Full range of motion (ROM) in the knee joint is critical for optimal function. A slight loss of knee motion can cause limited function and pain, and a more severe loss of knee motion will lead to significant impairment and disability. For optimum function, the knee should have ROM and strength that is symmetric to the opposite, normal knee. When something causes a loss of normal knee motion, a cascade of events often occurs, beginning with relative disuse of the involved lower extremity, increased pain, and subsequent loss of strength.
Loss of knee motion can occur for many reasons, including acute knee injury, lack of appropriate rehabilitation after a surgical procedure or an injury, arthrofibrosis (which commonly occurs after anterior cruciate ligament [ACL] reconstruction or lower extremity fractures), relative disuse due to injury or degenerative joint disease, displaced bucket-handle meniscus tears, or mucoid degeneration of the ACL or posterior cruciate ligament (PCL). Clinicians should be vigilant about detecting loss of ROM of the knee in any patient with knee pain or injury because by restoring normal, symmetric knee motion first, followed by restoring symmetric strength, many symptoms may subside or abate, negating the need for further surgical intervention. Use of this proactive approach helps patients avoid problems in the short term after a knee injury or surgery, and some evidence indicates that it may also prevent long-term problems, including knee osteoarthritis.
Early intervention for ROM loss requires early detection. To identify loss of knee motion, the opposite, normal knee must also be examined to establish a baseline for comparison, and the examination must include an assessment of knee hyperextension. Unfortunately, this step is sometimes overlooked. A recent study found that in patients who were seeking a second opinion for their knee problem, only 37% of them reported having their opposite, normal knee physically touched during the physical examination.
This chapter provides an overview of the diagnosis and treatment for loss of ROM of the knee. The reasons for loss of knee motion and thus the treatments are wide ranging. However, common themes regarding effective treatment remain the same regardless of the specific cause of loss of knee motion. Most cases of loss of knee motion can be effectively treated without surgery if proper rehabilitation is performed. In some cases, such as arthrofibrosis or displaced bucket-handle meniscus tears, surgical intervention is necessary to remove a mechanical block to knee ROM. The surgical treatment for arthrofibrosis after ACL reconstruction is outlined in detail in this chapter. The principles of rehabilitation for loss of knee motion remain the same whether or not surgical intervention is a part of the treatment plan, and these rehabilitation principles are discussed in this chapter.
Patients with loss of knee motion may present with varying subjective histories. It is important to determine how long the ROM loss has been present. This information can be difficult to elicit from patients because they are often unaware that their ROM is lacking, so we ask patients how long they have felt like they have had a bad knee. Generally speaking, the longer the ROM loss has been present, the more slowly it may respond to treatment. However, long-term ROM loss does not always mean that more aggressive forms of treatment are necessary; rather, it is important for both the clinician and patient to understand that progress may occur at a slower pace.
In patients who have had previous knee surgery, it is important to obtain pertinent details about the surgical procedure. When loss of motion is present it is perhaps even more important to ascertain what, if any, pre- and postoperative rehabilitation was performed. In our experience, many patients with persistent pain after a knee arthroscopy or other knee surgery have loss of knee motion that was likely present before surgical intervention but was overlooked and not treated.
In patients who have not had a previous knee surgery, a careful subjective history can often identify a precipitating injury that may not have seemed significant at the time but may have led them to begin favoring their knee. When patients favor their knee, they stand with their weight shifted away from the involved lower extremity, holding the knee slightly bent. Over time, this habit slowly leads to increasing amounts of knee extension loss. Without full terminal knee extension, it is not comfortable to stand with the body weight shifted toward the involved knee because the patient loses the ability to “lock out” the knee, and therefore they cannot relax the quadriceps muscles during stance as they can for the opposite, normal knee. This scenario feeds the vicious cycle of disuse, increased pain, and further loss of strength.
Other times the subjective history reveals a significant injury to which the patient can attribute the ROM loss with certainty. A displaced bucket-handle meniscus tear blocks the intercondylar notch, resulting in the inability to fully extend the knee. Although this scenario may not always be caused by a specific injury, patients can usually identify exactly when this mechanism occurred and report that their knee feels “locked.”
When a patient does not have a history of a specific injury, the ROM loss may be associated with degenerative joint disease. Another potential cause of ROM loss is mucoid degeneration of the cruciate ligaments, most commonly the ACL. This pathology presents as a gradual loss of knee flexion combined with posterolateral knee pain. An effusion is usually not present.
The physical examination for any knee problem should include a careful assessment of the knee ROM of both knees, including an assessment of knee hyperextension. The uninvolved knee should always be examined before the involved knee; this examination is important to establish a baseline of what the ROM should be for the involved knee. It is also important that both knees be fully exposed (to the level of the mid thigh) for the examination.
Knee extension (including hyperextension) is assessed in two ways. First, the examiner should perform a passive assessment of hyperextension ( Fig. 107-1 ). The examiner stabilizes the thigh on the examination table with one hand, while the other hand passively lifts the heel off the table, assessing the amount of movement available and the quality of the end feel. When ROM is limited, the patient should be asked if the discomfort is perceived posteriorly or anteriorly when a stretch is applied. Posterior discomfort indicates capsular and soft tissue tightness, whereas anterior discomfort may indicate an intraarticular mechanical blockage. Second, knee extension should be measured with the patient lying supine, with both heels propped up on a 6- to 8-inch bolster, allowing the knees to fall into hyperextension. This position allows for visual assessment of knee extension symmetry, as well as goniometric measurement of knee extension.
It is important to note that knee hyperextension is normal. DeCarlo and Sell studied a group of healthy young athletes and found that 95% of males and 96% of females have some degree of knee hyperextension. The mean knee hyperextension was 5 degrees for males and 6 degrees for females. Therefore treatment to restore normal knee ROM should include restoration of hyperextension when it is present in the opposite knee.
Knee flexion is assessed with the patient lying supine or in a long-sitting position. The patient should be asked to grasp the front of his or her ankle with both hands (or use a towel looped around this area if necessary) and pull the heel as far as possible toward the buttocks. Goniometric measurement can be made once maximal flexion is reached. Another method for assessing knee flexion is to ask the patient to sit on his or her heels ( Fig. 107-2 ). Patients with full flexion of both knees are able to comfortably sit back onto their heels without any pelvic tilt. Knee flexion loss leads to minor to severe tilting of the pelvis away from the involved extremity. This method of assessing flexion is also very helpful for patients to self-assess their knee flexion and adjust their activity levels accordingly.
For the purposes of this chapter, we focus on the examination for ROM deficits, but a full knee examination should also be performed, including observation of gait, observation for disuse of the lower extremity when arising from a chair or with habitual standing postures, observation of patella alignment and mobility, palpation for crepitus, assessment for a joint effusion, and special testing for meniscal pathology and ligamentous laxity.
Bilateral radiographs, including weight-bearing posteroanterior, lateral, and Merchant views, are routinely obtained. Again, even in the absence of bilateral symptoms, it is important to obtain bilateral radiographs to provide a baseline for comparison with the involved knee.
When osteoarthritis is suspected, we also recommend obtaining an anteroposterior view. A study by Rosenberg and colleagues showed that the posteroanterior view is more sensitive for detecting joint space narrowing of the tibiofemoral joint. This view is more sensitive because it is taken with the knees bent to a 45-degree angle, allowing for weight bearing with the tibiofemoral joint aligned in a position where more cartilage degeneration is likely. The anteroposterior view is not as sensitive for detecting joint space narrowing but provides information regarding the amount of joint space remaining when the knee is in a fully extended position.
In cases of long-standing ROM loss, the Merchant view radiograph can provide useful information by providing a visual comparison of the bone density of the patellae. When a patient has been favoring one knee for any considerable length of time, disuse osteopenia is evident on the Merchant view ( Fig. 107-3 ).
In patients with severe ROM loss, it is important to observe for signs of patella baja on the lateral-view radiographs. Again, comparison with the opposite knee is important to determine the height of the patella compared with Blumensaat’s line and the apparent length of the patellar tendon based on measurements from the inferior pole of the patella to the tibial tubercle. Although normal ranges have been established for each of these measurements, what is normal for each patient varies and should be based on the measurements for the uninvolved knee.
Magnetic resonance imaging (MRI) is useful when arthrofibrosis is present. In patients with arthrofibrosis types 1 or 2, the MRI can help identify the presence of a cyclops lesion, which is commonly present in patients with arthrofibrosis after ACL reconstruction. In persons with arthrofibrosis types 3 or 4, the MRI provides valuable insight about the extent of scar tissue formation in the fat pad.
Despite the wide range of pathologies that can cause limited knee ROM, a vast majority of cases of limited knee motion can be effectively treated with a directed rehabilitation program. One exception to this is in the case of a displaced bucket-handle meniscus tear, which would need to be arthroscopically reduced and removed or repaired.
Another condition to consider is arthrofibrosis, particularly in patients who have had any previous knee surgeries, including ACL reconstruction, but also fractures around the knee. Arthrofibrosis is an abnormal proliferation of fibrotic tissue in the knee joint. The fibrotic tissue is commonly found in the extrasynovial space anteriorly in a fibrotic fat pad or near the intercondylar notch, presenting as a cyclops lesion at the base of the reconstructed ACL. Arthrofibrosis can cause a loss of knee extension alone, or knee extension and flexion may both be limited. Shelbourne et al. developed a classification for arthrofibrosis to help guide treatment ( Table 107-1 ). Most patients with type 1 arthrofibrosis respond to nonoperative rehabilitation and do not need surgery, but most cases of types 2, 3, or 4 require a combination of rehabilitation and operative treatment to achieve satisfactory results. In these patients, pre- and postoperative rehabilitation is a vital component of the treatment process. In nearly all other cases of knee ROM loss that were not caused by a previous surgery, a directed rehabilitation program completed under the supervision of a well-trained knee therapist resolves significant deficits and provides a corresponding improvement in function.
|Type||Knee Flexion||Knee Extension||Other Features|
|1||Normal||≤10° deficit *||Able to fully extend with overpressure|
|2||Normal||>10° deficit *||Unable to fully extend with overpressure|
|3||≥25° deficit *||>10° deficit *||Decreased medial/lateral patellar mobility|
|4||≥30° deficit *||>10° deficit *||Patella infera evident on radiographs|
Not all rehabilitation programs are designed the same way, but the foundation of a rehabilitation program for limited knee motion should be to work on regaining symmetry in three distinct, sequential phases: (1) knee extension, (2) knee flexion, and (3) knee strength. Our experience has shown us that these phases of rehabilitation should not overlap; rather, one should focus only on extension ROM until symmetry is restored, and then shift toward working on flexion ROM while maintaining full extension. Finally, once full ROM symmetry is achieved, unilateral strengthening exercises should be initiated until strength symmetry is restored. This rehabilitation program is described in greater detail in the “Authors’ Preferred Technique” and “Postoperative Management” sections.
If ROM progress plateaus before symmetric knee extension is achieved, surgical intervention may be needed to remove a mechanical blockage to extension. When degenerative joint disease is present, the mechanical blockage may be caused by an osteophyte on the anterior tibia or near the intercondylar notch.
Mucoid degeneration of the ACL is a rare condition but presents with a classic history. Patients with this condition are typically middle aged and report an insidious onset of gradual loss of knee flexion accompanied by posterolateral knee pain. Some knee extension loss may be present, but it is usually mild and easily resolves with rehabilitation using either a towel stretch or a passive knee extension device (Elite Seat, Kneebourne Therapeutics, Inc., Noblesville, IN) ( Fig. 107-4 ). The appearance on MRI is often described as a “celery stalk” feature, with a striated appearance on T2-saturated images indicating fluid between the ACL fibers. An enlarged, bulbous area is usually present proximally ( Fig. 107-5 ). Literature on this topic is sparse and mostly includes case reports regarding debridement or resection of the ACL, but residual instability has been an undesirable aftereffect of this procedure. We have found that this condition responds favorably to oral or injected steroids and rehabilitation using the principles described in detail later in this chapter.
Nonsurgical treatment with a carefully planned rehabilitation program is the first line of treatment for most patients with loss of knee ROM. As discussed in the previous section, surgery may be necessary in some cases to allow full, symmetric ROM to be regained, particularly in cases of type 2, 3, or 4 arthrofibrosis after an ACL reconstruction or when a bucket-handle meniscus tear becomes displaced and is blocking the intercondylar notch.
The following surgical interventions have been described for loss of knee motion: anterior interval release, notchplasty and/or removal of a cyclops lesion, posterior capsular release, peripatellar release, and manipulation with the patient under anesthesia.
The anterior interval is defined as the space posterior to the patellar tendon and extending to the anterior tibia and transverse meniscal ligament. Trauma to the infrapatellar fat pad can lead to fibrotic formation in this area of the knee, limiting both knee extension and flexion. This presentation is most commonly seen in patients who have undergone arthroscopic ACL surgery, with fat pad trauma occurring as a result of repeatedly passing instruments through the fat pad. Although arthroscopic ACL surgery is believed to be less traumatic for the patient, the trauma to the fat pad is underestimated. Fat pad trauma can lead to fat pad fibrosis, and in its most severe form, fibrosis in this area can lead to infrapatellar contracture syndrome, which further limits patellar mobility and knee flexion. If full knee flexion is not emphasized immediately after surgery, patellar mobility decreases and permanent flexion deficits may occur. Anterior interval release can be performed arthroscopically with use of a 30-degree scope and portals that are slightly farther away from midline than usual to allow for better visualization of this area. Abnormal tissue may be removed with a basket forceps, meniscal shaver, or electrothermal probe.
Under normal circumstances, the ACL and PCL fit perfectly within the intercondylar notch, completely occupying this space when the knee is in terminal extension. Occasionally after ACL reconstruction, a mismatch occurs between the size of the graft and the width of the intercondylar notch, or a cyclops lesion forms, blocking full knee extension. A cyclops lesion is a fibrous nodule that forms on the anterior aspect of the ACL graft ( Fig. 107-6 ). We theorize that this complication can be prevented after ACL reconstruction by ensuring that full, symmetric knee extension is restored prior to and immediately after surgery. These lesions can be carefully excised during arthroscopy until terminal extension is regained. If the intercondylar notch width is not adequate to handle the size of the ACL graft and the PCL, a notchplasty can also be performed.