The Effect of Prolonged Knee Extension Immobilization on Knee Active Range of Motion: A Case Study on Arthrofibrosis
A 71-year-old female presented to our physical therapy clinic with postoperative right knee pain, stiffness, and weakness after suffering a severe, high-energy hyperextension-type injury to the knee on January 29, 2013. The postoperative report that included a description of the injury confirmed rupture of the medial collateral ligament (MCL), lateral collateral ligament (LCL), and posterior cruciate ligament (PCL), along with tearing of the posterior tibial artery at the level of the popliteal fossa. The patellar tendon and patella both suffered damage as well but to a lesser extent. Figure 1 shows the anatomy of the knee.
The patient underwent emergency surgery a few hours after the accident, with the vascular event taking precedence, followed by the orthopedic reconstruction of the PCL and MCL ligaments. The LCL was left unrepaired. The patient’s knee was immobilized using external fixation device (outrigger) to allow the patella and extensor mechanism to heal without further incident. The outrigger device was worn by the patient for 12 weeks after the surgery (Figure 2).
In early February 2013, she went to a rehabilitation facility for 1 week to begin early-phase physical therapy followed by home rehabilitation for the next 9 weeks. This involved home care services including physical therapy. On May 20, 2013, the patient had the stabilizing hardware removed and was fitted with an immobilizer brace locked at zero degrees extension, which weeks later, was followed with a hinged brace that could accommodate gradual knee flexion range of motion. At this time, the patient was using a wheelchair to get around. She was also referred to outpatient physical therapy to improve strength and mobility of the knee.
The patient presented to outpatient physical therapy with an orthopedic prescription to treat right knee pain, weakness, and limited active range of motion (AROM). The clinical exam revealed a 15-degree arc of available motion in knee flexion (ie, AROM flexion 15, extension 0 [normal]) in the right knee. The knee was mildly swollen, primarily in the supra-patellar pouch, and had mild to moderate tender areas, including the LCL, MCL, quadriceps/patellar tendons, and posterior knee joint. The tenderness correlated with the areas of injury and subsequent surgical repair, along with contact points from her hinged brace.
The most striking functional deficit in this particular case was the knee flexion range of motion loss that resulted from “positional gelling” secondary to post surgical scarring/fibrosis as a result of protracted immobilization in knee extension. Although there were deficits in other domains such as strength, balance, and gait, the most dramatic loss was definitely in knee joint motion. As she started physical therapy, she was wheelchair bound due to lack of right knee mobility and pain, leading to weakness on the right side. Weakness in her case had a twofold origin: neurologically mediated reflex inhibition caused by both edema in the joint and nociceptive input, and atrophic changes in muscle tissue as measured by girth differences between the 2 limbs. The culmination of the 2 factors manifested as weakness of the quadriceps, hamstring, hip adductors, and hip abductors, with resultant decreases in general motor control.
As a result of poor knee motor control, the patient had problems in both gait and dynamic balance, with both domains needing attention and inclusion in the care plan. At the time of intake (first visit), strength scores were documented as 2+/5 for quadriceps and 3- for hamstrings. The “red flag” was clearly the gross limitation in knee flexion that had been caused by positional locking of the knee in extension for long periods of time (Figures 3-5). The trade off made by the orthopedic and vascular team (stability over mobility) optimized the environment for subsequent knee soft tissue contracture. Indeed, both the posterior tibial artery and the soft tissue structures (ligaments and tendons) that were injured would require a lengthy period of immobility to ensure biological healing. The downside in this management plan is that postoperative immobilization (outrigger/bracing), which is designed to protect the repaired elements, can have a devastating effect on collagen-based elements of the knee. This will require force loading (mechanobiology) in cycles of stretching and shortening, which is critical to mobility and, ultimately, functional recovery down the line.
Our treatment approach evolved from a shared team perspective that was shaped by the context of the case presentation: the knee had suffered catastrophic musculoskeletal injury that required extensive surgical interventions, which later necessitated a prolonged exposure time (14 weeks) of immobilization in knee extension.
At approximately 2 months into physical therapy, the patient’s progress leveled off. During those 2 months progress was slow and steady until it abruptly halted. Continued manual passive range of motion (PROM) exer-cises began to cause pain and swelling. Shorter but more aggressive bouts of flexion PROM efforts resulted in knee joint irritation leading to edema and motor control inhibition. We tried to vary both the duration and magnitude of applied stretch force to the knee, consistent with our understanding of collagen creep. The idea of prolonged low force application for extended periods of time is the rationale behind dynamic tension devices where both force and time of application can be controlled by the patient. This intervention yielded no net gains in AROM in flexion beyond what we previously achieved with manual PROM methods. Her symptoms (pain, swelling, tenderness, redness) were clearly being exacerbated by persistent passive stretch to the knee and she identified the medial joint line and quadriceps/patellar tendon extensor mechanism as tender/pain sites during stretching. Table 1 lists possible differential diagnoses.
The primary lesion and main obstacle to mobility progression was a thick, taut (palpable) band of scar tissue (arthrofibrosis), which was confirmed (verified and measured) using ultrasonography.
From May to August 2013, the patient was diligent with physical therapy that included therapeutic exercises for lower extremity strengthening and knee stabilization, along with ultrasound and ice after exercises to reduce activity-induced inflammation. When the knee was able to reach 80 degrees flexion, it became apparent that it was not going to give any further. At that point we changed tack and concentrated primarily on gaining motion and began to apply high-level acoustic compression therapy. The rationale for choosing this treatment was to weaken or break down the offending scar tissue that was binding up the extensor mechanism of the knee and causing the extension contracture. When this failed, we reverted to dynamic flexion splinting for approximately 1 month. This also failed—the contracture was deep and had set.