Extensor tendon rupture after total knee arthroplasty

Etiology

The incidence of extensor tendon rupture (Figure 1) after TKA has been reported in a range of 1–12% [1, 2]. Their etiology is complex and multifactorial, and poor results emphasize the importance of prevention [3–5]. Often, the rupture occurs during a traumatic event, which may be obvious, eg, a fall on the flexed knee, or trivial, eg, arising from a chair or carrying a heavy weight. Usually, the event causes the rupture because of preexisting fragility in the tendon [6].

The underlying reasons can either be patient-related or structural factors. When patient-related factors are the cause, several years may elapse between the TKA and the tendon rupture. When structural factors are the cause, the rupture often occurs early in the recuperative period [7].

Patient factors include obesity and other comorbidities. Obesity will lead to higher loads on the extensor, which it may not be able to withstand. On the other hand, several systemic diseases have an effect on soft-tissue quality, be it through their impact on blood supply, or through triggering inflammatory processes. Many comorbidities have been implicated in extensor tendon ruptures, including hyperthyroidism, diabetes mellitus, rheumatoid arthritis (RA), connective tissue disorders like systemic lupus erythematosus, and chronic renal failure [6, 8]. Additionally, long-term high-dosage glucocorticoid or fluoroquinolone use, or repeated intraarticular glucocorticoid injections can weaken collagenous tissues, and thus predispose patients for tendon ruptures [3].

Structural factors are often related to prior knee surgeries. To maintain good tissue quality of the extensor tendons in the long run, an optimal blood supply is vital. However, multiple surgical interventions around the extensor mechanism, including distal realignment procedures, will weaken and contribute to reduction of the blood supply [8]. The more extensive the dissection, the higher the compromise of the vascularization.

Yixin Zhou, Professor and Chairman of Department of Adult Reconstructive Surgery, Beijing Jishuitan Hospital, points out: “Patients with the known relevant comorbidities, with stiff knees and a weak extensor mechanism, as well as male patients over 40 with tendinopathy, should raise red flags for surgeons and make them doubly careful with every maneuver avoiding overtension of the extensor. It is obvious that an impairment of vascularization has deleterious effects on any patient. However, in patients suffering from these conditions, the risk of subsequent tendon failure is so much higher. Therefore, every effort should be undertaken to be as vascularization-sparing as possible.”

Upon performing the TKA surgery, various vascular structures are imperiled (Figure 2). First, the medial and descending genicular arteries are at risk during medial arthrotomy. Second, the lateral-inferior genicular artery and the anterior-tibial recurrent artery are at risk during fat-pad excision. Third, the lateral-superior genicular artery is at risk during release of the lateral retinaculum [6, 8–11].

Etiology

The incidence of extensor tendon rupture (Figure 1) after TKA has been reported in a range of 1–12% [1, 2]. Their etiology is complex and multifactorial, and poor results emphasize the importance of prevention [3–5]. Often, the rupture occurs during a traumatic event, which may be obvious, eg, a fall on the flexed knee, or trivial, eg, arising from a chair or carrying a heavy weight. Usually, the event causes the rupture because of preexisting fragility in the tendon [6].

The underlying reasons can either be patient-related or structural factors. When patient-related factors are the cause, several years may elapse between the TKA and the tendon rupture. When structural factors are the cause, the rupture often occurs early in the recuperative period [7].

Patient factors include obesity and other comorbidities. Obesity will lead to higher loads on the extensor, which it may not be able to withstand. On the other hand, several systemic diseases have an effect on soft-tissue quality, be it through their impact on blood supply, or through triggering inflammatory processes. Many comorbidities have been implicated in extensor tendon ruptures, including hyperthyroidism, diabetes mellitus, rheumatoid arthritis (RA), connective tissue disorders like systemic lupus erythematosus, and chronic renal failure [6, 8]. Additionally, long-term high-dosage glucocorticoid or fluoroquinolone use, or repeated intraarticular glucocorticoid injections can weaken collagenous tissues, and thus predispose patients for tendon ruptures [3].

Structural factors are often related to prior knee surgeries. To maintain good tissue quality of the extensor tendons in the long run, an optimal blood supply is vital. However, multiple surgical interventions around the extensor mechanism, including distal realignment procedures, will weaken and contribute to reduction of the blood supply [8]. The more extensive the dissection, the higher the compromise of the vascularization.

Yixin Zhou, Professor and Chairman of Department of Adult Reconstructive Surgery, Beijing Jishuitan Hospital, points out: “Patients with the known relevant comorbidities, with stiff knees and a weak extensor mechanism, as well as male patients over 40 with tendinopathy, should raise red flags for surgeons and make them doubly careful with every maneuver avoiding overtension of the extensor. It is obvious that an impairment of vascularization has deleterious effects on any patient. However, in patients suffering from these conditions, the risk of subsequent tendon failure is so much higher. Therefore, every effort should be undertaken to be as vascularization-sparing as possible.”

Upon performing the TKA surgery, various vascular structures are imperiled (Figure 2). First, the medial and descending genicular arteries are at risk during medial arthrotomy. Second, the lateral-inferior genicular artery and the anterior-tibial recurrent artery are at risk during fat-pad excision. Third, the lateral-superior genicular artery is at risk during release of the lateral retinaculum [6, 8–11].