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Traumatic Patellar Tendon Rupture - Case Study and Management

Case Report

Introduction

Traumatic patellar tendon rupture is as a result of severe overloading of the knee extensor mechanism. The occurrence of bilateral spontaneous ruptures is rare with approximately 50 cases in the current literature, most of which are isolated case reports. The vast majority of these ruptures occur in persons with concomittent disease or corticosteroid use, with the smallest percentage in those without any predisposing factors [1]. The majority of bilateral ruptures occur in patients with co-existing conditions, such as renal failure, lupus and rheumatoid arthritis [2, 3].

The published cases of bilateral traumatic ruptures without any systemic diseases have all had a common history of long-term patellar tendinopathy type pain. This has been the proposed aetiology of tendon ruptures without any predisposing factors. Due to the rarity of this condition, clinical suspicions are low, resulting in the majority of these being misdiagnosed initially with a reported incidence of 28% [4]. As a result, careful history and examination techniques are paramount to ensure the optimal outcome in such patients. This case highlights the importance of early diagnosis of such patients and reviews the literature for early diagnosis and optimal management.

A 42 year-old man presented to the Sangre Grande hospital after sustaining an injury to his both knees during a basketball game. The mechanism of his injury was landing on flexed knees after jumping. He reported an audible ‘pop’ after landing, followed by the inability to ambulate thereafter. There was no history of illnesses such as Diabetes Mellitus, rheumatoid arthritis, connective tissue disease or corticosteroid use that may have predisposed to his suspected tendon injury. The only history of significance was that of longstanding anterior knee pain which was aggravated by playing sport.  On examination, both of his knees were grossly swollen without any skin breaches or ecchymosis. His maximal tenderness was infra-patellar, however, due to the acute swelling and pain there was difficulty to appreciate any defects. There was inability to straight-leg raise bilaterally and he was unable to walk as a result.

Plain, 30° flexion lateral radiographs demonstrated patella alta bilaterally with no bony defects (figure 1). He was sent for Ultrasound Scanning which confirmed the suspicion of patellar tendon rupture. The patient was counselled and consented for open primary repair of his bilateral patellar tendons under general anaesthesia. The repairs were performed simultaneously by two surgeons, via midline approaches to the knee. The torn tendinous ends were noted to be frayed and thinner than the tendon body itself, which was suggestive of a previous longstanding tendinosis (figure 2). Thorough debridement of the tendon edges were performed prior to proceeding with primary repair.  Two drill holes were made longitudinally through the patellae with a 2.5 mm drill bit. Number 2 prolene sutures were used to perform four-row Krackow repair (figure 3). This repair was reinforced by a merseline tape suture passed from the patellar tendon substance through the drill holes made in the patellar bone, and knotted superiorly. The retinacular tears were then repaired using a number 2 Vicryl and the decision was made against augmentation using a tension band wire.  

Discussion

Post-operative radiographs demonstrated an appropriate patella-bone position in relation to the femur. The patient was then placed in cylinder plasters bilaterally with the knee in 15° flexion for two weeks. At the two-week follow-up visit, the casts were removed and replaced by locking, hinged knee braces. He was permitted a range of motion between 0-40° degrees initially, and increased by 30-40° every two to three weeks. Throughout the post operative period, full-weight bearing was permitted.  The brace was discontinued at 12 weeks post-operatively. At six months, the patient had a range of knee flexion from 0-95°on the right knee and 0-110° on the left, in addition to being able to ambulate without any assistance as well as participate in light sporting activity.

The patellar tendon is one of the most important in the body, not only functioning as an extensor of the knee, but as one of the main components in the gait cycle. It is a strong flattened structure that originates from the distal patellar bone and inserts onto the tibial tuberosity. It is approximately 4.5 cm in length and is separated from the synovial capsule of the knee by the infra-patellar fat pad, which also serves as a main source of blood supply. The quadriceps tendon split in its descent, to insert into either sides of the tibial tuberosity. The split portions loosely attach to the underlying capsule and are referred to as the patellar retinaculum [5]. Patients with chronic anterior knee pain, especially athletes usually have some degree of tendinopathy, which was the suspected pre-disposing factor in the index case.

The aetiology of tendinopathy is still unclear, but many authors have defined it as a degenerative disorder rather than an inflammatory one. This pathology was first described Blazina et al. and divided it into four stages ranging from pain after activity, to tendon rupture [6]. Histologically, there is disorganisation in the collagen fibrils with patchy fibrosis, and an increase in the vascular flow to accommodate a steady supply of inflammatory cells. Inflammation plays an important role in the early stages of tendonitis, but is poor in the latter stages of the disease process. Continuous forces on the tendon stimulate the production of cytokines as well as interleukins, resulting in collagen micro-tears. There is also an increased production of type III collagen as well as a disorganised regulation of matrix metallo-proteases which further insults the tendon. The loss of protein and collagen homeostasis results in tears, and the neo-vascularisation process results in pain from the constant supply of inflammatory cells [7].

In the younger population, patellar ruptures are more likely to be caused by indirect trauma. This is likely due to longstanding tendinopathy, from overuse mico-trauma. The forces on the tendon are comparatively higher at its insertion rather than the substance of the tendon itself, thus, avulsions are more likely to occur. The forces needed for a rupture to occur are usually greater than 17 times the body mass, according to Zernicke et al. Movements in sports such as sudden acceleration, deceleration, and jumping can result in forces of up to eight times the individual’s weight [8]. Men are more likely to rupture the tendon bilaterally as compared to women with an approximate ratio of 4:1. The tendon most commonly ruptures at the osseo-tendinous junction, however, in the case of chronic degeneration the tendon is more likely to rupture at its mid-substance, as seen in the aforementioned case [9].

Kanus and Józsa evaluated examined biopsies from patellar ruptures in 891 of persons and compared it to 445 cadaveric tendons. Histo-pathological analysis using polarised light and electron microscopy were performed in both groups. There were patterns that were similar amongst the ruptured tendons, with 97% being found to have degenerative changes. These changes demonstrated zones of degeneration and areas of patchy calcification suggesting a background of long-term mico-trauma. He concluded that, in individuals older than thirty to thirty-five years these changes are more common, and are likelier to result in rupture [10].

Järvinen et al. analyzed the calibre of the collagen fibres of 66 tendons in which there were spontaneous ruptures. He found, that in the ruptured tendons there were zones demonstrating collagen thinning, decreased crimp angle with loss of continuity, as well as other changes that make the tendon susceptible for rupture below the ultimate tensile strength [11]. The aforementioned patient had a mid-substance tear in the absence of other predisposing factors apart from the history of longstanding anterior knee pain which may have been attributed to chronic degenerative tendinopathy. The factor of age being greater than 40 years at the time of rupture also correlates to the study done by Kanus et al.

A multitude of studies have shown that the diagnoses of bilateral ruptures are commonly missed on the initial assessment. A study by Siwek and Rao et al. showed a missed diagnosis rate on examination of 28% in patients with bilateral ruptures [4]. Often they present with pain, an intra-articular effusion and the loss of knee extension, coupled with high-riding patellae. As the patella is high-riding bilaterally, missed diagnosis is common as there is an absence of a comparatively normal knee. Palpation may reveal a defect, however, due to the presence of a large haemarthrosis it can be difficult to appreciate. In addition, there may be an inability to perform a straight leg raise, however, in cases where there are retained retinacula, extension can still be possible.

The suspicion of bilateral ruptures can be seen on x-rays by 30° flexion lateral films, showing patella alta. The ratio as described by Insall-Salvati, uses a ratio of the longest patella bone-length compared to the length of its accompanying tendon. A patellar bone: tendon ratio >1.2 may confirm the suspicion of rupture. Another method for determining patella alta uses the Blumensaat's line, which is a line drawn in distal femur at the physeal scar in the intercondylar notch. The suggestion of patellar alta is present when the inferior pole of the patella is >2cm above Blumensaat's line. Another method uses the Blackburne and Peel ratio, which compares the perpendicular distance from the patella’s articular margin to the tibial plateau. The majority of the population have a ratio ranging from 0.54 to 1.06, signifying patella alta or rupture with a value higher than the stated normal range [1].

A dynamic Ultrasound scan (USS) can be useful for diagnosis of ruptures; however, it is user dependent and is difficult to reproduce. Thus, the considered gold standard is a MRI scan; however, it is more expensive, with longer waiting times and may result in delay of surgical management. A Computed tomography (CT) scan is only indicated in cases where there is a suspicion of inferior pole avulsions, but is usually unnecessary. Patellar tendon ruptures must be diagnosed early and surgically managed in order to obtain the best functional outcome. Non-operative management can be considered in patients with incomplete ruptures, and preservation of function. However, in cases where there are functional deficits or a confirmed total rupture; surgical repair gives the best chance to return to the pre-morbid state.

In cases of mid-substance ruptures, one surgical option includes a Krackow suture repair with patellar bone tunnelling and securing the suture superior to the patella. Another option includes the use of a non-absorbable wire placed through the patella and then to the proximal tibia with the goal of providing protection to the primary repair. This method was avoided in the index case, as it necessitates further surgery for its removal.  Augmentation can also be used for management, but is mainly reserved for chronic ruptures. This method involves the use of a semi-tendinosus autograft. In this technique, similar to the cerclage wire technique, the tendon is passed through the patella and then to the tibial tuberosity, along with primary repair [12].

Conclusion

In conclusion, this young active male presented with bilateral patellar tendon ruptures without any predisposing factors, and will add to the literature of rare case reports. The history of chronic anterior knee pain in athletes may indicate long term patellar tendinitis, which is a risk factor for rupture as seen in the index case. A high index of suspicion is imperative to allow for a satisfactory functional outcome via early operative repair.

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