LITHUANIAN UNIVERSITY OF HEALTH SCIENCES MEDICAL ACADEMY
FACULTY OF MEDICINE
DEPARTMENT OF ORTHOPAEDICS AND TRAUMATOLOGY
AUDRIUS POŠKEVIČIUS
ALLOGRAFT TRANSPLANTATION IN CASES OF INSUFFICIENCY OF KNEE EXTENSOR MECHANISM
FOLLOWING TOTAL KNEE ARTHROPLASTY MASTER’S THESIS
MEDICINE
THESIS SUPERVISORS DR. VALDEMAR LOIBA AO. UNIV.-PROF. DR. WOLFGANG HACKL
KAUNAS 2020
CONTENT
1. ABSTRACT...3
2. CONFLICTS OF INTEREST...4
3. ABBREVIATIONS...5
4. INTRODUCTION...6
5. OBJECTIVE AND TASKS...6
6. CASES AND METHODS...7
7. RESULTS...10
8. DISCUSSION...12
8.1 Anatomy of the knee extensor mechanism...12
8.2 Kinematics of the patellofemoral joint...14
8.3 Injuries of the knee extensor mechanism...15
8.4 Insufficiency of the knee extensor mechanism as a complication following TKA...18
8.5 Management of the knee extensor mechanism insufficiency following TKA...20
8.6 Allograft transplantation as an alternative to reconstruct the insufficient knee extensor mechanism following TKA...23
9. CONCLUSIONS...24
10. REFERENCES...25
11. FIGURES AND TABLES...29
ABSTRACT
Background: Rupture of the knee extensor mechanism following total knee arthroplasty (TKA) is rare, but serious and devastating complication. Classification includes three types of rupture: suprapatellar (quadriceps tendon rupture), transpatellar (patellar fracture) and infrapatellar (patellar ligament rupture).
Management of the knee extensor mechanism insufficiency ranges from conservative treatment to various reconstruction techniques. In this article we will try to describe our experience with the allograft transplantation and evaluate this technique as a method to reconstruct insufficient extensor mechanism following TKA.
Methods: A retrospective analysis of three patients with the insufficient knee extensor mechanism after TKA, who underwent reconstruction surgery with the knee extensor mechanism allograft at the Department of Orthopedics, the University Hospital of Innsbruck, Austria.
Results: Our cases showed ambigous results with the first patient achieving great success and satisfying functional results, the second one, who did not manage to reach the great functional lever, highly possible due to previous medical conditions and old age, and lastly the third patient, who did not avoid several postoperative complications.
Conclusions: Just like most of the studies in the litarature, we are also not able to draw definitive conclusions, nevertheless, with the adequate patient choice, a great success may be reached. We would recommend allograft transplantation technique as a useful alternative to treat insufficient knee extensor mechanism, however, more bigger case series or systematic reviews have to be done, in order to evaluate, which of the many techniques promise the best outcome.
CONFLICTS OF INTEREST
The author declares no potential conflicts of interest referring to this article.
ABBREVIATIONS
1. TKA – total knee arthroplasty 2. TEP – total endoprosthesis 3. ROM – range of motion 4. CT – computed tomography
5. MRI – magnetic resonance imaging 6. DOF – degrees of freedom
7. PFJRF – patellofemoral joint reaction force 8. BMI – body mass index
INTRODUCTION
Rupture of the knee extensor mechanism following TKA is rare, but serious and devastating complication. From the anatomical point of view, this injury can happen in any of the knee extensor mechanism components, which include the quadriceps muscle, its tendon, the patella, the patellar ligament, the tibial tuberosity and all the soft tissues attached to the patella. Classification includes three types of rupture: suprapatellar (quadriceps tendon rupture), transpatellar (patellar fracture) and infrapatellar (patellar ligament rupture). Risk factors that are generally involved in this situation: prior operations or revisions, which result in major scarring or stiffness, infections, patella baja, obesity, rheumatoid arthritis, diabetes, hypothyroidism, local corticosteroid injection and use of floroquinolone [Parker et al.][1]. Management of the knee extensor mechanism insufficiency ranges from conservative treatment to various reconstruction techniques. It is always challenging to find the best technique for the patient, as there are many factors included (general condition, functional demand, delay, instability).
Since the orther surgical treatment techniques have been described to lead to functionally unacceptable results (primary repair, soft tissue augmentation, autograft reconstruction), the new techniques as synthetic material augmentation (Marlex Mesh) and allograft reconstruction have gained popularity and closer attention [Abdel et al.; Maffulli et al.; Matsuda et al.][2–4]. However, only small case series reffering to these techniques are available and no definitive conclusions have been drawn [Shau et al.][5].
In this article we will try to describe our experience with the allograft transplantation and evaluate this technique as a method to reconstruct insufficient extensor mechanism following TKA.
OBJECTIVE AND TASKS
Objective: To overview and evaluate allograft transplantation as a method to reconstruct insufficient extensor mechanism following TKA
Tasks:
1. To analyse the cases with allograft transplantation of the insufficient knee extensor mechanism following TKA and compare results with the international experience
2. To review relevant anatomy of the knee extensor mechanism 3. To analyse kinematics of the patellofemoral joint
4. To review injuries of the knee extensor mechanism
5. To overview insufficiency of the knee extensor mechanism as a complication following TKA 6. To review management of the knee extensor mechanism insufficiency following TKA
7. To evaluate allograft transplantation as an alternative to reconstruct the insufficient knee extensor mechanism following TKA
CASES AND METHODS
A retrospective analysis of three patients with the insufficient knee extensor mechanism after TKA, who underwent reconstruction surgery with the knee extensor mechanism allograft at the Department of Orthopedics, the University Hospital of Innsbruck, Austria. The cases are described below:
Case 1
68-year-old male patient underwent follow-up 6 months after left knee-total endoprosthesis (TEP) change and osteotomy in the area of tibial tuberosity in the presence of arthrofibrosis/patella infera and chronic anterior knee pain (Fig. 1). Primary prosthesis was implanted at the age of 56 years and removed after 5 years with prosthesis loosening and successfully reinserted (clinically 4 years after surgery: minor pain, extensor lag of 5-10o; radiologically: no prosthesis loosening, patella baja) (Fig. 2). During the follow-up the patient reported a fall 2 days ago. Active knee extension was not possible. Radiologically, a stable prosthesis was found, but the tibial tuberosity/screw was torn out (Fig. 3). After 3 weeks, the allograft transplantation of the distal extensor mechanism with Achilles tendon and calcaneal bone block (fresh-frozen) was performed. The operation was performed under general anesthesia, the skin was cut in the area of pre-existing scar. During the subcutaneous dissection, the exposed joint cavity was immediately revealed. Both the tibial tuberosity and the patellar ligament were ruptured. Therefore, first of all resection and debridement as well as removal of the cerclages were performed. The allograft was prepared to the suitable size and the Achilles tendon with calcaneal bone block allograft was fixed in the area of the desired tibial tuberosity height with 1 small fragment screw with washer and 2 1.6mm cerclages. The Achilles tendon was thus guided proximal. The latter was formed into 3 strands and reinforced (Fig. 4). The middle strand was pulled through a 6mm tunnel and fixed in the sense of an aperture fixation with an interference screw 6mm coming from distally. In addition, the Achilles tendon was proximal diverted and wound into the quadriceps aponeurosis side-to-side from anterior. The medial and lateral rods were guided laterally around the patella (frame-like) and sutured to the periosteum/retinaculum. The wound was closed in layers with drainages. Postoperatively, the patient was immobilized in extension with a knee brace. From the first postoperative day mobilization was
performed with the help of physiotherapy with a range of motion (ROM) of 0/0/0o under partial load and passive movement in the supine position with ROM of 0/0/30o.
Case 2
68-year-old female patient appeared for ambulant check-up 5 months after desarthrodesis and left knee- TEP (Fig. 5) in condition after left knee arthrodesis about 20 years ago (in presence of primary chronic polyarthritis) and implantation of left knee tissue expander 2 months ago (Fig. 6). Postoperatively after the knee-TEP insertion, a nonirritated wound situation as well as a regular radiographic result were observed, towards the end of the stay the passive ROM of the left knee of 0/0/70o could be achieved in 3 weeks. Until follow-up in 6 weeks a loading of 1/3 of the body weight and a mobility of 0/0/90o during lying or sitting was allowed, the knee brace was adjusted in full extension. The patient already achieved good results until the first follow-up, passive ROM was 0/0/80o, active knee extension strength grade 4.
Several follow-ups were performed almost every month and the patient was always satisfied, she always showed a stable situation, only minor pain, no increased inflammation values, no wound healing disorder, no swelling, no redness, no burning, ROM of 0/0/90o as well as knee extension grade 4 was achieved. However, the patient presented herself for the already mentioned check-up and reported of a painful deterioration and swelling of the left knee, since then a clear regression in the function of the left knee joint. Status showed local swelling, passive ROM at the knee joint 0/0/95o, active knee extension strength grade 2, palpable dent infrapatellar with painful palpation in the area of the lower patellar margin. After sonography, complete lesion of the patellar ligament was detected (Fig. 7). 2 months later the allograft implantation of the whole knee extensor mechanism (fresh-frozen) was performed. The operation was performed under general anesthesia. The incision was made in the area of the pre-existing skin scar from a parapatellar joint access with excision of patella as well as the chronically ruptured patellar ligament. Afterwards, the tibial tubertosity was exposed and the cerclages were loosened and removed. The tuberosity was removed. The allograft was used with its entire tibial bone block in terms of length and width. However, the thickness was slightly reduced to allow an anatomical fit. The tuberosity of the allograft was fixed with screws and cerclages in a suitable position with respect to tension. The patella height was verified in the lateral beam path by means of a C-arm. Tight suturing into the quadriceps tendon mirror was then carried out in absolute extension by means of fiber-reinforced sutures and wound closure in layers (Fig. 8). Subsequently, an application of a long leg cast. The postoperative movement therapy was carried out in a strictly relieving manner until the cast was removed after 6 weeks.
Case 3
56-year-old male patient presented for follow-up a total of 2.5 years after primary right knee-TEP (Fig.
9) (in case of a right knee gonarthrosis in condition after anterior and posterior cruciate ligament lesion (Fig. 10)) and several postoperative complications that occurred during the course. After the knee-TEP surgery, massive pain and swelling of the right knee was observed. Sonographically a haematoma was confirmed which was surgically removed in one week, which quickly led to an alleviation of symptoms.
After 2 weeks of stationary treatment a flexion of 103o was achieved. 2 months later the patient reported an improvement in pain, but there was a tendency to swelling due to stress. Status showed a secure free gait, retropatellar crepitus, passive flexion improved to 130o. 4 months later the patient appeared with increasing pain, minimal swelling tendency and a worsening of the flexion to 90o, the Zohlen sign clearly positive, signs of effusion minimally positive. Retropatellar arthritis was detected after a computed tomography (CT). A total of 18 months after the knee-TEP implantation, a secondary patella back surface replacement and inlay change was performed. The first check-up in 6 weeks showed no complications, the operated knee was well movable with ROM of 0/0/130o, knee compression was strength grade 4. Immediately afterwards the patient reappeared and reported acute pain in the area of the right thigh, which led to a clear effusion formation at the right knee joint, whereby the knee extension was no longer possible. A quadriceps tendon rupture was confirmed sonographically. Surgically, a quadriceps tendon suture/refixation and postoperative immobilization by knee brace were then performed, locked in full extension. During the 9 months many follow-ups were performed every 6 weeks and the pain history, mobility and strength of the right knee always improved up to the ROM of 0/0/90o and strength grade 4 of the knee extension. The patient always complained of persistent pain and smouldering, physiotherapy was no longer successful. Finally, the patient took part in the follow-up mentioned at the beginning and reported a deterioration of the strength situation. Radiologically a clear patella low position showed up, in the comparison over the last 8 months clear descensus. A magnetic resonance imaging (MRI) confirmed a thinned quadriceps tendon on the right (Fig. 11). An allograft transplantation of the entire right knee extensor mechanism (fresh-frozen) was decided. The surgical procedure was performed 2 months later under general anesthesia and started with the incision in the area of the pre-existing scar. Then the extensor mechanism was sparingly cut out. The allograft was initially coffin-shaped in the are of the tibial tuberosity and fitted into the recipient site. There in a good fit the fixation with bicortical small fragment screws was performed. A physiological patella height of the graft was observed (Fig. 12). Subsequently, suturing was performed in the medial and lateral retinaculum as well as in the quadriceps (Fig. 13). The soft tissue fixations were performed under maximum tension in full extension. Proximal fixation was performed with fiber-reinforced sutures strength 2. Layerwise - wound closure via drainage (Fig 14). A knee brace was placed over the bandage
in a locked, extended position while still under anaesthetic. Mobilization was allowed by partial loading with half body weight in the knee brace adjusted for at least 4 weeks.
RESULTS
Case 1
We would consider this case a success. No postoperative infection or wound healing disorder developed.
Radiologically there was no material fracture or loosening (Fig. 15). The patient presented with a clearly swollen knee in the area of the calf for follow-up 6 weeks after surgery. He did not report any physiotherapy and did not use a knee brace. The knee joint was mobile 0/0/30o. Further physiotherapy and use of the knee brace with the setting 0/0/0o was requested. One month later, the patient presented for a check-up and reported progress in physiotherapy and compliance with the brace use. The knee joint was well mobile 0/0/90o with active knee extension up to 20o extensor lag possible. Radiologically there were no changes from the last follow-ups (Fig. 16). Further physiotherapy was performed, the knee brace was extended to the ROM of 0/0/60o. After another 3 months, the patient appeared for a check-up with a well mobile knee joint with ROM of 0/0/100o and active knee extension of 90o away up to approximately 20o extensor lag. A total of 9 months after the operation, the last follow-up was carried out, the patient was satisfied, no complaints, active extension was well possible, flexion to 90o possible.
From then on the patient did not appear for more than one year for the follow-up, assuming that he had no further complaints.
Case 2
This case is quite complicated to judge, but in our opinion it was also a success. At the first follow-up 6 weeks after the operation, the long leg cast was removed and the wound was nonirritated, the mobility was 0/0/35o, but the function of the extensor mechanism was intact. Radiologically, a sufficient position of the graft was proven. Physiotherapy was requested in the range up to a maximum of 60o passive or actively assisted knee extension. After one month passive ROM improved to 0/0/70o, knee extension strength grade 3 was achieved. The patient reported ongoing physiotherapy and still pain. After 2 more months the patient was very satisfied, ROM was 0/0/85o, after 6 weeks afterwards - 0/0/90o. A total of 7 months after the operation, the patient reappeared for a check-up and reported pain in the left knee for 3 weeks. Clinically no worsening was noticed, passive extension was still 90o, but she could not extend the knee completely with the leg lifted and thus had an extensor lag of about 15o. Sonography showed
an incomprehensible rupture of the extensor at the base of the graft. After another 1 month, an MRI was performed, but the rupture was not detected. At the last check-up (8 months postoperatively) the patient still had minor complaints: limping gait pattern, pain during loading, ROM was 0/0/90o as before, strength grade 3 of the knee extension. Clinically in palpation the extensor mechanism was continuous, both surpra- and infrapatellar. Since then, the patient has never appeared for check-ups for the next 2 years. There were no postoperative complications, radiologically there was always a stable implant position, a regular patella height and fixation of the graft. Clinically, good mobility and sufficient strength were achieved. Recurrence of pain or relative insufficiency is explained by the complicated history, which suggests limited clinical results.
Case 3
In this case it was not managed to avoid the postoperative complications. Postoperatively, there were no complications until the 6th week, when a fissure of the tibia in the area of the stepped incision was radiologically detected during a follow-up (Fig. 17). Consequently, the placement of a long leg cylinder cast was performed in full extension. 3 months later, an osteosynthesis of the right proximal tibia was performed (Fig. 18). 2 months after the osteosynthesis it proceeded again without complications, knee extension strength grade 4 and passive flexion of 85o were achieved. Each follow-up was always better, 8 months after osteosynthesis knee extension strength 5 and passive ROM of 0/0/125o were achieved.
In total, 1 year after osteosynthesis, the patient presented for follow-up and reported deterioration. At status one saw a limping gait pattern, passive ROM deteriorated to 0/5/95o. Radiologically there were no changes compared to the last check-ups. It was suspected that the patient had implant-related complaints. The osteosynthesis material was removed 6 months later. At the first follow-up 6 weeks after the operation, the patient did not report any alleviation of his complaints, performance of the knee was the same as before. 3 weeks after the operation, the patient was hospitalized due to suspicion of knee-TEP infection, but the infection was ruled out after the knee puncture. One month later the patient reappeared for a follow-up with existing functional deficits of the right knee and 2 options were suggested: knee brace right with Swiss lock or arthrodesis of the right knee joint. For the time being, the patient did not want to take advantage of any of these options. 3 weeks later, the patient presented for a check-up and reported palpatory sensation of the anterior ossicle at the right knee. Radiologically, a 1x1x1cm ossicle was found, corresponding to an avulsion of the most cranial fragment of the bone block of the tibial tuberosity. An osteosynthesis of the tibial tuberosity on the right knee was immediately performed. Tibial tuberosity was fixed with 2 screws and additionally secured with a McLaughlin loop/Cerclage. Postoperatively radiologically a tearout of the refixed fragment was visible, therefore a reconstruction of the patellar ligament with Achilles tendon and calcaneal bone block allograft was
performed after 3 days without complications (Fig. 19). 6 weeks after the revision, the patient came to the control with healed wound situation, palpatory continuous patellar ligament. Mobilization in the range of 0/0/30o and partial loading with 50% of the body weight was allowed. During a guided check- up 4 weeks after the procedure, the radiologically regular height of the patella and stable fixation of the allograft to the tibial head were observed (Fig. 20). An extension of the ROM to 60o both in the knee brace and with physiotherapy was requested. Further rehabilitation took place in a specialized clinic.
From then on the patient did not appear for 4 months for a check-up in the hope that he would experience an improvement. Basically there were several complications after the first allograft reconstruction and we could not judge that as a success. After the last operation the patient was doing well, but the follow- up is too short to draw early conclusions.
DISCUSSION
Anatomy of the knee extensor mechanism
Basically, the knee extensor mechanism consists of four quadriceps muscles, quadriceps tendon, patella and patellar ligament. In addition to that, it also includes tibial tuberosity and all the soft tissues attaching to patella (restrictor ligaments, infrapatellar fat pad, bursae und plicae) [Andrikoula et al.][6].
All quadriceps muscles are innervated from the femoral nerve, which arises from the nerve roots at the second to fourth lumbar vertebrae (L2 to L4). The arterial supply is mainly ensured by the femoral, popliteal and anterior tibial arteries. The primary vascularization to the whole extensor mechanism comes from the descending genicular, superior and inferior medial genicular, superior and inferior lateral genicular arteries and the recurrent branch of the anterior tibial artery [Nam et al.][7].
Quadriceps muscle is composed of four muscles: rectus femoris, vastus medialis, vastus lateralis and vastus intermedius [Waligora et al.][8]. The vastus medialis can be more particularly divided into two following: the vastus medialis longus and the vastus medialis obliquus. Nevertheless there is no evidence that these two structures are independent from a functional point of view [Andrikoula et al][6].
These muscles form a trilaminar structure called quadriceps tendon, which inserts into the patella. The superficial layer is made of rectus femoris, which inserts into the superior pole and superior third of the anterior surface of the patella. Vastus lateralis and vastus medialis make the intermediate layer, which inserts into the base of the patella. The deep layer contains the vastus intermedius, which inserts into the base of the patella posterior to the other layers [Astur et al.][9].
Patella is the largest sesamoid bone in the body and is located deep to the fascia lata within the quadriceps tendon in front of the knee joint, providing an attachment point for tendons of quadriceps
and patella. It is triangular in shape with its apex pointing downwards, while its base lies proximally.
The posterior surface is divided into a medial and a lateral facet. From the inferior pole originates the patellar ligament, also known as a patellar tendon, which inserts on an anterior prominence of the proximal tibia, onto the tibial tuberosity [Cox et al.][10]. The superior part of this strong, thick band, which is actually a continuation of the quadriceps tendon, overlies the infrapatellar fat pad, while the inferior part overlies the deep infrapatellar bursa.
Restrictor ligaments, that are attaching to the patella, also belong to the knee extensor mechanism. The main medial restraint on the patella is the medial patellofemoral ligament, which is responsible for 53% of the containment force [Astur et al.][9]. It originates from the medial femoral epicondyle, distal to the adductor magnus tendon insertion onto the adductor tubercle and proximal to the origin of the superficial medial collateral ligament, and inserts on the superior medial border of the patella, as it underlies the distal portion of the vastus medialis obliquus. Secondary medial stabilizers of the patella include the medial retinaculum, patellomeniscal ligament and the patellotibial ligament. The medial retinaculum consists of the fibrous expansion of the vastus medialis obliquus and the quadriceps tendon. It inserts onto the superior medial border of the patella. The medial patellomeniscal ligament whereas originates in the distal third of the patella and inserts on the inferior portion of the patella and the anterior cornu of the medial meniscus. The medial patellotibial ligament has been described as expanding from the inferior medial edge of the patella to the insertion area 1,5cm distally to the joint line in the anteromedial region of the tibia. Contrary to the medial compartment, the lateral retinaculum includes two major components: the superficial oblique and the deep transverse retinaculum. The superficial oblique one is made of the fibrous expansion from the vastus lateralis and iliotibial band, which inserts into the lateral border of the patella, while the deep transverse retinaculum consists of three major components: transverse patellofemoral ligament (epicondylopatellar band), the deep transverse retinaculum and the patellotibial band.
Infrapatellar fat pad (also Hoffa’s fat pad) is one of the knee fat pads, the other two being the anterior suprapatellar and posterior suprapatellar fat pads. It is located posterior to the patellar tendon and anterior to the capsule. This intracapsular structure plays a role in stabilizing the patella and, as it is richly innervated, is one of the sources of anterior knee pain [Draghi et al.][11]. A bursa is a fluid-filled structure that is present between either skin and tendon or bone and tendon. There are three bursae around the patella: prepatellar bursa, the superficial and deep infrapatellar bursae, and the suprapatelar bursa. The prepatellar one is located between the patella and the surrounding subcutaneous tissue, the superficial infrapatellar bursa expands from the tibial tubercle and the overlying skin, while the deep infrapatellar one locates between the posterior part of the patellar tendon and the tibia, lastly the suprapatellar bursa is located betwen the quadriceps tendon and the fumur [Chatra][12]. Plicae are thin and almost transparent foldings of the synovium into the knee joint, which occur with inconsistent
frequency. The four types of knee plicae are known to exist: suprapatellar, medial parapatellar, infrapatellar and lateral parapatellar plica. The suprapatellar one runs from the lateral patellar tendon to the medial wall of the knee, the medial parapatellar expands from the medial wall of the knee joint to the infrapatellar fat pad, the infrapatellar plica extends from the intercondylar notch to the infrapatellar fat pad while the lateral parapatellar one transverses from the fat pad towards the superior aspect of the lateral patellar recess [Schindler][13].
Kinematics of the patellofemoral joint
The patellofemoral joint is a diarthrodial joint, consisting of the trochlear surface of the distal anterior femur and the posterior surface of the patella. The function of the patella is multifaceted and its purpose is to serve as a mechanical pulley for the quadriceps as the patella changes the direction of the extension force throughout the knee range of motion. It also centralizes the divergent quadriceps forces during flexion, as the patella engages within the trochlea. In addition to that, the patella increases the area of force distribution.
As a gliding joint, patella has movement in multiple planes. During knee flexion and extension six degrees of freedom (DOF) are involved in patellar kinematics. These include (a) flexion, (b) tilt, (c) rotation, (d) medial-lateral shift, (e) anterior-posterior translation, and (f) proximal-distal translation (Fig. 21). According to DOF classification, the first three movements are also considered to be rotations, while the last three can be described as translations [Yu et al.][14]. Patellar flexion is defined as the rotation around the femoral flexion axis such that anteriorly directed motion of the superior pole of the patella results in positive values for flexion. Patellar tilt stands for the rotation about the patellar long axis in such way, that posteriorly directed motion of the medial border of the patella results in positive values for tilt. Patellar rotation whereas is described as the rotation of the patella around the anterior- posterior axis, what makes the medially directed motion of the superior pole of the patella end up in positive values for spin. Medial-lateral shift is the transverse displacement of the patellar center point along the component of the vector directed along the flexion axis of the femur, so that the lateral movement is positive. Anterior-posterior translation is defined as the displacement along the component of the vector, which is directed along the third axis of the femur such that created anterior movement is positive. Lastly, proximal-distal translation is known as the displacement along the component of the vector directed along the long axis of the femur such that proximal movement is positive [Loudon][15].
The kinematic characteristics of the patellofemoral joint are considered to be the result of a complex interplay of components. It means, that it is all about the balance of the knee extensor mechanism: once any part of the system is changed, all the remaining ones are affected and the excessive
patellofemoral joint stress may occur. The stress placed on the patellofemoral joint is evaluated by patellofemoral joint reaction force (PFJRF) divided by the joint contact area and is measured as force per unit area. PFJRF is the compression force, acting on the joint and it depends on muscle tension and knee joint angle (Fig. 22). When the PFJRF increases (due to the changes in the lever system) or the contact area between the patellar surface and the trochlea decreases (due to poor patellar positioning), it results in excessive patellofemoral joint stress, which may be harmful to the joint cartilage and cause patellofemoral pain syndrome [Petersen et al.][16].
Numerous factors can make an impact on patellofemoral kinematics and change the balance of the knee extensor mechanism. Firstly, it depends on the morphology of throchlear groove and the patella.
At patellar zero position the patella is not congruent with the femoral trochlea. During the flexion the patella enters the groove, shifts medially, then laterally. The flat lateral facet of the trochlear groove and different forms of dysplastic patella are associated with subluxation and dislocation [Andrish][17].
Besides the osseous structures, the soft tissues surrounding the patella play a vital role in patellar tracking at the initial period of flexion. These include quadriceps (especially the vastus medialis and vastus lateralis, which influence patellar spin and tilt with less influence over translation), patellar tendon (the angle between the patellar and quadriceps tendons help to adjust the flexion and extension of the patella in order to maintain the patellar contact area perpendicular to the patellofemoral joint reaction force), medial retinaculum (guides the patella as it rotates medially), lateral retinaculum (contributes 10%
restraint of lateral displacement), and medial patellomeniscal ligament, which is the primary restraint to the lateral displacement of the patella during the initial 30 degrees of knee flexion (56%) [Lorenz et al.;
Philippot et al.][18,19]. Lastly, the interaction betweet patellofemoral and tibiofemoral joints is also though to influence the patellar kinematics. It has been reported, that tibial rotation and varus, as well as valgus, can make an impact on patellar tracking. When the tibia rotates medially with respect to the femur, the patella tends to move to the lateral side towards the tibial tubercle. That means, that tibial medial rotation could cause patellar lateral shift [Yu et al.; Keshmiri et al.][14,20].
Injuries of the knee extensor mechanism
The knee exensor mechanism consists of many structures and once any of them is injured, the function of the whole mechanism is disrupted. The injuries of the knee extensor mechanism are quite common and may occur due to acute trauma, overuse injuries or chronic degenerative disease. The most common and basic injuries are the rupture of quadriceps tendon and patella ligament, and the patella fracture.
The rupture of the quadriceps tendon makes 28,9% of all extensor mechanism injuries and tends to occur in patients older than 40 years with an avarage of 61. Many authors report men being almost 10 times more likely to sustain a rupture than women. It affects the non-dominant limb twice more often than the dominant one [Garner et al.][21]. Antomically ruptures frequently begin in the rectus femoris tendon extending to vastus intermedius or move transversely to either medial or lateral patellar retinaculum. Most ruptures of the quadriceps tendon occur while attempting to regain balance in order to avoid a fall. Forced and rapid contraction of the quadriceps muscle in a semiflexed position is the typical mechanism of the injury. Risk factors include hyperparathyroidism, diabetes mellitus, chronic renal failure, obesity and coricosteroids use [Nori][22]. Diagnostically it is extremely important to diagnose the rupture as early as possible, while delayed surgical repair is linked with adverse outcomes.
The triad of symptoms include acute knee pain, palpable suprapatellar gap and loss of active extension.
The rupture may also be accompanied by large haemarthrosis which obscures clinical findings. The weak extension also might be elixted, if the patellar retinaculum remains intact. Also partial ruptures may occure, which follow with a palpable supratellar defect but the active knee extension remain normal.
The diagnosis is clinical, but radiographs provide the evidence of an acute rupture. Positive findings on a lateral radiograph with the injured knee flexed to 30o include obliteration of the quadriceps tendon shadow, suprapatellar mass and an inferiorly displaced patella.In unclear diagnoses magnetic resonance imaging (MRI) or ultrasound may be used. MRI is the gold standart, while the ultrasound is operator dependent, even though it is cheap and readily available diagnostic tool [Rodriguez-Merchan][23].
Partial rupture of the quadriceps tendon can be treated conservatively, which involve cylinder cast or brace immobilisation in full extension for aproximatelly 4 to 6 weeks. It is followed by physiotherapy in order to promote knee flexion and increase quadriceps strenght [Egol et al.][24]. Complete rupture whereas require urgent surgical repair, while if it is delayed, the tendon retracts and binds down to the femur, which makes surgical repair difficult and functional outcomes poor. The surgical method includes the reapproximation of the tendon to bone using nonabsorbable sutures passing through the bone tunnels.
The tendon must be repaired close to the articular surface in order to avoid the patellar tilting. The midsubstance tears may undergo end-to-end repair, but the edges must be freshened and slightly overlapped. Most repairs are also reinforced with a distally based partial thickness triangular flap of tendon, which is then reflected over the suture line (Scuderi repair). Chronic tears may require a V-Y advancement of a retracted quadriceps tendon (Codivilla V-Y-plasty technique). Postoperatively a knee is immobilized in full extension for 5-6 weeks which then follows with the physiotherapy [Hak et al.][25]. Many retrospective case series have shown good to excellent functional outcomes, but some complications may occur. These include rerupture, loss of knee motion, persistent quadriceps atrophy and infection [Nori][22].
Patellar ligament ruptures are quite rare and only make 12,3% of all knee extensor mechanism injuries. Most patients are younger than 40 years old with men making 95,5% of all the cases [Garner et al.][21]. The injury is also often described in athletes. Anatomically the most common site of rupture is at the junction between the tendon and the inferior pole of the patella. An indirect mechanism of injury is the most common, the rupture is usually caused by sudden contraction of the quadriceps muscle with the knee in slight flexion (sudden imulsion, sprint, avoiding a fall) [Tuong et al.][26]. Pre-existing patellar tendonitis and degenerative tendinosis are major risk factors, the others include rheumatoid arthritis, systemic lupus erythematosus, diabetes, chronic renal failure, systemic corticosteroid therapy and local steroid injection [Rosso et al.][27]. Symptomatically the pattelar tendon ruptures present with pain, swelling and bruising in and around the patella. Physical examination may reveal a palpable defect distal to the inferior pole of the patella and the patella migration proximally (patella alta) due to unopposed quadriceps contraction. In addition to that one can notice hemarthrosis, partial or complete loss of active extension, painful passive knee flexion and quadriceps artrophy by chronic injury.
Radiographic examination shows patella alta on lateral X-ray view. Most effective method is MRI, especially if other intra-articular or soft tissue injuries are suspected. Nevertheless ultrasonography can also distinguish between partial and full thickness tears [Rodriguez-Merchan][23]. Treatment can be conservative (immobilization in full knee extension for 3 to 6 weeks) by partial tears when full active knee extension is present. Otherwise early repair is extremely important as it shows overall better outcome. Surgical technique includes primary repair of the tendon through a midline incision in which tendon and retinacular tears are exposed, frayed edges and hematoma are debrided and the tendon ir repaired with nonabsorbable sutures. The repair can also be reinforced with a cerclage wire or cable in order to alleviate tension on the suture line and protect the repair. This also allows to do more aggressive postoperative rehabilitation. Delayed repair cases have more surgical options which include hamstring and fascia lata autograft augmentation of primary repair or Achilles tendon allograft. Postoperatively follows knee immobilization for 6 weeks with possible active flexion at 2 weeks (more conservative management by delayed repairs). Complications happen much more often by delayed repairs and may include knee stiffness, rerupture, infection, persistent quadriceps atrophy and patella baja [Egol et al.;
Rosso et al.][24,27].
Patellar fractures are relatively common with 58,8% of all knee extensor mechanism injuries. Males suffer from this fracture two times more often than females with generally average age of 56,3 years [Garner et al.][21]. Classification depends on the fracture pattern and includes many different options, which often predict treatment (Fig. 23). The most common types are transverse, multifragmented and avulsion of the upper or lower pole fractures. Transverse fractures mostly appear in young patients with a good bone quality. Avulsion ones are functionally equivalent to disruptions of union tendon-bone of patellar or quadriceps tendon. Patellar fractures may be also classified as displaced
or non-displaced [Jarraya et al.][28]. Mechanism of injury may be due to direct or indirect trauma. Direct trauma may produce incomplete, simple, stellate or comminuted fracture patterns. Displacement is mostly minimal and active knee extension may be preserved. Indirect injuries occur due to forcible eccentric quadriceps contraction while the knee is in a semiflexed position (stumble or fall). A transverse fracture pattern is most common with this mechanism. The degree of displacement may be higher and active knee extension is usually lost. Combined direct/indirect traumas may also occur when the patient experiences both injuries at the same time (for instance a fall from a height) [Egol et al.][24]. Clinically physical examination shows swelling, tenderness of the affected knee, hemarthrosis, pain with palpation and a palpable defect. Radiographic evaluation includes standard anteroposterior and lateral radiographs, in which a fracture is seen. Other radiological tests are rarely indicated, only when other joint damage is suspected [Rodriguez-Merchan][23]. Treatment may be conservative (immobilization for 4 to 6 weeks), when the fracture is non-displaced or minimally displaced (2 to 3 mm) and the extensor mechanism is intact. Otherwise surgical intervention follows. Fractures with more than 3 mm fragment displacement with loss of active extension or open fractures are treated with open reduction and internal fixation.
There are many techniques to do that, including tension banding or circumferential cerclage wiring.
When the fracture includes a large, salvageable fragment in the presence of smaller, comminuted polar fragments in which it is impossible to restore the articular surface or to achieve stable fixation, the partial patellectomy is used. Total patellectomy is rarely indicated and is reserved for extensive and severely comminuted fractures. All the surgical techniques are normally followed by immobilization for 3 to 6 weeks [Henrichsen et al.][29]. Complications may occur which include symptomatic hardware, fixation failure, infection, non-union, refracture, osteonecrosis, posttraumatic osteoarthritis, loss of knee motion or strength and patellar instability [LeBrun et al.][30].
Insufficiency of the knee extensor mechanism as a complication following TKA
Extensor mechanism rupture is a rare but really devastating complication after TKA. Its incidence is reported to range from 1 to 12% in all the TKA patients [Parker et al.][1]. Classification includes three types of rupture: suprapatellar (quadriceps tendon rupture), transpatellar (patellar fracture) and infrapatellar (patellar ligament rupture). Although most of these injuries occur in the immediate postoperative period, it can also happen intra-operatively. Many factors increase the risk of an extensor mechanism rupture after TKA, which generally include: prior operations or revisions, which result in major scarring or stiffness, infections, patella baja, obesity, rheumatoid arthritis, diabetes, hypothyroidism, local corticosteroid injection and use of floroquinolone [Cottino et al.][31].
Quadriceps tendon rupture after TKA is really rare with 0,1% prevalence. Normally these ruptures in TKA are non-traumatic and most of the patients are elderly. It can also be caused by minor traumatic episode, nevertheless in these cases the patient mostly has an underlying degeneration of the tendon. That indicates the importance of a patient’s predisposing risk factors, which specifically include systemic disorders and prior surgical procedures (especially patellar over-resection, quadriceps snip, V- Y turndown) [Vaishya et al.][32]. Patients with a partial rupture and less than a 20o extensor lag can be successfully managed conservatively with immobilization of the knee in extension for 6 weeks. Greater than 20o extensor lag indicates that surgical repair will be necessary. It may include end to end method, suturing through drill holes or by using suture anchors (Fig. 24). Unfortunately, direct repair has shown poor results (35% re-rupture rate) with a high complication rate (33%) [Nam et al.][7]. This means, that augmentation is mandatory. Synthetic grafts or Achilles tendon/complete extensor mechanism allografts are the best options on this occasion [Rosenberg][33].
Patellar ligament ruptures following TKA are infrequent, affecting 0,7 to 2,5% of the TKA patients [Rodriguez-Merchan][23]. It can occur both intraoperatively and postoperatively. Intraoperative ruptures may happen due to overzealous dissection or failure to protect the tendon during the tibial cut.
Postoperative ones may be either traumatic or atraumatic. Traumatic ruptures are caused by direct trauma (mostly fall on a flexed knee), whereas non-traumatic ones affect degenerated tendons and result in intrasubstance lesions. The majority of the patellar ligament ruptures occur at the tibia tubercle insertion, less frequent are intrasubstance and infrapatellar avulsions. Specific risk factors include stiffness after primary TKA and previous revision procedures or extensor mechanism repairs. Hypovascularity is also a huge factor, which is the result of a medial parapatellar approach (3 out of 4 genicular vessels are sacrificed, the fat pad is removed) [Rhee et al.][34]. Treatment depends on many factors, which include acuity and location of the injury, the quality of the remaining tissue, physiologic age and activity demands of the patient. Conservative treatment with bracing may be used in patients with partial ruptures, who have low functional demands and are poor surgical candidates. In most of all the other cases surgical intervention is demanded. Direct repair may be used when a rupture occurs intraoperatively or in the immediate postoperative period. However it shows poor functional results, it often leads to re-rupture, deep infection and extensor lag [Anand et al.][35]. All the other cases require complete reconstruction with augmentation. Many options include hamstring autograft, fresh-frozen or freeze-dried Achilles tendon with bone block, complete extensor mechanism allograft and synthetic grafts such as Marlex Mesh. Synthetic augmentation with Marlex Mesh is broadly preferred technique [Browne et al.][36].
Periprostetic patellar fractures are rare and range from 0,68 to 5,5% in all the patients following TKA. They are more common in males than in females, possibly due to higher body mass index (BMI) and physical activity level. Patellar fracture may occur secondary to direct trauma to the anterior aspect
of the knee or secondary to a strong contraction of the quadriceps muscle with the foot fixed on the ground [Sayeed et al.][37]. An increased risk is known for resurfaced patellas, especially with excessive resection. Use of a patellar implant with a large central plug, use of a metal-backed cementless patellar component, component malalignment and avascular necrosis of the patella also stand for greater risk for the patellar fracture [Rodriguez-Merchan][23]. The Universal Classification System for periprosthetic fractures categorises these fractures into two main types: type A includes fractures at proximal (A1) or distal (A2) pole of the patella with no loosening of the patellar component. Type B1 includes non- displaced transverse fractures, stable component and intact extensor mechanism. B2 and B3 whereas suggest loosening of the patellar component, with B3 also including substantial bone loss [Duncan et al.][38]. Treatment is based on fracture location, pattern, remaining bone stock, implant stability, quality of the remaining bone stock and extensor mechanism integrity. Conservative management shows excellent results in patients with a stable implant and an intact extensor mechanism. Type B fractures, especially with disruption of the extensor mechanism, require surgical treatment. The most common technique of many is open reduction and internal fixation (Fig. 25). However, the complication rate for surgical treatment is 50%, prevalence of extensor lag is 58% and 42% of the cases end up in a reoperation [Nam et al.][7].
Management of the knee extensor mechanism insufficiency following TKA
Management of the knee extensor mechanism insufficiency ranges from conservative treatment to various reconstruction techniques. It is always challenging to find the best technique for the patient, as there are many factors included (general condition, functional demand, delay, instability etc.). Many case series have demonstrated inconsistent results of surgical repair and reconstructive techniques and the choice is usually tailored to the patient case by case.
Conservative treatment of the injured knee extensor mechanism requires the patient to depend on walking aids and/or knee braces. These braces are normally locked into extension and are unlocked only allowing the patient to sit [Bates][39]. It is rarely satisfactory for the active patient. However, it may be acceptable for elderly, sedentary patients or for those, who are unfit for surgical intervention.
Direct repair with a nonabsorbable suture, anchor or staple fixation may be attempted in patients with acute and partial knee extensor mechanism disruption. However, the poor outcomes of primary repair have been often reported in the literature, especially for chronic disruptions, where the tendon is retracted or the soft tissue is not sufficient to perform a good repair [Abdel et al.][2]. For this reason direct repair has been abandoned as a treatment option for chronic extensor mechanism disruption and even by fresh and partial disruptions other surgical techniques should be taken into consideration.
In cases when the knee extensor mechanism disruption is caused by patellar ligament rupture, soft tissue augmentation may be an option. The most commonly used surrounding soft tissues are semitendinosus, gracilis, and a turned down quadrideps tendon. The use of hamstring tendon has also been described in literature [Maffulli et al.][3]. Reconstruction using the semitendinosus tendon includes several techniques. Augmentation may be used with semitendinosus tendon alone or, when it is too short, together with gracilis tendon. When the autograft is harvested, a tunnel is created on the distal third of the patella bone and the graft is passed from the medial to lateral through the tunnel and sutured to itself (Fig. 26 (a)). If the patella bone is too thin or fragile for creation of a tunnel, the graft is passed through the quadriceps tendon on top of the patella bone (Fig. 26 (b)). However, quadriceps turndown has to be performed to maintain patellar tilt in this technique [Matsuda et al.][4]. Another fixation technique includes securing the graft to the tibia on the lateral side after it is passed through the tunnel in the patella (Fig. 26 (c)). The graft may also be secured with interference screw in the tunnel through the tibial tubercle [van der Zwaal et al.][40]. The augmentation with hamstring tendon uses similar technique, except the graft is crossed in the middle to create a figure-of-eight form [Mihalko et al.][41]. Turndown quadriceps tendon flap technique includes detaching of the middle third of the tendon from muscle junction and turning down to secure it either at the distal end of the patellar tendon or to drill into tibial tuberosity [Lin et al.][42]. In order to reduce the load on any reconstructed tendon, reconstruction may be combined with wire cerlage or metalwork. It allows early rehabilitation but requires a second surgery to remove the implanted material [Nguene-Nyemb et al.][43]. All of these grafts may be harvested from ipsilateral or contralateral leg. There are many different combinations of techniques and many different case series in the literature, which show good or excellent result with minimal or no extensor lag.
However, most of the series have many limitations, include only few cases and have poor level of evidence, which does not allow to draw definitive conclusions [Maffulli et al.; Samagh et al.; Woodmass et al.][3,44,45].
In addition to all the soft tissue augmentation techniques described above, where an autograft tendon is used, the most commonly used autograft for reconstruction of the injured knee extensor mechanism is bone-tendon-bone autograft from contralateral side. In this technique a graft of a block of tibial bone, middle third of the patellar ligament and a block of the patella is taken from the opposite knee. One way of it is then fixed to the tendon insertion at the tibial tubercle with srews, while the other is secured to the patella [Milankov et al.][46]. There are also many different fixation methods described in the literature. In many cases the construct is supported with metallic wire cerclage, which also allows early rehabilitation [Temponi et al.][47]. Generally, this technique allows anatomical patellar tendon reconstruction with its length serving as reference. However many complications as quadriceps weakness and anterior knee pain are common, also a normal contralateral knee is disrupted, even though some studies say, that it makes no impact to its function [Matsuda et al.][4].
Synthetic material augmentation is a great option for patients with poor soft tissue condition. It has many advantages as no donor site morbidity, no additional surgery time for harvesting donor, free from possible transmitted infection and no regulatory restriction. However, many materials are not available in all countries and they are prone to infection. There are many different synthetic materials used for augmentation (Leeds-Keio scaffold type artificial ligament, LARS etc.), but the one, which has gained popularity is polypropylene mesh (Marlex Mesh) [Abdel][48]. It is a knitted monofilament polypropylene heavyweight mesh commonly used for hernia and urological procedures. On this occasion a 25x35cm sheet of it is rolled 8-10 times onto itself and sewn together with 1 to 2 heavy, nonabsorbable sutures with a running-locked closure. The distal end is secured to a trough in the proximal tibia using cement and screw fixation. The proximal end is then tunneled from deep to superficial on the lateral aspect of the host patellar tendon and sutured to the quadriceps tendon proximally. The whole synthetic mesh graft is then ultimately covered with the medial and lateral laps of the host tissue [Browne et al.][36]. The rehabilitation includes immobilization in a long leg cast for 6 to 8 weeks, with only touch-down wight bearing allowed. This technique is inexpensive, easy to perform and the material is easily accessed in most of the countries. The clinical results are consistent and show good knee extensor lag recovery withouth lengthening of the graft. Only a mean postreconstruction extensor lag of 10o among a small subset of patient has been described [Abdel et al.][49]. No unique complications have been also noted, with low to zero reconstruction fail rate and 8-10% infection rate [Browne et al.; Abdel et al.][36,49].
Allograft reconstruction is another option to treat large defects of knee extensor mechanism. The whole knee extensor mechanism (proximal tibia, patellar ligament, patella and several centimeters of quadriceps tendon) or Achilles tendon with calcaneal bone block allograft may be used. Regardless of which type of allograft is used, it should be fresh-frozen, because inferior results have been reported with the use of freeze-dried grafts [Bates][39]. Allograft choice is based on the quality of the native patella: if the patella is intact and mobile (inferior pole can be brought down to within 2-3cm of the joint line), then it is preserved and the Achilles tendon graft may be used, otherwise, the whole patella is completely replaced using the whole extensor mechanism allograft [Cottino et al.][50]. During the surgery the host extensor mechanism is reached through a midline incision as retinaculum is dissected and medial and lateral flaps are created. After the residual extensor mechanism is exposed, the position of the allograft is simulated with the patient’s knee in extension and in 30o flexion to center the patella on the trochlea, in order to determine the optimal height and the position of the future graft. The 7cm long, 15mm wide and 2cm deep bone trough is then created on the native anterior tibial tubercle. At the same time the allograft is prepared as the quadriceps tendon is divided into two strands longitudinally and four anteroposterior holes and a transverse tunnel are drilled into the patella to allow future suture of the patellar retinaculum (Fig. 27). The allograft tibial bone block is impacted into the host tibial bone
trough for good primary stability and secured with double transosseur cerclage wire and two anteroposterior compression screws. Simultaneosly several heavy sutures are used to pull the host quadriceps distally and create maximal tension. The allograft is sutured afterwards to the overlying host quadriceps with heavy nonabsorbable sutures, a patellotibial cerclage whereas protects the allograft and is tightened at 30o flexion. Finally, previously elevated medial and lateral flaps are closed over the allograft. The patella is not resurfaced in order to avoid failure. Postoperatively, a brace is worn in full extension for 6-8 weeks, avoiding full weight bearing. Rehabilitation then follows, gradually increasing active flexion with full flexion achieved before 6 months [Murgier et al.; Cottinno et al.][51,52]. Surgical technique with Achilles tendon is almost the same, nevertheless there are several variations to fix proximal part of the allograft. After calcaneal bone block is fixed to the host tibia, proximal portion is normally secured onto the underlying extensor mechanism with heavy nonabsorbable sutures. The Achilles tendon itself can be also divided and passed through the extensor mechanism in a figure-of- eight fashion, sutured back on itself and tensioned in full extension. Alternatively, the graft may be passed through a slit in the posterior retinaculum (posterior and lateral to the host patellar ligament remnant) and pulled proximally anterior to the host patella and tensioned proximally in full extension.
Afterwards the host quadriceps is sewn over the allograft [Nam et al.][7]. Extensor mechanism allograft is an attractive option as it allows better restoration of the anatomical landmarks, does not rely on the intact patella and most case series have shown good clinical results following this repair. The mean postoperative extensor lag mostly varies from 10o to 15o. However some studies described extensor lag to reach 59o [Bates][39]. The risk rate of recurrent extensor mechanism disruption is also extremely inconsistent and varies between 5% and 100%. In addition, physiological lengthening of the graft resulting in instability has been described. Generally, allografts are quite difficult to find and this technique is much more expensive and complex compared to the others [Murgier et al.][51].
Allograft transplantation as an alternative to reconstruct the insufficient knee extensor mechanism following TKA
The whole knee extensor mechanism allograft reconstruction technique was first described by Emerson et al. [53]. Both fresh-frozen and freeze-dried techniques have been described. The surgical technique was then improved by Nazarian et al. in order to avoid the extensor lag of 20-40o [54]. The main improvement was allograft tensioning in full extension. In 2008 a new extensor mechanism reconstruction technique has been described by Malhotra et al. in which a composite allograft consisting of a patella-patellar ligament-tibial tubercle was used in order to repair the injured extensor mechanism in the presence of a good patellar bone stock [55]. However, they described delayed proximal graft
healing at the bone-tendon interface after reconstruction using this technique. Generally, many different techniques have been described, but the Achilles tendon with a calcaneal bone block and whole extensor mechanism allografts are most commonly used for reconstruction.
Since it was first described, the allograft reconstruction has become superior treatment method compared to primary repair, as it has shown much better outcome [Bates][39]. However, mid-term and long-term results have been inconsistent, with progressive extensor lag being noted. Further issues as availability, graft mismatch to host, immune reaction, disease transmission and cost have prompted surgeons to investigate synthetic material such as Marlex Mesh, which has gained popularity over the years, since it was first described by Browne et al. in 2011 [36]. This new technique has shown great clinical results and debate is open regarding which method is superior. Systematic literature review by Shau et al. has been made to compare these two techniques and have described quite similar results [5].
The success rate in the allograft group was described to be 76% compared to 74% in the mesh group.
Knee outcome scores have shown also no significant difference between the groups. Postoperative extensor lag was also similar (7,7o in the allograft group compared to 9,5o in the mesh group).
Complication rate have been described to be the same with 23% failure rate in both groups and 13%
infection rate in allograft group compared to 15% infection rate in the mesh group.
Basically, Marlex Mesh has shown equivalent extensor mechanism reconstruction success when compared to allograft but with lower cost, better availability, lack of disease transmission and potential for diminishing graft stretch-out. However, no conclusions can be drawn as most of the studies in the literature are level III or level IV small case series. Very often the choice between these two techniques depends on the material or graft availability, capability of the surgeons to perform reconstruction using one or another technique or just personal preference [Cottino et al.][52].
CONCLUSIONS
Our cases showed ambiguous results with the first patient achieving great success and satisfying functional results, the second one, who did not manage to reach the great functional lever, highly possible due to previous medical conditions and old age, and lastly the third patient, who did not avoid several postoperative complications. Just like most of the studies in the litarature, we are also not able to draw definitive conclusions, nevertheless, with the adequate patient choice, a great success may be reached.
We would recommend allograft transplantation technique as a useful alternative to treat insufficient knee extensor mechanism, however, more bigger case series or systematic reviews have to be done, in order to evaluate, which of the many techniques promise the best outcome.
REFERENCES
1. Parker DA, Dunbar MJ, Rorabeck CH. Extensor mechanism failure associated with total knee arthroplasty: prevention and management. J Am Acad Orthop Surg. 2003 Aug;11(4):238–47.
2. Abdel MP, Salib CG, Mara KC, Pagnano MW, Perry KI, Hanssen AD. Extensor Mechanism Reconstruction with Use of Marlex Mesh: A Series Study of 77 Total Knee Arthroplasties. The Journal of Bone and Joint Surgery. 2018 Aug;100(15):1309–18.
3. Maffulli N, Del Buono A, Loppini M, Denaro V. Ipsilateral Hamstring Tendon Graft Reconstruction for Chronic Patellar Tendon Ruptures: Average 5.8-Year Follow-up. The Journal of Bone and Joint Surgery-American Volume. 2013 Sep;95(17):e123-1–6.
4. Matsuda S, Lustig S, van der Merwe W. Soft tissue balancing in total knee arthroplasty. New York, NY: Springer Berlin Heidelberg; 2017.
5. Shau D, Patton R, Patel S, Ward L, Guild G. Synthetic mesh vs. allograft extensor mechanism reconstruction in total knee arthroplasty — A systematic review of the literature and meta- analysis. The Knee. 2018 Jan;25(1):2–7.
6. Andrikoula S, Tokis A, Vasiliadis HS, Georgoulis A. The extensor mechanism of the knee joint: an anatomical study. Knee Surg Sports Traumatol Arthrosc. 2006 Mar;14(3):214–20.
7. Nam D, Abdel MP, Cross MB, LaMont LE, Reinhardt K, McArthur BA, et al. The management of extensor mechanism complications in total knee arthroplasty. AAOS exhibit selection. The Journal of bone and joint surgery American volume. 2014;96(6):e47.
8. Waligora AC, Johanson NA, Hirsch BE. Clinical Anatomy of the Quadriceps Femoris and Extensor Apparatus of the Knee. Clin Orthop Relat Res. 2009 Dec;467(12):3297–306.
9. Astur DC, Oliveira SG, Badra R, Arliani GG, Kaleka CC, Jalikjian W, et al. UPDATING OF THE
ANATOMY OF THE EXTENSOR MECHANISM OF THE KNEE USING A THREE-DIMENSIONAL VIEWING TECHNIQUE. Rev Bras Ortop. 2015 Dec 6;46(5):490–4.
10. Cox CF, Hubbard JB. Anatomy, Bony Pelvis and Lower Limb, Knee Patella. In: StatPearls [Internet].
Treasure Island (FL): StatPearls Publishing; 2019
11. Draghi F, Ferrozzi G, Urciuoli L, Bortolotto C, Bianchi S. Hoffa’s fat pad abnormalities, knee pain and magnetic resonance imaging in daily practice. Insights Imaging. 2016 Mar 21;7(3):373–83.
12. Chatra PS. Bursae around the knee joints. Indian J Radiol Imaging. 2012;22(1):27–30.
13. Schindler OS. ‘The Sneaky Plica’ revisited: morphology, pathophysiology and treatment of synovial plicae of the knee. Knee Surg Sports Traumatol Arthrosc. 2014 Feb 1;22(2):247–62.
14. Yu Z, Yao J, Wang X, Xin X, Zhang K, Cai H, et al. Research Methods and Progress of Patellofemoral Joint Kinematics: A Review [Internet]. Journal of Healthcare Engineering. 2019
15. Loudon JK. BIOMECHANICS AND PATHOMECHANICS OF THE PATELLOFEMORAL JOINT. Int J Sports Phys Ther. 2016 Dec;11(6):820–30.
16. Petersen W, Ellermann A, Gösele-Koppenburg A, Best R, Rembitzki IV, Brüggemann G-P, et al.
Patellofemoral pain syndrome. Knee Surg Sports Traumatol Arthrosc. 2014 Oct;22(10):2264–74.
17. Andrish JT. Biomechanics of the Patellofemoral Joint. Operative Techniques in Sports Medicine.
2015 Jun;23(2):62–7.
18. Lorenz A, Müller O, Kohler P, Wünschel M, Wülker N, Leichtle UG. The influence of asymmetric quadriceps loading on patellar tracking--an in vitro study. Knee. 2012 Dec;19(6):818–22.
19. Philippot R, Boyer B, Testa R, Farizon F, Moyen B. The role of the medial ligamentous structures on patellar tracking during knee flexion. Knee Surg Sports Traumatol Arthrosc. 2012
Feb;20(2):331–6.
20. Keshmiri A, Maderbacher G, Baier C, Zeman F, Grifka J, Springorum HR. Significant influence of rotational limb alignment parameters on patellar kinematics: an in vitro study. Knee Surg Sports Traumatol Arthrosc. 2016 Aug 1;24(8):2407–14.
21. Garner MR, Gausden E, Berkes MB, Nguyen JT, Lorich DG. Extensor Mechanism Injuries of the Knee: Demographic Characteristics and Comorbidities from a Review of 726 Patient Records. The Journal of Bone and Joint Surgery-American Volume. 2015 Oct;97(19):1592–6.
22. Nori S. Quadriceps tendon rupture. J Family Med Prim Care. 2018;7(1):257–60.
23. Rodriguez-Merchan EC. Traumatic injuries of the knee. New York: Springer; 2013.
24. Egol KA, Koval KJ, Zuckerman JD, Koval KJ. Handbook of fractures. 4th ed. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins Health; 2010. 800 p.
25. Hak DJ, Sanchez A, Trobisch P. Quadriceps tendon injuries. Orthopedics. 2010 Jan;33(1):40–6.
26. Tuong B, White J, Louis L, Cairns R, Andrews G, Forster BB. Get a kick out of this: the spectrum of knee extensor mechanism injuries. Br J Sports Med. 2011 Feb 1;45(2):140–6.
27. Rosso F, Bonasia DE, Cottino U, Dettoni F, Bruzzone M, Rossi R. Patellar tendon: From
tendinopathy to rupture. Asia Pac J Sports Med Arthrosc Rehabil Technol. 2015 Aug 7;2(4):99–
107.
28. Jarraya M, Diaz LE, Arndt WF, Roemer FW, Guermazi A. Imaging of patellar fractures. Insights Imaging. 2016 Nov 30;8(1):49–57.
29. Henrichsen JL, Wilhem SK, Siljander MP, Kalma JJ, Karadsheh MS. Treatment of Patella Fractures.
ORTHOPEDICS. 2018 Nov 19;41(6):e747–55.
30. LeBrun CT, Langford JR, Sagi HC. Functional outcomes after operatively treated patella fractures. J Orthop Trauma. 2012 Jul;26(7):422–6.
31. Cottino U, Abdel MP, Hanssen AD. Chronic extensor mechanism insufficiency in total knee arthroplasty (TKA). Curr Rev Musculoskelet Med. 2015 Sep 18;8(4):368–72.
32. Vaishya R, Agarwal AK, Vijay V. Extensor Mechanism Disruption after Total Knee Arthroplasty: A Case Series and Review of Literature. 2016 Feb 4
33. Rosenberg AG. Management of extensor mechanism rupture after TKA. The Journal of Bone and Joint Surgery British volume [Internet]. 2012 Nov 1
34. Rhee SJ, Pham TH, Suh JT. Acute Patellar Tendon Rupture after Total Knee Arthroplasty Revision.
Knee Surg Relat Res. 2015 Jun;27(2):123–8.
35. Anand S, Kanwat M, Mishra A, Mittal R, Yadav CS. Management of Patellar Tendon Rupture after Total Knee Arthroplasty using Hamstring graft: A Case Report. J Orthop Case Rep. 2018;8(2):57–
60.
36. Browne JA, Hanssen AD. Reconstruction of patellar tendon disruption after total knee
arthroplasty: results of a new technique utilizing synthetic mesh. J Bone Joint Surg Am. 2011 Jun 15;93(12):1137–43.
37. Sayeed SA, Johnson A, Delanois RE. The Treatment of Patellar Fractures After Total Knee Arthroplasty. Seminars in Arthroplasty. 2010 Jun;21(2):139–41.
38. Duncan CP, Haddad FS. The Unified Classification System (UCS): improving our understanding of periprosthetic fractures. Bone Joint J. 2014 Jun;96-B(6):713–6.
39. Bates MD, Springer BD. Extensor Mechanism Disruption After Total Knee Arthroplasty. JAAOS - Journal of the American Academy of Orthopaedic Surgeons. 2015 Feb;23(2):95.
40. van der Zwaal P, van Arkel ERA. Recurrent patellar tendon rupture: Reconstruction using
ipsilateral gracilis and semitendinosus tendon autografts. Injury Extra. 2007 Sep 1;38(9):320–3.
41. Mihalko WM, Vance M, Fineberg MJ. Patellar tendon repair with hamstring autograft: A cadaveric analysis. Clinical Biomechanics. 2010 May;25(4):348–51.
42. Lin P-C, Wang J-W. Use of a Turndown Quadriceps Tendon Flap for Rupture of the Patellar Tendon After Total Knee Arthroplasty. The Journal of Arthroplasty. 2007 Sep;22(6):934–8.
43. Nguene-Nyemb AG, Huten D, Ropars M. Chronic patellar tendon rupture reconstruction with a semitendinosus autograft. /data/revues/18770568/v97i4/S1877056811000818/ [Internet]. 2011 Jul 6
44. Samagh SP, Huyke FA, Buchler L, Terry MA, Tjong VK. Treatment of a Neglected Patellar Tendon Rupture with a Modified Surgical Technique: Ipsilateral Semitendinosus Autograft Reconstruction with Suture Tape Augmentation. Case Rep Orthop [Internet]. 2018 Jul 8
45. Woodmass JM, Johnson JD, Wu IT, Krych AJ, Stuart MJ. Patellar Tendon Repair With Ipsilateral Semitendinosus Autograft Augmentation. Arthrosc Tech. 2017 Nov 13;6(6):e2177–81.
46. Milankov MZ, Miljkovic N, Stankovic M. Reconstruction of chronic patellar tendon rupture with contralateral BTB autograft: a case report. Knee Surg Sports Traumatol Arthr. 2007 Dec
1;15(12):1445–8.
47. Temponi EF, Camelo N, Tuteja S, Thaunat M, Daggett M, Fayard JM, et al. Reconstruction of chronic patellar tendon rupture with contralateral bone-tendon-bone autograft. Knee Surg Sports Traumatol Arthrosc. 2017 Aug 1;25(8):2468–73.
