Arthroscopic Approaches to Arthrofibrosis

Benjamin I. Chu

David S. Ryan

William R. Beach

INTRODUCTION

Motion loss in the knee can range widely, from slight loss of extension to significantly restricted motion. Historically, the term arthrofibrosis has been used to describe any loss of knee motion, in flexion, extension, or both. Most commonly, extension loss after anterior cruciate ligament (ACL) reconstruction, such as from a cyclops lesion or notch impingement, has been incorrectly referred to as arthrofibrosis.

For the purposes of this chapter, we define arthrofibrosis of the knee as a condition of diffuse, proliferative scar tissue formation that results in progressive loss of motion in both flexion and extension. The scar tissue associated with arthrofibrosis may form intra-articular and/or extra-articular. A key characteristic of arthrofibrosis is the progressive decrease in the total arc of knee motion. In contrast, motion loss from a focal lesion reaches a certain limit and then plateaus.

Normal Knee Motion

Normal arc of knee motion has been reported from hyperextension of 5° and 6° to flexion of 140° and 143°, for men and women, respectively (1). Passive flexion to 165° is seen in societies that require kneeling and squatting, as in Japan, India, or the Middle East. The functional arc of knee motion required for most daily activities is 10° to 125°.

Hyperextension is required for two important knee motions to occur. First, it permits the screw home mechanism to occur for normal tibiofemoral kinematics. Second, it enables the knee to lock out, allowing the quadriceps muscle to relax during the stance phase. Loss of 5° or greater of extension can cause patellofemoral pain and limping (2). With increasing degrees of knee flexion, greater quadriceps muscle force is required to stabilize the knee (3). Greater quadriceps muscle force results in increased compressive forces at the tibiofemoral and patellofemoral articulations.

Knee flexion of at least 125° is required for sitting and stair climbing. Loss of flexion beyond 125° may make squatting and kneeling difficult. In general, flexion loss is better tolerated than extension loss. However, athletes involved in running and jumping sports may not tolerate any loss of flexion, even less than 10°.

Pathophysiology

The exact pathogenesis of arthrofibrosis is not clearly understood, and the etiology is most likely multifactorial. Primary arthrofibrosis, which develops without an inciting event, has been reported although this is rare. The majority of cases of arthrofibrosis are secondary, following a knee injury, surgery, or prolonged immobilization.

After any trauma there is a normal inflammatory healing response. Arthrofibrosis may result from exaggerated inflammation. Microscopic examination of tissue from arthrofibrotic knees demonstrates a dense fibrous or fibrovascular tissue associated with inflammatory reaction (4, 5). Immunohistologic analysis of the infrapatellar fat pad after ACL injury demonstrates increased expression of fibrogenic cytokines, platelet-derived growth factor, and transforming growth factor-ß, which may promote an arthrofibrotic reaction (6).

Other studies have shown 10 times the amount of α-smooth muscle actin-containing myofibroblasts in the infrapatellar fat pad of arthrofibrotic knees (7). Myofibroblasts —highly differentiated fibroblastic cells—play a role in tissue contraction during wound healing as well as pathologic states such as Dupuytren’s contracture. Alman et al. (8) demonstrated proliferation of the abnormal fibroblasts in Dupuytren’s contracture with cyclic repetitive strain, which may explain the paradoxical decrease in range of motion with increased therapy. Increased levels of collagen type VI, which is upregulated in keloid formation and lung fibrosis, has also been implicated in the development of arthrofibrosis (9).

Incidence

The reported rate of loss of knee motion following trauma or surgery ranges from 2% to 35%. The true incidence of arthrofibrosis is more difficult to determine because of varying definitions of arthrofibrosis and mixed patient populations and varying tolerances for loss of motion. There are many potential causes of limited knee motion that must be ruled out before making the diagnosis of arthrofibrosis. These include mechanical block (incongruent articular surface, displaced bucket handle meniscus tear, and loose body), effusion, quadriceps inhibition, or neurologic deficit.

Risk Factors

Numerous risk factors have been associated with knee motion loss. In general, the magnitude of injury or surgery is correlated with the risk of knee stiffness. Loss of motion may also result from prolonged immobilization, infection, or complex regional pain syndrome.

Recent research suggests that some patients may have a genetic predisposition for developing arthrofibrosis. Skutek et al. (10) demonstrated a link between various human leukocyte antigen loci and the development of primary arthrofibrosis.

CLINICAL EVALUATION

Pertinent History

The primary symptom of arthrofibrosis is stiffness, which is often worse in the morning. As described earlier, the patients may report a progressive loss of knee motion, despite attempts at range of motion as part of a home exercise program or formal physical therapy. Patients will often experience significant pain, which may make arthrofibrosis difficult to differentiate from complex regional pain syndrome. Patients will also complain of warmth and swelling in the knee that is exacerbated by attempted motion or activity. These symptoms are often associated with complaints of weakness. The combination of limited motion, pain, and quadriceps weakness can significantly limit activities of daily living.

Physical Examination

Patients will present with a diffusely swollen knee that is warm and tender to touch. An effusion may or may not be present. Swelling is because of inflamed and thickened tissues that often make visualization and palpation of surface landmarks difficult (Fig. 81.1). The skin incision may demonstrate advanced healing or contracture compared with what is normally seen at that point postoperatively. The knee is often held in a slightly flexed position. The quadriceps muscle will be weak and atrophic, and the patient will walk with an antalgic, bent knee gait.

FIGURE 81.1. Diffuse swelling of the arthrofibrotic knee makes visualization and palpation of landmarks difficult.

Active and passive ranges of motion of the knee will be restricted. With passive range of motion, there may be a spring-like endpoint owing to the inflamed and thickened tissues. Patellar mobility is reduced as well, reflecting the diffuse nature of the scar tissue formation.

Imaging

Arthrofibrosis is typically diagnosed based on history and physical examination. Plain radiographs may demonstrate calcification in the soft tissues but often require more than 6 weeks following the injury to develop. Radiographs can be useful in identifying patella infera (baja) in cases of infrapatellar contracture syndrome (IPCS). In cases of stiffness following ACL reconstruction, radiographs to assess tunnel placement are helpful. MRI may be helpful in ruling out other causes of motion loss such as loose body, cyclops lesion, scarring of the fat pad, or graft impingement. One specific advantage of MRI is the ability to evaluate the articular cartilage surfaces, which may provide valuable information when counseling patients regarding their long-term expectations.

Classification

There are multiple classification systems for arthrofibrosis. The first classification system for arthrofibrosis was developed by Sprague et al. (11) and was based on pathoanatomy (Table 81.1).

Shelbourne et al. (12) more recently introduced a system of classification based on motion loss in comparison to the normal, contralateral side (Table 81.2). Paulos et al. (4) described IPCS, an extreme subset of arthrofibrosis. IPCS is characterized by restricted knee flexion, extension, and patellar entrapment, which progresses to patella infera.

We have found that classification is not critical as many patients will not fit into a single group. It is more
important to accurately identify the extent of motion loss in flexion, extension, and patellar mobility as this will influence management decisions.

Table 81.1 Sprague et al. (11) arthrofibrosis classification system

Group	Pathoanatomy Present at Arthroscopy
1	Discrete bands or single sheet of adhesions traversing suprapatellar pouch
2	Complete obliteration of suprapatellar pouch and peripatellar gutters
3	Group 2 combined with extracapsular involvement (bands of tissue from proximal patella to anterior femur)