Introduction

Quadriceps tendon rupture is a rare condition, with an incidence of approximately 1.37 per 100,000 individuals, predominantly affecting men over the age of 40 (1). This injury can result from direct trauma, particularly in sports-related activities (2), or may occur spontaneously in the presence of chronic conditions such as gout, systemic lupus erythematosus, hyperparathyroidism, and chronic kidney disease (CKD) (3-6). Additionally, the use of medications such as fluoroquinolones, corticosteroids, and anabolic steroids has been implicated as a risk factor for tendon rupture (7).

Diagnosis is primarily clinical, with the classic triad consisting of acute pain, an inability to actively extend the knee, and a palpable suprapatellar gap (8). When clinical suspicion arises, imaging modalities such as ultrasonography or magnetic resonance imaging (MRI) are utilized to confirm the diagnosis (9).

In patients with CKD undergoing dialysis, quadriceps tendon rupture has been linked to secondary hyperparathyroidism, which disrupts bone and tendon homeostasis (5,10). However, despite this association, tendon rupture in patients with CKD remains uncommon and is primarily documented through case reports.

Herein, we present a case of bilateral, simultaneous quadriceps tendon rupture in a middle-aged patient with chronic kidney disease following low-energy trauma.

In March 2021, a 37-year-old man presented to our hospital with an inability to walk following a fall. He reported a two-week history of bilateral knee pain and swelling after falling. Initially, he assumed that his symptoms would resolve spontaneously, leading to a two-week delay in seeking medical attention. However, during this period, his inability to bear weight persisted.

The patient had a seven-year history of end-stage renal disease (ESRD) secondary to hypertension and was undergoing hemodialysis. He had previously undergone a kidney transplant six years ago, which failed after eight months, necessitating a return to dialysis three times per week.

On physical examination, the patient exhibited significant bilateral knee swelling and was unable to actively extend his legs. A palpable suprapatellar gap was present bilaterally. Additionally, he was unable to perform the straight leg raise (SLR) test on both sides. Upon palpation, a noticeable depression was observed in the superior aspect of both knees at the quadriceps tendon insertion site (Fig. 1).

Figure1: Bilateral depression of the suprapatellar area

Based on the patient's symptoms and physical examination findings, a suspicion of bilateral quadriceps tendon rupture was raised. Consequently, X-ray (Fig. 2) and MRI (Fig. 3) were ordered for further evaluation.

Figure 2: Preoperative X-ray of both knees of the patient in lateral (a) and anterior (b) views and calculation of the insall-salvati ratio (c and d)

Figure 3: Preoperative MRI of the patient

The X-ray showed no evidence of fracture, cartilage damage, or patellar dislocation but revealed significant joint effusion. MRI findings confirmed bilateral quadriceps tendon ruptures, with clear detachment of the tendons from their insertion sites.

Given the patient's history of chronic renal failure and ongoing dialysis, additional laboratory tests were ordered. His metabolic and hematological profiles were within normal limits, but elevated parathyroid hormone (PTH) levels were noted.

A clinical diagnosis of bilateral quadriceps tendon rupture was confirmed based on the combination of physical examination findings and radiological imaging. The patient was scheduled for surgical repair the following day.

The repair was performed using the Krackow method, with three parallel tunnels and two size-five anchor sutures (Fig. 4and Fig. 5).

Figure 4: Surgery process of both knees

Figure 5: Schematic diagram of surgery process

The patient underwent outpatient physiotherapy to regain strength and improve the range of motion. Four months postoperatively, the patient was able to walk without difficulty, achieving full bilateral knee extension (0°) and 100° of bilateral flexion. He reported no limitations in daily activities and had fully recovered.

Discussion

Bilateral quadriceps tendon rupture is a rare injury in otherwise healthy individuals. Simultaneous bilateral quadriceps tendon rupture is more commonly observed in men over 50 years old, particularly those who are obese, diabetic, or have age-related tendon abnormalities (11). However, cases have also been reported in younger individuals with chronic conditions such as gout, hyperparathyroidism, and chronic renal failure (11). Other contributing factors include the use of anabolic steroids, local steroid injections, and a history of persistent tendinitis (12-14). These predisposing factors promote tendon degeneration by impairing collagen production or strength, resulting in tendon sclerosis, fibrosis, fatty degeneration, necrosis, or calcification (11, 15).

The first documented case of simultaneous bilateral quadriceps tendon rupture in a patient with chronic renal failure and secondary hyperparathyroidism was reported by Preston and Adikoff in 1962 (16). Since then, numerous studies, particularly in recent years, have highlighted this issue (17-21). Early research emphasized the association between the duration of hemodialysis and the occurrence of spontaneous tendon ruptures, attributing the mechanism to tendon weakness caused by malnutrition and the accumulation of uremic toxins—classic complications of long-term hemodialysis (22, 23). A study by De Franco et al. also reported secondary hyperparathyroidism in these patients and attributed tendon rupture to this condition (24).

Secondary hyperparathyroidism is a common complication of chronic renal failure. Its development is driven by several factors, including calcitriol deficiency, phosphorus retention, decreased calcium receptor activation in the parathyroid, and skeletal resistance to the calcemic effects of parathyroid hormone. The reduction in calcitriol also diminishes intestinal calcium absorption, contributing to hypocalcemia and stimulating increased parathyroid hormone production (25). Elevated PTH levels activate osteoclasts at the tendon attachment site, weakening the bone at the tendon insertion, which makes it more susceptible to rupture even with minimal trauma (5). In our patient, a fall from a flat surface led to the mild trauma that resulted in bilateral quadriceps tendon rupture.

Diagnosing bilateral quadriceps tendon rupture can be challenging due to its rarity, the absence of obvious trauma, and the difficulty of performing a thorough physical examination, especially with knee swelling and bilateral involvement, which prevents a comparative examination (17). Consequently, diagnosis may be delayed, underscoring the importance of imaging studies. In this case, we ordered an MRI of both knees for a definitive diagnosis. Other case reports have similarly relied on MRI for diagnosis (17, 19). Zribi et al. also employed knee ultrasonography in conjunction with MRI (18), while Lim et al. diagnosed bilateral quadriceps tendon rupture through X-ray, physical examination, and elevated PTH levels (19). Nevertheless, we recommend MRI as the gold standard for confirming the diagnosis in this patient population. In settings where MRI is unavailable or has a long waiting period, ultrasound can be used as a diagnostic tool, although its sensitivity is lower compared to MRI.

This case highlights that secondary hyperparathyroidism, as a complication of chronic renal failure, likely contributes to tendon weakening and may even lead to spontaneous tendon rupture. Preventive measures should be considered for high-risk patients with chronic renal failure to mitigate the risk of such injuries.

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