. A 0.7 cm × 2.0 cm strip was harvested and preserved in saline-soaked gauze. The fascia lata defect was closed with a 3-0 polydioxanone suture in a simple continuous pattern. The subcutaneous tissue and skin of right hindlimb were closed routinely.

The fascial strip was sutured to the distal triceps brachii tendon using a 3-0 polypropylene suture with a three-loop pulley pattern (Fig. 4B). The origins of the anconeus and flexor carpi ulnaris muscles were elevated from the olecranon to allow bone tunneling. A 1.2-mm Kirschner wire was used to create a bone tunnel in the proximal olecranon, directed laterally to medially (Fig. 4C). With the elbow joint extended, the distal part of the graft secured to the bone tunnel using a modified three-loop pulley pattern with a 3-0 polypropylene suture (Fig. 4D) (16). To reduce the risk of suture failure, the residual free distal end of the graft was fixed to the olecranon with periosteal sutures in a locking loop pattern using 4-0 polydioxanone, and the free proximal end of the graft was sutured to the distal triceps tendon with a 4-0 polydioxanone. The repaired tendon was tested for integrity by flexing the elbow joint, which remained stable. The subcutaneous tissues and skin were closed routinely.

Postoperative radiographs confirmed proper bone tunnel placement without complications (Fig. 5A). Postoperative care included CRI of fentanyl (2-3 µg/kg/h) until discharge from the hospital three days later. Discharge instructions included oral enrofloxacin (10 mg/kg, SID), gabapentin (10 mg/kg, BID), and trazodone (3.5 mg/kg, BID) for 10 days, alongside strict exercise restriction and bandage care. A spica splint was applied postoperatively to immobilize the right forelimb, with the elbow maintained in extension for 6 weeks.

Figure 5. (A) Immediate postoperative radiograph demonstrating proper placement of the bone tunnel within the olecranon (arrow). (B) Eight-week postoperative radiograph.

Follow-up examinations were performed every 2 weeks until 10 weeks post-surgery. Six weeks post-surgery, after splint removal, a custom-made elbow brace was applied for an additional 4 weeks. Further follow-up examinations were also performed at 5 months and 1 year after surgery. Immediately after the removal of spica splint 6 weeks post-surgery, the dog showed a grade 4/4 lameness at both walk and trot, but was capable of extending the elbow joint on its own and displayed partial weight-bearing of the limb while standing. Although muscle atrophy was noted, there was no pain on palpation of the elbow joint, and the range of motion was mildly decreased. Additionally, no skin problems from the external coaptation. Then, the dog was restricted to house confinement for 4 weeks. Due to the owner's circumstances, rehabilitation therapy was not performed. Eight weeks post-surgery, the dog exhibited a grade 3/4 lameness at both walk and trot, and palpation revealed a firm triceps tendon. The elbow joint could not be flexed while maintaining shoulder extension, suggesting successful tendon healing and restored function. Radiographs and ultrasonography at 8 weeks post-surgery confirmed tendon continuity at the olecranon without complications (Figs. 5B, 6). At 10 weeks post-surgery, the dog showed a grade 2/4 lameness at both walk and trot. The owner was advised to initiate gradual leash walks for 2 weeks, progressively increasing in frequency and duration. At 5 months and one year post-surgery, the dog showed no lameness or pain, exhibited normal range of motion (Supplementary Video 2), and the owner was satisfied with the clinical outcome.

Figure 6. Eight-week postoperative ultrasound image showing normal triceps tendon continuity and attachment to the olecranon (arrowhead).

Triceps brachii tendon disruption is rare in small animals (1,7-9,14). Trauma is a common contributing factor; however, iatrogenic causes such as local or systemic corticosteroid administration have also been implicated (7,9,14). In this case, the owner was unaware of the cause of the triceps tendon disruption. During history taking, no iatrogenic factors were identified, and the dog displayed acute non-weight bearing lameness, suggesting a likely trauma cause. Typically, tendinopathy does not result in the formation of a fistula or open wound, which raises the suspicion that an acute traumatic event, potentially in the form of a penetrating injury such as a stab wound, may have led to the disruption of the tendon, subsequently causing inflammation. This could explain the absence of an open wound and potentially result in the later development of one.

Surgical repair is necessary to restore functional elbow extension in humans with complete triceps tendon disruption (21). In quadrupeds, the triceps tendon is essential for bearing weight and extending the elbow during standing and movement. A complete disruption of the triceps tendon leads to significant functional deficits, such as an inability to bear weight on the limb and difficulty with ambulation. This loss of function often necessitates surgical intervention to repair the tendon and restore normal function.

Successful triceps brachii tendon repair requires meticulous surgical techniques to restore anatomical integrity and functional elbow extension. Early surgical intervention is ideal; however, chronic tendon injury presents significant challenges and is associated with a historically guarded prognosis (18). Delayed diagnosis often results in tendon retraction, inadequate tissue for reconstruction, and excessive scar tissue formation, including fibro-adipose tissue, which requires excision prior to repair. Excessive scar tissue and soft tissue contracture can further compromise the success of primary repair (10,22). In such cases, augmentation with autogenous or synthetic materials may be necessary to bridge defects and provide additional support (1,4,5,15,20).

The decision to use an autogenous fascia lata graft for this chronic triceps tendon disruption was based on multiple factors. A 1 cm post-debridement defect precluded primary repair. Although tendon lengthening techniques could potentially repair a 1-cm defect, this procedure was not performed for the following reasons: the chronic nature of the tendon injury raised concerns regarding compromised blood supply and impaired healing. Furthermore, approximately 1.5 cm of tendon segment is required to achieve a 1-cm tendon elongation with Z-plasty, while U-T-plasty necessitates approximately 2 cm of tendon segment (11). However, considering the small size of the patient at 1.8 kg, the distal tendon remnant did not reach these lengths. An autogenous graft avoids the risks of foreign body reactions, rejection, and increased infection risk associated with synthetic materials.

The established success of autogenous fascia lata grafts in tendon repair, which has been extensively documented in both human and veterinary medicine, provided strong support for this technique (4,5,15,20). Firstly, when performing traction, if the ends come together, the suturing can be carried out, followed by covering the sutured area with fascia lata to provide reinforcement (5,15). Secondly, if a gap remains even with traction, one end of the fascia lata graft can be sutured to one side of the tendon, while the opposite end of the fascia lata graft is affixed to the opposite tendon or bone. In employing this method, the length of the graft is generally kept longer than the gap to ensure adequate coverage of the tendon or bone and facilitate additional suturing (4,20).

This approach is well-established for common calcaneal and patellar tendon repairs in veterinary surgery (5,15,20); however, its use in triceps tendon repair is novel. Finally, the ease of harvesting autogenous fascia lata with minimal donor-site morbidity reinforced this choice and likely contributed to the successful repair outcome. Human surgical literature also supports the use of fascia lata for triceps brachii tendon repairs (3,4).

In a canine triceps tenotomy model, postoperative immobilization is necessary to protect the repair from excessive weight-bearing forces because tendon healing is slow, achieving only 56% of its original strength at 6 weeks (6). Several methods for postoperative immobilization of the elbow joint following triceps tendon repair have been reported, including transarticular external skeletal fixation (TAESF), and spica splints (1,7,8,14). However, practical considerations, particularly the patient's small size (1.8 kg), led to the selection of a spica splint over TAESF. A custom-made elbow brace was applied for 4 weeks after 6 weeks of spica splint immobilization to minimize the risk of joint ankylosis and promote optimal healing, as complete osteotendinous integration following tendon avulsion may take up to 12 weeks for optimal structural integrity (17).

This case report is a single case, which presents the following limitations. Firstly, because it is a single case, it may be difficult to apply the findings to dogs with different conditions. Additionally, the absence of a control group makes it challenging to accurately determine the efficacy of the intervention, highlighting the need for further research to explore these aspects in the veterinary literature.

This case study is the first to report the successful surgical repair of chronic triceps tendon disruption with a defect in a dog using an autogenous fascia lata graft. Postoperative assessment showed significant improvement in lameness and gait, which were maintained during a one-year follow-up period without complications. Although this is a single-case study, the findings indicate that augmentation with an autogenous fascia lata graft may be a viable treatment option for chronic triceps tendon disruptions with a defect in dogs.

This work was supported by the research fund of the Haemaru Referral Animal Hospital.

The authors have no conflicting interests.