Primary arthrofibrosis is caused by an exaggerated inflammatory response to an injury or surgical procedure, followed by the production of fibroblastic cells and an increase in the deposition of extracellular matrix proteins.¹⁴⁷ Proliferative scar tissue or fibrous adhesions form within the joint, which can result in either localized or diffuse involvement of all of the compartments of the knee and the extra-articular soft tissues (Fig. 41-1). In the most severe cases, dense scar tissue obliterates the normal peripatellar recesses, suprapatellar pouch, intercondylar notch, and articular surfaces. Formation of dense scar tissue in the infrapatellar region may result in a patella infera and permanent limitation of normal knee flexion and extension. The consequent pain and restricted knee motion resulting from arthrofibrosis may lead to disabling events including severe quadriceps atrophy, loss of patellar mobility, patellar tendon adaptive shortening, patella infera, and articular cartilage deterioration.^105,¹⁰⁶

FIGURE 41-1 Proliferative formation of scar tissue requiring arthroscopic débridement and lysis of adhesions. A contracture of medial and lateral parapatellar soft tissues is shown, along with patella and trochlear cartilage deterioration.

The incidence of arthrofibrosis after ligament reconstructive surgery varies according to several factors, which are discussed. Two of the most commonly noted factors are knee dislocations and major concurrent operative procedures performed with the ligament surgery such as reconstruction of other knee ligaments, complex meniscus repair, or high tibial osteotomy (Table 41-1).^7,⁹¹^–¹⁰³ Publications show wide disparity among authors regarding the treatment of this problem, especially the time postoperatively that intervention is warranted and what type of treatment should be implemented for losses of knee extension and flexion and loss of patella mobility.

TABLE 41-1 Incidence of Knee Motion Problems after Knee Operations: Authors’ Clinical Studies

Critical Points INTRODUCTION

• Arthrofibrosis implies a loss of knee flexion, extension, or both compared with the contralateral normal knee.

• Primary arthrofibrosis is caused by an exaggerated inflammatory response to an injury or surgical procedure, followed by the production of fibroblastic cells and an increase in the deposition of extracellular matrix proteins. Proliferative scar tissue or fibrous adhesions form within the joint, which can be either localized or diffuse.

• Incidence of arthrofibrosis after ligament reconstructive surgery varies.

• Wide disparity exists among authors regarding the treatment of this problem.

• Limitations in knee motion may occur owing to reasons other than arthrofibrosis:

Mechanical block from a displaced bucket-handle meniscus tear.

Impinged or improperly placed ACL graft.

Cyclops lesion.

Improper ACL graft tensioning.

Contracture of posterior capsular structures.

• If not resolved, these problems may result in the development of secondary arthrofibrosis.

• Most individuals have some amount of hyperextension to allow the normal “screw-home” mechanism to occur: knee stabilized in extension during the stance phase, with the quadriceps muscle relaxed.

• Normal knee flexion averages 140° in men and 143° in women.

• Patients not involved in athletics tolerate small flexion deficits. Significant flexion deficits < 90° cause problems with squatting, stair-climbing, and sitting.

• Loss of just 5° of extension may produce a flexed-knee gait, fatigue the quadriceps muscle, and cause patellofemoral pain.

• Prevention of knee arthrofibrosis is paramount and preferred over the current treatment options for this complication.

ACL, anterior cruciate ligament.

It is important to note that limitations in knee flexion and extension may occur owing to reasons other than arthrofibrosis. Any acute injury causing pain and swelling may cause a short-term loss of knee motion, which usually resolves as symptoms subside. Other factors influencing the restoration of knee motion include a mechanical block from a displaced bucket-handle meniscus tear, an impinged or improperly placed anterior cruciate ligament (ACL) graft, a cyclops lesion,⁶⁵ improper graft tensioning that constrains normal knee joint motion,²⁰ and graft fixation at 30° or more of extension.⁵ In addition, contracture of the posterior capsular structures may limit knee extension. If not resolved, these problems may result in the development of what is termed secondary arthrofibrosis, complicating the course of treatment.

Normal knee motion varies, but most individuals have some amount of hyperextension, which averages 5° in men and 6° in women.^30,^31,⁷⁴ This degree of hyperextension is required so that the normal “screw-home” mechanism can occur that allows the knee to be stabilized in extension during the stance phase, with the quadriceps muscle relaxed. Normal knee flexion averages 140° in men and 143° in women. It is generally assumed that at least 125° of knee flexion is required for activities of daily living.^31,⁷⁴ Rowe and coworkers¹²⁰ measured knee kinematics during functional activities in a group of 20 subjects aged 49 to 80 years and reported that 90° of flexion is required for gait and slopes, 90° to 120° for stairs and sitting, and 135° for bathing. Patients not involved in athletics tolerate small flexion deficits. Significant flexion deficits of less than 90° cause problems with squatting, stair-climbing, and sitting. Athletes have a poorer tolerance for even minor losses of flexion, which affect running and jumping. Cosgarea and associates²⁴ reported that deficits of 10° or more of flexion were associated with decreased running speed.

All patients, regardless of their activity level, have greater problems with loss of knee extension. A loss of just 5° of extension may produce a flexed-knee gait, fatigue the quadriceps muscle, and cause patellofemoral pain.^63,^66,^86,^89,¹²¹ Limitation of more than 20° may cause a functional limb-length discrepancy.²⁴ Many years ago, Perry and colleagues¹¹⁴ demonstrated the effect of a loss of extension on joint contact pressures, quadriceps muscle activity, and fatigue. These investigators measured the extensor forces required to stabilize the flexed knee during simulated weight-bearing in cadaver specimens. The quadriceps force required to stabilize the knee was 75% of the load on the head of the femur at 15° of flexion, which increased to 210% at 30° of flexion, and to 410% at 60° of flexion. The quadriceps force was equal to 20% of the average maximum quadriceps strength at 15° of flexion, but increased to 50% at 30° of flexion. Surface pressure in the tibiofemoral and patellofemoral joints also increased with greater amounts of knee flexion.

It has become evident that the prevention of knee arthrofibrosis is paramount and preferred over using the currently available treatment options for this complication. This chapter discusses the risk factors and preventive measures for loss of knee motion after knee injury and surgery. In addition, conservative medical and therapeutic treatment intervention strategies are discussed that are usually successful in resolving a transient limitation of knee motion if initiated early postoperatively. Surgical procedures for severe cases of restriction of knee motion are presented. The authors’ clinical studies involving 650 ACL-reconstructed knees are included to provide support for treatment recommendations.

TERMINOLOGY AND CLASSIFICATION SYSTEMS

A variety of terms have been used to describe, define, or classify a limitation of knee flexion and extension including arthrofibrosis, flexion contracture, ankylosis, infrapatellar contracture syndrome, and motion loss. Some of the terms indicate a specific process whereas others simply imply a limitation of motion compared with the contralateral normal knee. Ankylosis is one such generic term that indicates stiffness of joints that occurs for any reason and may represent loss of knee flexion, extension, or both. The term motion loss is another general phrase used to describe deviations from the amount of flexion and extension compared with the contralateral normal knee. Conversely, arthrofibrosis describes a specific cause for a limitation of knee motion, which is the formation of diffuse scar tissue or fibrous adhesions within a joint.^63,^111,¹¹⁵ Flexion contracture indicates a loss of extension due to any cause and is accompanied by a relative shortening of the posterior soft tissues (in either the capsule or the muscles). Petsche and Hutchinson¹¹⁵ stated that arthrofibrosis and flexion contracture are general terms, and it is necessary to indicate a specific cause for loss of motion.

Critical Points TERMINOLOGY AND CLASSIFICATION SYSTEMS

• Terms used to describe limitation knee motion: arthrofibrosis, flexion contracture, ankylosis, infrapatellar contracture syndrome, motion loss.

• The term arthrofibrosis describes a specific cause for a limitation of knee motion, which is the formation of diffuse scar tissue or fibrous adhesions within a joint.

• Classification systems describe limitations in knee motion, based on either the anatomic location of scar tissue and adhesions or the amount of knee motion in the affected joint.

• Authors’ classification system is based on the anatomic sites where scar tissue, adhesions, and adaptive shortening of soft tissues occur.

Classification systems have been proposed by various authors to describe limitations in knee motion, based on either the anatomic location of scar tissue and adhesions or the amount of knee motion in the affected joint (Table 41-2).^12,^33,^111,^132,¹⁴¹ Sprague and coworkers¹⁴¹ first introduced a system based on the arthroscopically observed location of scar tissues and adhesions in 24 patients who had a severe limitation of knee motion. Paulos and associates¹¹¹ described three stages of knee motion restrictions due to infrapatellar contracture syndrome. Del Pizzo and colleagues³³ and Shelbourne and coworkers¹³² developed classification systems based on the deviation of knee motion compared to the opposite knee. Blauth and Jaeger¹² described a system based on the total arc of motion in the affected knee.

TABLE 41-2 Classification Systems of Arthrofibrosis

Reference	Classification System
Sprague et al., 1982¹⁴¹	I: Discreet bands or a single sheet of adhesions traversing the suprapatellar pouch II: Near-complete obliteration of suprapatellar pouch and peripatellar gutters with masses of adhesions III: Multiple bands of adhesions or complete obliteration of suprapatellar pouch with extracapsular involvement

Del Pizzo et al., 1985³³ Based on deviation from full extension and amount of flexion present:

Mild: <5° extension, >110° flexion

Moderate: 5°–10° extension, 90°–100° flexion

Severe: >10° extension, <90° flexion

Paulos et al., 1987¹¹¹ Three stages of infrapatellar contracture syndrome:

I: Prodromal stage (2–8 wk postoperative) hardened synovium, fat pad, retinaculum marked by painful motion, restricted patellar mobility, quadriceps muscle lag

II: Active stage (6–20 wk postoperative) peripatellar swelling, severely restricted patellar motion, hardening anterior tissues, step-off between patellar tendon and tibial tuberosity

III: Residual stage (>8 mo postoperative) fat pad atrophy, patellofemoral crepitus and arthrosis, patella infera, quadriceps atrophy

Blauth & Jaeger, 1990¹² Based on total arc of motion:

I (mild): >120°

II (moderate): 80°–120°

III (severe): 40°–80°

IV (extreme): <40°

Shelbourne et al., 1996¹³² Based on deviation from full flexion and extension of opposite, normal knee:

I: <10° extension, normal flexion

II: >10° extension, normal flexion

III: >10° extension, >25° loss of flexion

IV: >10° extension, >30° loss of flexion, patella infera

The authors developed a classification system based on the anatomic sites at which scar tissue, adhesions, and adaptive shortening of soft tissues occur (Fig. 41-2 and Table 41-3). This system is advantageous because it highlights the areas that must be addressed surgically, as is discussed.

FIGURE 41-2 Multiple areas of soft tissue contracture, adhesions, and scar tissue formation with knee arthrofibrosis.

TABLE 41-3 Authors’ Anatomic Classification System of Arthrofibrosis

Loss of Flexion

Quadriceps muscle

• Shortens due to scar tissue and intramuscular changes, limiting normal muscle lengthening.

Suprapatellar pouch

• Scar tissue may form underneath quadriceps VMO, VLO, limiting muscle extensibility.

• Scar tissue from the superior pole of the patella produces patellar clunk, may extend as a band just above the femoral trochlea.

• Scar tissue and adhesions obliterate the suprapatellar pouch.

Medial and lateral capsular pouches

• Scar down and become adhesive to the medial and lateral side of the femur.

Patellar retinaculum and associated ligaments

• Scar tissue forms with thickening, shortening, limiting patellar mobility.

Patellar tendon

• Tendon shortens or may adhere to the tibia.

• Infrapatellar scar tissue inferior pole to tibia just anterior to fat pad.

Medial and lateral extra-articular ligament structures

• Scar tissue, adhesions, adaptive shortening.

Loss of Extension

Posterior capsule

• Scar tissue, adhesions, shortening of structures.

Femoral notch

• In-growth scar tissue, cyclops lesion.

Hamstrings muscle

• Shortening of musculotendinosus unit.

Cruciate ligaments

• ACL, PCL adaptive shortening.

ACL, anterior cruciate ligament; PCL, posterior cruciate ligament; VLO, vastus lateralis obliquus; VMO, vastus medialis obliquus.

RISK FACTORS AFTER KNEE LIGAMENT RECONSTRUCTION

A variety of factors appear to influence the requirement for treatment intervention for knee motion limitations (Table 41-4) and the final amount of knee flexion and extension gained after ligament reconstruction. These factors are related to the severity of the injury, the timing of surgery, preoperative treatment, technical aspects of the ligament reconstruction, and the postoperative course and rehabilitation. Although it remains uncertain why some knees are more likely to form an abnormal scar response to trauma and surgery than others, knowledge of these factors may help reduce this problem.

TABLE 41-4 Risk Factors for the Development of Knee Arthrofibrosis

ACL, anterior cruciate ligament; MCL, medial collateral ligament.

Severity of the Injury

Patients who sustain knee dislocations are at increased risk for developing motion complications (Fig. 41-3).^23,^35,^83,^97,^127,¹³⁶ These injuries frequently occur from high-energy accidents that produce extreme soft tissue swelling and edema, hematomas, muscle damage, and other multiple trauma that must be resolved before consideration of knee soft tissue reconstructions. Early operative intervention when possible is advisable for multiple ligament injuries that involve the lateral and posterolateral structures where acute repair and augmentation procedures are performed (see Chapter 22, Posterolateral Ligament Injuries: Diagnosis, Operative Techniques, and Clinical Outcomes). For all other dislocations, surgery is delayed with the limb immobilized in a posterior plaster splint or bivalved cast with a posterior pad to prevent posterior tibial subluxation. Even in these severe knee injuries, it is possible to start immediate range of motion and prevent scar tissue formation that may compromise the outcome of a subsequent ligament reconstruction. Too often, these serious knee joint injuries are not treated with an early motion and function program. When surgical treatment is elected, the reconstructive and repair procedures of torn ligaments, capsular structures, and menisci are performed in a manner that allows immediate knee motion to be instituted postoperatively.⁹⁷

FIGURE 41-3 Acute knee dislocation results in severe disruption of soft tissues, swelling, hemorrhage, and muscle damage always resulting in motion problems and risk of arthrofibrosis.

Preoperative Issues

Performing ACL and other knee ligament reconstruction within a few weeks of the injury or before the resolution of swelling, pain, quadriceps muscle atrophy, abnormal gait mechanics, and motion limitations has been noted by many authors to correlate with postoperative knee motion problems.^25,^54,^86,^129,^130,^134,^144,¹⁵² Shelbourne and associates¹³⁴ noted an increased rate of arthrofibrosis in patients who underwent acute ACL reconstruction (within 1 week of the injury) compared with those in whom the reconstruction was delayed for at least 21 days. Similar findings were reported by Wasilewski and colleagues¹⁵² who noted that arthrofibrosis was found in 22% of acutely reconstructed knees versus 12.5% of knees reconstructed with chronic ACL deficiency. Mohtadi and coworkers⁸⁶ found that ACL reconstructions performed less than 6 weeks postinjury had a higher rate of knee stiffness than those done more than 6 weeks postinjury (11% and 4%, respectively). Harner and associates⁵⁴ reported a 37% rate of motion complications after acute ACL reconstructions (done within 1 month of the injury) compared with a 5% rate in chronic ACL-deficient knees.

Critical Points RISK FACTORS AFTER KNEE LIGAMENT RECONSTRUCTION

• Severity of injury: knee dislocations increase risk for developing motion complications. Surgery is delayed in all cases except those with ruptures to the posterolateral structures.

• Preoperative issues: performing knee ligament reconstruction within a few weeks of the injury or before the resolution of swelling, pain, quadriceps muscle atrophy, abnormal gait mechanics, and motion limitations correlates with postoperative knee motion problems.

• Technical factors at surgery: improper ACL graft placement, overtensioning graft at surgery, performing concurrent MCL repair with ACL reconstruction.

• Postoperative course and rehabilitation: immobilization is detrimental to all of the knee joint structures and may result in a permanent limitation of knee motion, prolonged muscle atrophy, patella infera, and articular cartilage deterioration. Begin knee motion, patellar mobilization, and muscle-strengthening exercises the day after surgery. Treat joint effusion immediately.

• Postoperative infection, complex regional pain syndromes, and reflex sympathetic dystrophy may cause knee motion problems.

ACL, anterior cruciate ligament; MCL, medial collateral ligament.

Although Bach and colleagues ⁶ did not observe a significant difference in knee motion complications between acute and chronic ACL-reconstructed knees, the authors stressed the need to delay surgery until patients achieved 120° of knee motion and swelling had resolved. The authors found “no advantage to performing urgent acute ACL reconstruction.”⁶ Sterett and coworkers¹⁴³ found no association between surgical timing and postoperative motion problems. However, in their series, all patients had achieved at least 0° to 120°, had good quadriceps control, and could perform a straight leg raise without an extensor lag before undergoing surgery. Eight percent of the patients in this investigation’s acute subgroup required arthroscopic débridement of scar tissue. Meighan and associates⁸¹ also found no advantage in performing early ACL reconstruction and noted an increased rate of complications in patients who underwent surgery within 2 weeks of the injury compared with those who had surgery between 8 and 12 weeks postinjury. The delayed group had a faster return of knee motion and quadriceps strength.

A few authors have not found a higher rate of postoperative motion problems after acute ACL reconstruction.^18,^62,⁷⁵ However, it appears that delaying surgery until knee motion is regained, swelling is resolved, and a good quadriceps contraction is demonstrated is advantageous in decreasing the risk of postoperative arthrofibrosis. The inflammatory response to the initial injury varies among patients. Whereas some have little effusion and swelling, others have an exaggerated inflammatory response characterized by pain, soft tissue edema, and redness and increased warmth to tissues surrounding the knee. These knees are placed into an initial conservative treatment program to resolve these problems first and are also carefully monitored after ACL reconstruction for a similar exaggerated inflammatory reaction postoperatively. Knees with isolated ACL ruptures that have little swelling and demonstrate normal motion early after injury may be considered for earlier reconstruction. In addition, knees with multiple ligament ruptures that include the posterolateral structures are also candidates for early surgical repair, as discussed in Chapter 22, Posterolateral Ligament Structures: Diagnosis, Operative Techniques, and Clinical Outcomes.

Technical Factors at Surgery

Improper ACL graft placement has been frequently noted as a cause of loss of knee motion.* On the tibia, grafts placed anterior to the native ACL insertion result in impingement on the roof of the intercondylar notch when the knee is extended.^59,^60,⁷⁸ Yaru and colleagues¹⁵⁴ recommended that with passive extension, there should be a 3-mm clearance between the anterior portion of the intercondylar notch and the graft to prevent impingement. Grafts placed lateral to the insertion site impinge on the lateral wall of the notch. In addition, Romano and coworkers¹¹⁹ found that ACL grafts placed too far anterior in the tibial tunnel can cause knee extension deficits, and grafts placed too far medially in the tibial tunnel can cause knee flexion deficits. On the femur, an excessive anterior graft placement causes deleterious forces on the graft, leading to limitations in flexion and potential graft failure (Fig. 41-4).

FIGURE 41-4 Lateral radiographs show excessive anterior placement of the femoral tunnel limiting knee flexion and the anterior tibial tunnel limiting knee extension. The graft failed as motion was regained postoperatively.

Overtensioning ACL grafts may lead to abnormal knee kinematics.^84,¹¹⁵ In addition, the degree of knee extension during graft tensioning and fixation may affect postoperative motion.^5,^20,^47,^82,⁸⁹ Austin and associates⁵ noted in a cadaver study that the amount of graft tension (44 N or 89 N) did not effect knee extension; however, tensioning the graft in knee flexion was associated with extension deficits. The authors reported that grafts tensioned and fixed at 30° of flexion had more than a 12° increase in knee flexion after ACL reconstruction compared with those tensioned and fixed at 0° of flexion. From a two-part biomechanical and clinical study, Nabors and colleagues⁸⁹ suggested that grafts tensioned in full extension result in a low incidence of knee motion loss. In their series of 57 patients who underwent patellar tendon autograft ACL reconstruction, only 1 patient had a mild (5°) loss of extension.

Concurrent medial collateral ligament (MCL) repair with ACL reconstruction has been associated with an increased risk of knee arthrofibrosis.^54,^98,¹²⁸ Harner and associates⁵⁴ postulated that concurrent MCL primary repair may cause a limitation of knee motion due to the disruption of the medial capsule, because the procedure does not restore the normal tissue planes, resulting in scar formation and a heightened pain response. The studies of Shelbourne and coworkers^128,¹³³ and the authors of this chapter⁹⁸ led to the recommendation many years ago to treat the majority of combined ACL-MCL ruptures conservatively. This allows healing of the medial-side injury, followed by ACL reconstruction in appropriately indicated patients (see Chapter 24, Medial and Posteromedial Ligament Injuries: Diagnosis, Operative Techniques, and Clinical Outcomes). There are exceptions to this rule, and any surgical procedure on the medial side of the knee joint should be carefully observed postoperatively for a limitation of motion or, in acute knee injuries, the development of heterotopic soft tissue ossificiation requiring treatment.^126,¹⁵⁰

Postoperative Course and Rehabilitation

There is consensus in the literature that immobilization is detrimental to all of the knee joint structures and may result in a permanent limitation of knee motion, prolonged muscle atrophy, patella infera, and articular cartilage deterioration.^25,^51,^67,^104–106,^112,¹²² Early knee joint motion decreases pain and postoperative joint effusions, aids in the prevention of scar tissue formation and capsular contractions that can limit normal knee flexion and extension, decreases muscle disuse effects, maintains articular cartilage nutrition, and benefits the healing ACL graft.^† Modern rehabilitation programs (see Chapters 12, Scientific Basis of Rehabilitation after Anterior Cruciate Ligament Autogenous Reconstruction; 13, Rehabilitation of Primary and Revision Anterior Cruciate Ligament Reconstructions; and 14, Neuromuscular Retraining after Anterior Cruciate Ligament Reconstruction) incorporate immediate knee motion and muscle-strengthening exercises the day after surgery, both of which have been shown to be safe and not deleterious to healing grafts. Importantly, the immediate motion program must include patellar mobilization (inferior, superior, medial, and lateral directions) to avoid an infrapatellar contracture.

Patient compliance with postoperative rehabilitation is essential in recovering full knee motion. In the authors’ experience, the small percentage of patients who have permanent restrictions in extension or flexion have often been unwilling to perform the required motion, strengthening, and patellar mobilization exercises postoperatively. In addition, in instances in which an early postoperative limitation of motion has been recognized, these patients are also unwilling to undergo treatment recommendations such as overpressure exercises, extension casts, and other modalities that are usually effective in resolving these problems.^101,¹⁰² Thus, in a majority of cases, the inflammatory and fibrotic response that follows surgery and initially limits knee motion is treatable if no delay occurs in instituting a gentle motion and overpressure program along with appropriate anti-inflammatory medications. There is a distinct group of patients, probably in the range of 1% to 2%, who demonstrate a pathologic exaggerated fibrous tissue proliferative response from a genetic basis, in which the treatment is prolonged and may not be successful. This unique group of patients are discussed in a later section of this chapter.

Significant lower extremity muscle atrophy represents an unresolved problem after ACL reconstruction, because the magnitude of quadriceps atrophy and strength loss may exceed 20% to 30% in the first few months postoperatively.^39,^40,^50,^81,¹¹⁷ Prolonged quadriceps atrophy may affect the ability to regain normal knee motion and maintain knee extension. Chronic swelling may also cause a limitation of knee motion by inhibiting the function of the quadriceps muscle.^29,^110,^140,^145,¹⁴⁶ It is important that a knee joint effusion be treated to lessen its deleterious effect on quadriceps function.

Infection may result in loss of knee motion after ACL reconstruction. The rule followed in the authors’ clinical practice is to always consider first that an exaggerated inflammatory response with joint swelling, synovitis, and early limitation of joint motion is caused by a joint infection until proved otherwise. Even when an infectious process appears to have been excluded, a knee joint that does not respond to the gentle modalities to regain knee motion, or that has continued pain or lack of patellar mobility, should undergo repeat aspiration, cell count, culture, and diagnostic studies. In the authors’ experience, the most severe cases of arthrofibrosis that initially are presumed to be on a genetic basis are subsequently proved to have an occult unrecognized infectious etiology. In patients with an established infectious process, the principles of treatment have been discussed (see Chapter 7, Anterior Cruciate Ligament Primary and Revision Reconstruction: Diagnosis, Operative Techniques, and Clinical Outcomes), and it is important that gentle motion and overpressure programs continue to maintain the joint motion. Even in knees with swelling of soft tissues and the initial host response to an infection, it is possible within days after instituting arthroscopic lavage, débridement, and appropriate antibiotics to initiate motion exercises and prevent a flexion contracture or patella infera. Although aggressive management of this complication usually leads to resolution of the infection, studies report permanent loss of extension and flexion in the majority of patients treated, which may be avoidable.^80,^125,^148,¹⁵³

Complex regional pain syndromes and reflex sympathetic dystrophy may cause knee motion problems as a result of quadriceps atrophy, chronic swelling, and an increased sensitivity to pain.^49,¹⁰⁷ These issues are discussed in detail in Chapter 43, Diagnosis and Treatment of Complex Regional Pain Syndrome. Appropriate management using a variety of medical specialists is essential to diagnose and treat these problems.

PATHOPHYSIOLOGY

In 1972, Enneking and Horowitz ³⁶ published one of the first studies on the pathophysiology of a joint contracture after immobilization in humans. The investigators described in a series of case reports the presence of fibrofatty connective tissue in the infrapatellar fat pad, suprapatellar pouch, and posterior recesses of the knee joint with eventual obliteration of the joint cavity. Over time, this tissue was replaced with mature fibrous connective tissue.

Tissue homeostasis is maintained by the normal level of cell growth and proliferation along with the production and turnover of the extracellular matrix.^13,¹⁵ Polypeptides known as cytokines or growth factors are responsible for the constant signaling that occurs both between local cells (paracrine) and within cells (autocrine). Cytokines exist as small proteins that signal cells in response to injury and infection. One cytokine, interleukin-1, has been found to stimulate platelets and macrophages to release a variety of growth factors, including transforming growth factor–β (TGF-β). TGF-β is thought to be one of the factors (among others^19,^68,¹²⁴) mediating Dupuytren’s Contracture.³ Cytokines regulate all aspects of tissue remodeling and may act positively or negatively on tissue damage. This variability results in a wide range of potential responses to injury between patients.

Critical Points PATHOPHYSIOLOGY

• Cytokines or growth factors responsible for constant signaling occurring both between local cells and within cells.

• TGF-β is a key cytokine that initiates and ends the process of tissue repair. Its actions enhance the deposition of extracellular matrix and regulate the actions of other cytokines.

• Overexpression of TGF-β₁ results in progressive accumulation of matrix in tissues and an elevated number of myofibroblasts, leading to fibrosis.

• Specific ASMA-expressing myofibroblasts generate tissue contraction, are responsible for collagen overproduction during fibrotic diseases. TGF-β is capable of up-regulating ASMA and collagen in fibroblasts.

• ASMA is involved in scar formation and scar tissue contraction during the course of primary arthrofibrosis.

• Collagen type VI could play a contributory role in the deposition of extracellular matrix that leads to arthrofibrosis.

• Primary arthrofibrosis may be the result of an immune response.

• It appears that in the future, chemical agents will become available to treat fibrotic response to injury by controlling elevated levels of myofibroblast unregulators and fibrogenic growth factors

ASMA, α-smooth muscle actin; TGF-β, transforming growth factor–β.

TGF-β, released by platelets, tendon fibroblasts,^137,¹³⁸ and the joint capsule,^52,⁵³ has been identified as a key cytokine that both initiates and ends the process of tissue repair. Although other growth factors are involved in tissue remodeling, TGF-β is unique in its actions that enhance the deposition of extracellular matrix and regulate the actions of other cytokines.^118,¹³⁸ An overexpression of TGF-β₁ results in progressive accumulation of matrix in tissues and an elevated number of myofibroblasts, leading to fibrosis.^13,^15,^52,^57,^58,⁸⁷ Border and Noble¹³ believe that repeated injury or trauma may also cause autoinduction of TGF-β beyond normal levels, creating a “chronic, vicious circle of TGF-β overproduction,” resulting in tissue fibrosis that may also occur in organ systems such as the kidney, liver, and lung. Investigators have documented that elevated levels of myofibroblasts and TGF-β occur rapidly, within 2 weeks after injury in experimental models, and that these changes are similar to those observed in humans with chronic elbow joint contractures.^52,^57,⁵⁸

There is evidence that during the exaggerated fibrotic response that occurs in knee arthrofibrosis, a certain amount of tissue contraction or shrinkage occurs.^16,^111,¹³¹ Specific α-smooth muscle actin (ASMA)–expressing myofibroblasts generate tissue contraction during wound healing and are responsible for collagen overproduction during fibrotic diseases.^28,^34,^38,⁴⁶ TGF-β is capable of up-regulating ASMA and collagen in fibroblasts.

Unterhauser and associates ¹⁴⁷ measured the amount of ASMA-containing fibroblastic cells in arthrofibrotic tissue to determine whether the number of these cells was increased over that found in normal tissue. Tissue biopsies were obtained from 9 patients who underwent surgery for arthrofibrosis that had developed after ACL reconstruction. The patients all had primary arthrofibrosis and underwent the débridement procedure between 4 and 12 months after the ACL reconstruction. Tissue samples were also taken from 5 patients who underwent ACL reconstruction for chronic ligament deficiency and from 8 patients who had follow-up arthroscopy after ACL reconstruction for meniscus pathology; all 13 of these control patients showed no signs of arthrofibrosis. A significantly higher expression of ASMA-positive fibroblastic cells were found in the collagen bundles and remaining fatty tissue in the study group compared with both control groups (23.4% of the total cell count vs. 2.3% and 10.8%, respectively; P < .001). The authors concluded that this cell type is involved in scar formation and scar tissue contraction during the course of primary arthrofibrosis. They speculated that the expression of ASMA is most likely variable according to the time from the onset of the disease to tissue biopsy and probably decreases as the disease progresses.

Unterhauser and associates ¹⁴⁷ also reported that the fatty tissues in the arthrofibrotic knees were replaced by a dense collageneous network with parallel fiber orientation. A significantly higher total cell count and lower vessel density were measured in the arthrofibrotic knees compared with the control group who underwent ACL reconstruction. Similar findings were noted by Mariani and colleagues⁷⁶ who biopsied 17 knees with arthrofibrosis that occurred after a variety of surgical procedures. The tissue samples were obtained less than 6 months from the onset of stiffness in 9 patients, from 6 to 12 months in 5 patients, and more than 12 months in 4 patients. The histologic evaluations demonstrated collagen-producing fibroblastic tissue with differing amounts of cellularity and vascularization. This study supports the hypothesis that arthrofibrotic tissue undergoes progressive remodeling and acquires the characteristics of mature collagen, all within the first 6 months after the onset of joint stiffness. There was no association between the amount of knee motion and the time from surgery or the degree of tissue maturation. The severity of loss of motion was associated only with the location and amount of adhesive tissue in the knee joint.

Unterhauser and associates ¹⁴⁷ concluded that the ratio of myofibroblasts to the total cells in connective tissue is a factor in the onset of arthrofibrosis. The authors suggested that future antifibrosis agents (such as decorin) be evaluated, because they inhibit the signaling pathway of TGF-β. Decorin is a human proteoglycan that inactivates the effect of TGF-β and may have a beneficial effect in arthrofibrotic tissues. Fukushima and coworkers⁴⁵ reported that injection of decorin improved both the muscle structure and the function of lacerated muscle to near-complete recovery in mice. Several other experimental models have demonstrated the effectiveness of decorin in inhibiting adhesion formation in intra-articular adhesions,⁴⁴ kidneys,^14,⁶⁴ and lungs.⁴⁸ However, the effectiveness of this agent in humans with early or later-stage arthrofibrosis has not been investigated to date.⁵⁸

In an in vivo small animal model, Bedair and associates ⁸ showed that an antiotension II systemic receptor blocker decreased fibrosis and enhanced muscle regeneration in acutely injured skeletal muscle and hypothesized that the blocker modulated TGF-β₁. Hagiwara and colleagues⁵³ reported that the joint capsule has the potential to produce TGF-β₁ and connective tissue growth factor, both of which play a role in causing fibrosis.

Zeichen and coworkers ¹⁵⁵ compared tissue samples of 13 patients with arthrofibrosis, obtained a mean of 16 months after the inciting knee ligament surgery, with those of 8 patients undergoing primary ACL surgery. Histologic examination from the patients with arthrofibrosis showed marked synovial hyperplasia, infiltration of inflammatory cells, and vascular proliferation with an increased level of collagen types VI and III. None of the control subjects demonstrated these findings. The authors noted that this confirmed the observations of Murakami and associates⁸⁸ regarding the association between an inflammatory process and the proliferation of fibroblasts. The suggestion was made that collagen type VI could play a contributory role in the deposition of extracellular matrix that leads to arthrofibrosis.

Bosch and colleagues ¹⁷ advanced the hypothesis that primary arthrofibrosis is the result of an immune response. Tissue samples obtained from 18 patients between 4 and 48 months from the triggering event to surgical débridement demonstrated synovial hyperplasia with fibrotic enlargement of the subintima and infiltration of inflammatory cells. The authors believed their findings supported an immune response as the cause of capsulitis leading to formation of diffuse scar tissue. The clinical implication was to avoid further surgery or aggressive manipulation while patients are suffering from acute capsulitis and to wait 3 to 6 months for the inflammatory response to resolve before débridement is considered. As is discussed, too often, there is a delay in treatment that results in a permanent limitation of knee motion. Unfortunately, even though a delay in treatment may allow tissues to “quiet down,” the resulting fibrotic tissue that forms becomes well organized and dense and treatment becomes more difficult. It appears that in the future, chemical agents will become available to treat fibrotic response to injury by controlling elevated levels of myofibroblast up-regulators and fibrogenic growth factors.^8,^22,^42,^45,^52,^57,^58,^70,⁹⁰

PREVENTION

Preoperative

After an acute ACL tear and before reconstruction, the surgeon-therapist team must manage pain, effusion, quadriceps weakness, knee motion limitations, and gait abnormalities. Effusion and hemarthrosis are treated with appropriate nonsteroidal anti-inflammatory drugs (NSAIDs), cryotherapy, compression, and limb elevation. Patients work with physical therapists to learn safe and effective muscle-strengthening exercises (such as straight leg raises, bicycling, mini-squats, wall-sits, calf raises, knee extensions from 90°–30°, hamstring curls, and swimming) and must demonstrate good quadriceps control without an extensor lag before consideration for surgery. Regaining normal or nearly normal knee motion is essential and may take several weeks after an ACL rupture. The exceptions are knees with a mechanical block to motion, such as a displaced meniscus tear, in which early surgical intervention is warranted to preserve and repair the meniscus. A decision regarding future ACL reconstruction is based on the patient’s activity goals and other factors (see Chapter 7, Anterior Cruciate Ligament Primary and Revision Reconstruction: Diagnosis, Operative Techniques, and Clinical Outcomes). Other exceptions are knees with concomitant posterolateral ligament ruptures who are candidates for surgical intervention within 7 to 10 days of the injury. Knees with concomitant MCL tears are treated conservatively for at least 4 to 8 weeks to allow the medial side structures to heal and regain motion and muscle strength before proceeding to ACL reconstruction (see Chapter 24, Medial and Posteromedial Ligament Injuries: Diagnosis, Operative Techniques, and Clinical Outcomes).

Critical Points PREVENTION

Intraoperative

The principles of correct graft placement, tensioning, and fixation are paramount to avoid a limitation of knee motion postoperatively (see Chapter 7, Anterior Cruciate Ligament Primary and Revision Reconstruction: Diagnosis, Operative Techniques, and Clinical Outcomes). The ACL graft is placed within the femoral and tibial footprint, occupying the central two thirds or more of the footprint, to achieve an anatomic position that allows the graft to control the pivot shift and anterior tibial translation. To achieve an anatomic graft placement in the center of the tibial attachment may require a limited notchplasty to avoid a limitation of knee extension. For the femoral tunnel, an anteromedial portal drilling technique or a two-incision procedure is favored to obtain a central anatomic femoral footprint placement. An endoscopic transtibial drilling technique is not recommended.⁵⁵ In most chronic ACL-deficient knees, there is an overgrowth of cartilage and spur formation in the femoral notch, which necessitates a notchplasty to prevent ACL graft impingement.

The ACL graft is conditioned after femoral fixation by placing approximately 44 N tension on the distal graft sutures and flexing the knee from 0° to 120° for 30 flexion-extension cycles. The arthroscope is used to verify that the graft position is ideal and there is no impingement against the lateral femoral condyle or notch with full hyperextension. The knee is placed at 20° flexion and the tension on the graft is reduced to approximately 10 to 15 N in order to avoid overconstraining tibial anteroposterior (AP) translation. Alternatively, the graft can be tensioned to a higher load with knee extension. After graft fixation, a Lachman test is performed and anterior tibial translation of 2 to 3 mm should be elicited, indicating that the graft has not been overtightened. If the graft has a “bow-string,” tight appearance with no anterior tibial translation on testing, the distal tensioning and fixation procedure is repeated with less tension placed on the graft.

In knees that undergo concomitant meniscus repair, the sutures are tied with the knee at 30° of flexion to prevent capsular shortening or increased pain with postoperative extension exercises. If an associated lateral extra-articular procedure is required, care is taken to avoiding overtensioning the iliotibial band graft and to place the graft in the correct position on the femur to allow restoration of normal knee flexion (see Chapter 7, Anterior Cruciate Ligament Primary and Revision Reconstruction: Diagnosis, Operative Techniques, and Clinical Outcomes). Posteromedial and posterolateral capsular plication procedures are performed in a manner that will not result in a limitation of knee extension, which is tested at the operative table.

Postoperative

The 1st week after ACL or other knee ligament reconstruction represents a critical time period for patients to control knee joint pain and swelling, regain adequate quadriceps muscle contraction, initiate immediate knee motion exercises, and maintain adequate limb elevation (see Chapter 13, Rehabilitation of Primary and Revision Anterior Cruciate Ligament Reconstructions). A bulky compression dressing (cotton-Ace Brand [Becton, Dickinson and Company, Franklin Lakes, NY] elastic bandage–cotton–Ace Brand elastic bandage) is used for 48 hours, followed by antiembolic compression stockings and supplemental Ace bandage. Cryotherapy is begun in the recovery room after surgery. NSAIDs are used for 5 days along with pain medication to allow the immediate exercise protocol to be successfully implemented. Electrogalvanic stimulation or hi-volt electrical muscle stimulation may be used along with ice, compression, and elevation to control swelling.¹⁰⁹

On the 1st postoperative day, patients perform passive and active range of motion exercises in a seated position for 10 minutes a session, approximately four to six times per day. This is accompanied by patellar glides (mobilization), which are performed in all four planes (superior, inferior, medial, and lateral) with sustained pressure applied to the appropriate patellar border for at least 10 seconds (Fig. 41-5). The goal is to achieve 0° to 90° of knee motion by the 7th postoperative day. Patients who are unable to achieve this amount of extension and flexion are immediately placed into an overpressure motion program, described in detail later in this chapter. In the authors’ experience, the exercises and modalities in the overpressure program resolve the majority of knee motion limitations when initiated early postoperatively. In 650 knees that underwent ACL reconstruction, described elsewhere in this chapter, only 18 (3%) required a gentle manipulation under anesthesia and 6 (<1%) underwent surgical débridement and lysis of adhesions after the overpressure program failed to resolve knee motion limitations.

FIGURE 41-5 Patellar mobilization is performed by the therapist during physical therapy visits and at home by the patient or family member several times daily.

Hamstring and gastrocnemius-soleus flexibility exercises are begun immediately, as are straight leg raises in all four planes of hip movement. Partial weight-bearing is permitted as long as pain and swelling are controlled and a voluntary quadriceps contraction demonstrated. Isometric quadriceps contractions are also begun the 1st postoperative day and are performed on an hourly basis following the repetition rules of 10-second holds, 10 repetitions, 10 times per day. The remainder of the rehabilitation program is detailed in Chapter 13, Rehabilitation of Primary and Revision Anterior Cruciate Ligament Reconstructions.

DIAGNOSIS AND CLINICAL PRESENTATION

The early detection of a limitation of knee motion after ACL reconstruction is paramount for resolving the problem and preventing permanent arthrofibrosis. The establishment of specific knee flexion and extension goals according to the amount of time that has elapsed postoperatively and concurrent major operative procedures performed is required. In all knees, full passive knee extension must be obtained immediately to avoid excessive fibrous tissue proliferation in the intercondylar notch and posterior capsular contracture. In patients with physiologic bilateral knee hyperextension, the authors recommend the gradual return of 3° to 5° of hyperextension in the reconstructed knee and not more than 5° of hyperextension owing to potentially deleterious forces on the healing graft. Specific range of knee motion goals after ACL reconstruction (Table 41-5) are communicated to the patient before surgery and during postoperative assessments. Knee motion is carefully documented by the therapist in a closely supervised postoperative rehabilitation program so that detection of a knee motion problem occurs in a timely manner. Failure to meet these goals prompts entering the patient in an overpressure program using appropriate medical and therapeutic measures, to be described.

TABLE 41-5 Authors’ Goals for Restoration of Knee Motion after Anterior Cruciate Ligament Reconstruction

Operative Procedure Details	Weeks Postoperative	Range of Knee Motion Goal*
ACL B-PT-B autograft reconstruction, isolated or with meniscus repair, patient desires to return to strenuous athletics as soon as possible	1–2	0°–110°
	3–4	0°–120°
	5–6	0°–135°
ACL revision reconstruction (any graft source) ACL primary reconstruction with allograft or semitendinosus autograft Complex reconstructions with concomitant operative procedures Knees with noteworthy articular cartilage lesions

1–4 0°–90° 5–6 0°–120° 7–8 0°–135° ACL reconstruction with posterior cruciate ligament reconstruction (see Chapter 21, Posterior Cruciate Ligament: Diagnosis, Operative Techniques, and Clinical Outcomes) 1–2 0°–90° 3–4 0°–110° 5–6 0°–120° 7–8 0°–135° ACL reconstruction with posterolateral procedure (see Chapter 22, Posterolateral Ligament Structures: Diagnosis, Operative Techniques, and Clinical Outcomes) 1–4 0°–90° 5–6 0°–110° 7–8 0°–120° 9–12 0°–135°

ACL, anterior cruciate ligament; B-PT-B, bone–patellar tendon–bone.

* In patients with physiologic bilateral knee hyperextension, the authors recommend the gradual return of 3°–5° of hyperextension in the reconstructed knee. Greater than 5° of hyperextension is not recommended owing to potentially deleterious forces placed on the healing graft.

Critical Points DIAGNOSIS AND CLINICAL PRESENTATION

• Early detection limitation of knee motion after ACL reconstruction is paramount for resolving the problem.

• Full passive knee extension obtained immediately to avoid excessive fibrous tissue proliferation in the intercondylar notch, posterior capsular contracture.

• Joint aspiration with cell analysis and culture for any indication of joint redness, warmth, limitation of knee motion.

• Initial phase primary arthrofibrosis (transient) occurs within first few weeks after surgery. Limitations in knee motion usually resolve with conservative measures with compliant patient.

• If not treated, condition becomes more established, requires operative management. Findings:

Shortening of the posteromedial and posterolateral capsule, ACL graft, quadriceps muscles.

Significant growth of fibroproliferative tissue into intercondylar notch.

• Comprehensive débridement and lysis of adhesions, in-patient epidural and physical therapy program, weeks of outpatient therapy may be successful in achieving significant gains in knee motion.

• Final phase of arthrofibrosis (established) involves patellar infera and articular cartilage damage. Requires comprehensive evaluation, appropriate radiographs, bone scans, and MRI. Determine patellar vertical height, location grafts, presence cyclops lesion.

ACL, anterior cruciate ligament; MRI, magnetic resonance imaging.

Joint aspiration with cell analysis and culture are important with any indication of joint redness, warmth, and limitation of knee motion. A serum sedimentation rate is usually not reliable after surgery, because it is elevated for a number of weeks. If surgery is required, multiple tissue specimens are sent for culture and microscopic evaluation. As already discussed, an occult infectious process is not excluded by a single negative joint aspirate, and repeat joint aspirations, culture, and blood studies are required.

The initial phase of primary arthrofibrosis occurs within the first few weeks after surgery. The condition at this time is transient, because limitations in knee flexion and extension are usually resolved with conservative measures as long as the patient complies with the recommended program. However, if knee motion deficits are untreated for a few weeks, the condition becomes more established and eventually requires operative management. Findings include shortening of the posteromedial and posterolateral capsule, blocking extension; significant ingrowth of fibroproliferative tissue into the intercondylar notch; shortening of the ACL graft, preventing normal anterior tibial translation with extension; obliteration of the suprapatellar pouch; and shortening of the quadriceps muscles, limiting flexion. A comprehensive débridement and lysis of adhesions, followed by an in-patient epidural and physical therapy program and many weeks of continued outpatient therapy, may still be successful in achieving significant gains in knee motion. The final phase of arthrofibrosis involves patellar infera and articular cartilage damage, which are exceedingly difficult to treat and the loss of knee motion is usually permanent.

Patients who present with an established arthrofibrosis condition require a comprehensive evaluation, including appropriate radiographs (Fig. 41-6), bone scans, and magnetic resonance imaging (MRI) to determine whether the condition is primary or secondary, as previously discussed. The examination may demonstrate diffuse edema, increased warmth, constant pain, limited patellar mobility (Fig. 41-7), contracture of peripatellar and infrapatellar soft tissues, tenderness in the fat pad, and limits in both extension and flexion compared with the contralateral normal knee (Fig. 41-8). Anterior knee pain, stiffness, pain with attempted knee motion, a flexed-knee gait, and severe quadriceps atrophy are common findings.

FIGURE 41-6 Anteroposterior (AP; A) and lateral (B) radiographs of a knee with a severe flexion contracture and development of advanced joint arthritis after anterior cruciate ligament (ACL) reconstruction. The patient was not a candidate for surgical soft tissue releases and subsequently underwent total knee arthroplasty.

FIGURE 41-7 Limited patellar mobility is demonstrated in this patient, referred after undergoing ACL reconstruction elsewhere. The normal patellar medial glide allows at least 10–15 mm medial translation with the knee at 20° of flexion. A normal lateral glide of up to 10–15 mm is possible. A loss of either medial or lateral translation occurs with contracture of peripatellar tissues. There is usually a limitation of proximal-distal glide due to an infrapatellar contracture.

FIGURE 41-8 A severe limitation of knee extension (A) and flexion (B) demonstrated after ACL reconstruction in a patient referred for treatment 10 wk after surgery. An arthroscopic débridement, lysis of adhesions, and posteromedial and capsular releases were required. Unfortunately, the motion deficits were not resolved in the first few weeks after ACL surgery.

Patellar vertical height is determined using the radiographic method described by Caton and coworkers ²¹ and Linclau.⁷¹ In Figure 41-9, Left, the patellar vertical-height ratio is calculated by dividing line segment A, the distance between the most ventral rim of the tibial plateau and the lowest end of the patellar articular surface, by line segment B, the maximum length of the patellar articular surface. An alternative method described by Blackburne and Peel¹¹ locates the tibial reference point at an anterior central location on the tibial plateau (shown in Fig. 41-9 as line segment C). Using this method, the patellar vertical-height ratio equals C/B. The senior author conducted a study to determine normal right to left patellar vertical height ratios within the same individual in a group of 51 patients (102 knees).¹⁰⁶ The difference in the vertical-height ratio of the patella between these two methods ranged from 0 to 9%, with an average difference of 3%. Large variations existed in the ratios between individual patients (range, 0.75–1.46). Therefore, the diagnosis of patellar infera requires analysis of patellar height ratios compared with those of the opposite knee and subsequent radiographs compared with the same knee at different time periods (Fig. 41-10). A decrease in the vertical-height ratio of 14% to 15%, depending on the method used (Table 41-6), indicates a patella infera condition because this amount of difference is greater than 2 standard deviations of the normal difference between knees. An alternative method for the calculation of patellar height is the patellotrochlear index,¹⁰ expressed as a percentage at knee extension (Fig. 41-9, Right).

FIGURE 41-9 Methods used to determine patellar vertical-height ratio on a lateral radiograph. Left, The numerator (line segment A) is the distance between the most ventral (anterosuperior) rim of the tibial plateau and the lowest end of the patellar articular surface. The denominator (line segment B) is the maximum length of the patellar articular surface. An alternative numerator (line segment C) locates the tibial reference point on the middle of the tibial plateau. The patellar vertical-height ratio equals A/B or C/B. Right, The numerator (A) is the superiormost aspect of the trochlear cartilage that is in contact with line segment B. The denominator (line segment B) is the maximum length of the articular patellar surface. Using this method, the mean index is 32 ± 12%, >50% is a patellar infera, and <12% is a patella alta.¹⁰

FIGURE 41-10 Lateral radiographs document a 22% decrease in patellar vertical-height ratio after a combined ACL reconstruction and medial meniscus repair in a 14-year-old female gymnast. A, The injured knee before the reconstruction. B, Four wk postoperative, the patient was referred to our center with significant quadriceps atrophy, difficulty performing knee motion exercises, and limited patellar mobility. The patient was treated with daily physical therapy and required an arthroscopic débridement, peripatellar release, lysis of adhesions, and removal of infrapatellar scar tissue. Nine months postoperative, the patient had regained full knee motion, had no pain symptoms, and had returned to recreational activities. However, the patellar infera remained unchanged. The patient is being followed for signs of patellofemoral arthritis and need for further treatment.

(A and B, From Noyes, F. R.; Wojtys, E. M.; Marshall, M. T.: The early diagnosis and treatment of developmental patella infera syndrome. Clin Orthop 265:241–252, 1991.)

TABLE 41-6 Differences between Three Radiographic Methods of Computing Patellar Vertical-Height Ratios

MRI is useful in assessing the extent and location of scar tissue formation (Fig. 41-11). The infrapatellar band of scar tissue frequently found in the patellar infera state is just anterior to the fat pad and attaches from the inferior patellar pole to the anterior aspect of the tibia. Obliteration of the fat pad, with the patellar tendon attaching directly to the anterior tibia, is a poor prognostic sign, because the patella may adhere to the proximal tibia, which markedly restricts medial-to-lateral mobility. Thick peripatellar tissues are frequently observed. The location of prior ACL or posterior cruciate ligament (PCL) grafts must be determined. Important signs of an infectious process or unexplained edema and fluid in soft tissues or bone or about fixation implants are specifically evaluated to exclude an infectious etiology.

FIGURE 41-11 Magentic resonance imaging (MRI) of a knee with patella infera. A, Thickening of the medial and lateral peripatellar tissues. B, Note the infrapatellar tissues are replaced with dense fibrotic connective tissue. There is loss of the normal patellar tendon outline, because the tendon is encased with scar tissue and attached to the proximal tibia. The infrapatellar scar extends from the inferior pole to the anterior tibia. This patient required arthroscopic débridement of the suprapatellar pouch, followed by open débridement of infrapatellar scar tissue and Z-plasty lengthening of the medial and lateral parapatellar tissues. The decrease in patellar tendon length is permanent.

Patients who present with arthrofibrosis secondary to a cyclops lesion or an impinged or improperly placed ACL graft require surgical débridement of the lesion or graft and scar tissue, followed by several months of physical therapy to regain normal knee motion and muscle function. The decision may then be made regarding the necessity for revision ACL reconstruction. In addition, patients with established primary arthrofibrosis require surgical management of the condition, described in detail elsewhere. These two groups of patients will not be successfully managed with conservative treatment measures. However, patients who fail to meet the knee motion goals established after ACL reconstruction (see Table 41-5) and in whom the arthrofibrosis is in the early, transient stage may usually be effectively treated with the exercises and modalities described later. The key is the early detection of the limitation of knee motion, as soon as the 7th postoperative day if 0° to 90° is not demonstrated.

CONSERVATIVE MANAGEMENT OF LIMITATION OF KNEE EXTENSION

If the patient has not achieved at least 0° by the 7th postoperative day, she or he is placed into an overpressure extension program. The goal is to produce a gradual stretching of posterior capsular tissues, but not to induce soft tissue tearing and further injury because this could lead to an inflammatory response and worsen the condition. One effective exercise involves hanging weights, in which the foot and ankle are propped on a towel or other device to elevate the hamstrings and gastrocnemius, which allows the knee to drop into full extension (Fig. 41-12A). This position is maintained for 10 to 15 minutes and repeated at least eight times per day. Initially a 10-pound weight is used, which may be progressed up to 25 pounds to the distal thigh and knee to provide overpressure to stretch the posterior contracted tissues. Full knee extension is usually obtained by the 2nd to 3rd postoperative week. A commercial extension appliance (see Fig. 41-12B) is also an option.

FIGURE 41-12 A, Hanging weights. B, Extension board. C, Drop-out cast.

If these treatment measures are not effective, a drop-out (bivalved) cast (see Fig. 41-12C) is implemented for continuous extension overpressure. The advantage of this technique is that the patient is in control of the process and can apply or delete wedge material as tolerated and may bathe. A hyperextension splint may be used in the same manner; however, the authors believe that the bivalved cast offers superior benefits. Casting is not recommended in knees that have greater than a –12° extension deficit with a hard block to terminal extension. These knees are usually 3 or more months postoperative, and dense scar tissue has formed posteriorly with posterior capsular contracture requiring surgical releases and débridement. In knees with a rigid block to extension, extension casts have the potential to produce high tibiofemoral compressive forces and articular cartilage damage. Extension casts are also not effective when there is proliferative ingrowth of fibrous tissue in the femoral notch. These cases require arthroscopic débridement.

Critical Points CONSERVATIVE MANAGEMENT OF LIMITATION OF KNEE EXTENSION

• If at least 0° is not achieved by the 7th postoperative day, the patient is placed into an overpressure extension program. Goal is to produce gradual stretching of posterior capsular tissues, but not induce soft tissue tearing and further injury because this could lead to an inflammatory response and worsen the condition.

• Hanging weights: foot and ankle propped on a towel to elevate the hamstrings and gastrocnemius allows the knee to drop into full extension, use 10–25 lb weight on distal thigh.

• Bivalved cast (within first 4 weeks) if hanging weight is ineffective. Not used in knees that have > –12° extension deficit with a hard block to terminal extension or in knees with proliferative ingrowth of fibrous tissue in the femoral notch. These knees require posterior capsulotomy through a limited medial and lateral approach.

• Cylinder cast, if bivalved cast ineffective. Applied 36–48 hr, anterior wedges used. Convert to night splint for 7–10 days.

When indicated, the cast is used within the first 4 weeks for cases resistant to the other overpressure extension modalities. The goal is to resolve all extension problems by 4 weeks postoperatively. In select knees, the extension deficit may return and, accordingly, the drop-out cast is repeated. On occasion, the drop-out cast will not be effective and it is necessary to use a cylinder cast and serial wedges to gain extension. The cast is well padded to prevent skin breakdown. An anterior wedge is used every 12 to 24 hours to gradually achieve extension. The cast is applied for 36 to 48 hours and then removed to resume knee flexion and extension motion exercises. Again, some knees do not have a rigid block to full extension requiring surgery. Once extension is regained, the cast is converted into a posterior night splint, which is used for an additional 7 to 10 days. In some knees, full extension is regained but then gradually lost over the course of several weeks. In these cases, a repeat cast application may resolve the problem.

The treatment algorithm for limitations of knee extension is shown in Figure 41-13. The goal is to resolve the loss of knee extension by 4 weeks, using the modalities outlined. Frequently, it is necessary to repeat steps in the treatment protocol, because the return in a knee extension deficit may occur. It is rare that manipulation or continuous epidural is necessary when the program is followed; however, these steps are provided for the most resistant cases. The most difficult problem is the knee joint that does not respond and, despite the overpressure program, continues to show a lack of full extension. If the lack of knee extension is 10° or less, the overpressure program will usually be successful. However, it is important to identify the knee in which there is a rigid hard block to extension and the deficit is greater than 10°. In these knees, it is better to proceed with a posterior capsulotomy through a limited medial and lateral approach, to be described.

FIGURE 41-13 Treatment algorithm of limitations of knee extension.

CONSERVATIVE MANAGEMENT OF LIMITATION OF KNEE FLEXION

Because full knee flexion is present at the end of the ACL reconstruction, any limitation in the early postoperative period is due to intra-articular adhesions and contracture of peripatellar tissues and muscle spasm or pain. The early detection of a limitation of flexion (<90° by the 7th postoperative day) necessitates an overpressure flexion program. A rolling stool exercise (Fig. 41-14A) may be done in which the patient sits on a small stool close to the ground, the knee is flexed to the maximum position possible and held in that position for approximately 1 minute or as long as the patient is able to tolerate mild discomfort. Then, the patient rolls the stool forward without moving the foot position on the floor to achieve a few more degrees of flexion. The procedure is performed for 10 to 12 minutes and repeated six to eight times a day. Wall-slides are another effective exercise to achieve flexion. The patient lies on his or her back and places the foot of the reconstructed knee on a wall as shown in Figure 41-14B. The foot of the opposite leg is used to gently slide the opposite foot and flex the reconstructed knee in a gradual manner. Commercial knee flexion devices (see Fig. 41-14C and D) may also be used as available to further promote overpressure. In addition, a figure-four overpressure exercise is effective (see Fig. 41-14E). A 4-inch tubular stocking is used, double-wrapped around the foot and ankle, that allows the patient under his or her own power to flex the knee. The patient shown in Figure 41-14E had 90° of flexion, and an arthroscopic release was successful in achieving 135°. After the débridement and placement of an epidural, the surgeon sets a mark on the thigh by gentle pressure to establish the flexion goal for that day. The mark on the thigh in the photograph demonstrates the 135° flexion position, which is the overall goal. The mark on the distal portion of the patella in the photograph demonstrates the starting position, which in this case was 90°. The goal of these exercises and modalities is to gradually and passively stretch tissues in a controlled manner, while not inducing pain or tearing of tissues. Patients who have difficulty achieving 90° by the 3rd to 4th week require a gentle ranging of the knee under anesthesia (not a forceful manipulation) in which full flexion is easily obtained with only light loads applied. This stretches out early joint adhesions, markedly reduces postoperative pain, and allows the patient to regain motion.

FIGURE 41-14 A, Rolling stool exercise. B, Wall-slides. C, Flexion seat. D, Knee flexion overpressure device. E, Figure-four knee flexion overpressure exercise.

Critical Points CONSERVATIVE MANAGEMENT OF LIMITATION OF KNEE FLEXION

• Overpressure program indicated < 90° flexion by 7th postoperative day.

• Rolling stool exercise, wall-slides, commercial knee flexion devices, figure-four exercise usually effective.

• Patients who have < 90° by 3–4 wk require a gentle ranging of the knee under anesthesia (not a forceful manipulation) in which full flexion is easily obtained with only light loads applied.

• Associated peripatellar contracture must be immediately treated to prevent patella infera.

• Knees with no patellar mobility: operative release of tight contracture peripatellar tissues indicated.

• Chronic cases of arthrofibrosis require open medial Z-plasty release.

The treatment algorithm for a limitation of knee flexion is shown in Figure 41-15. The first step is to determine whether there is associated contracture of patellar tissues, which makes the treatment more difficult. The loss of knee flexion when there is no peripatellar contracture is more easily resolved. With the treatment protocol shown, it is rare to progress to the necessity for an arthroscopic débridement and release of peripatellar tissues. When there is an associated peripatellar contracture, it is important that the condition be immediately treated because this can result in a patella infera. A conservative patellar mobilization program with oral steroids is performed for a week. If the limitation of motion and peripatellar contracture persists, a gentle manipulation under anesthesia is performed; however, no more than “two to three fingers of pressure” is placed at the distal tibia to achieve knee flexion. If more force is necessary, it indicates that the peripatellar contracture is composed of more dense, resistant scar that requires arthroscopic débridement. An aggressive manipulation under higher forces risks damaging the patellofemoral articular cartilage, because the tight contracted tissues increase patellofemoral contact forces with knee flexion. Knee flexion is gained, but at the expense of possibly damaging the patellofemoral joint. This is also true for pushing knee flexion in the clinic when there is no patellar mobility. Again, an operative release of tight contracture peripatellar tissues is indicated instead of overzealous flexion exercises or a knee manipulation with high flexion loads.

FIGURE 41-15 Treatment algorithm for a limitation of knee flexion.

It should be noted that there are select knees, most commonly chronic cases of arthrofibrosis, in which the peripatellar scar tissue is thick and contracted and an attempted arthroscopic release would result in too extensive a release on both the medial and the lateral peripatellar tissues. If a major release is necessary, extending to the proximal aspect of the patella, the senior author recommends an open medial Z-plasty release in which the more normal tissue laxity is restored and the abnormal scar tissue is excised. In addition, the Z-plasty procedure prevents the occurrence of a major capsular defect with joint communication to subcutaneous tissues, which is a complication of an extensive medial or lateral arthroscopic release.

ROLE OF ORAL CORTICOSTEROIDS

There is a subset of patients who develop postoperatively an exaggerated inflammatory soft tissue response with excessive pain, joint stiffness, soft tissue edema, warmth, and redness about the knee. The inflammation is not resolved by the standard treatment methods of cryotherapy, anti-inflammatory medications, elevation, and compression. It is first recommended to use a maximum dose of an NSAID for 1 week. If this is not successful, a trial of oral steroids is indicated. It is important that before and during the treatment of these resistant cases, an occult infectious process is ruled out, with appropriate serial diagnostic tests (aspiration, sedimentation rate) performed as necessary.

A 6-day dose pack of 4-mg methylprednisolone tablets (Watson Laboratories, CA) is effective if used early in the phase. Six tablets are taken on the 1st day of treatment, five on the 2nd, four on the 3rd, three on the 4th, two on the 5th, and one on the 6th. During this treatment period, forceful and aggressive physical therapy is avoided. Gentle knee motion and lighter overpressure exercises are performed. In select cases, the 6-day dose pack may be repeated.

Critical Points ROLE OF ORAL CORTICOSTEROIDS

• Indications: knees with exaggerated inflammatory soft tissue response with excessive pain, joint stiffness, soft tissue edema, warmth, and redness about the joint.

• Inflammation not resolved by cryotherapy, anti-inflammatory medications, elevation, and compression.

• A 6-day dose pack of 4-mg methylprednisolone tablets (Watson Laboratories, CA) is effective if used early. Avoid forceful and aggressive physical therapy.

• Consider oral corticosteroids (prednisone 5 mg [UpJohn, Kalamazoo, MI]) for 4 wk if the inflammatory symptoms return or are more severe.

• In cases of severe arthrofibrosis, oral corticosteroids may be required for 2–3 months in an effort to avoid repeat surgery.

Another option is to use oral corticosteroids (prednisone 5 mg, UpJohn, Kalamazoo, MI) for 4 weeks if the inflammatory symptoms return or are more severe. The usual daily dose is 30 mg in the 1st week (two tablets taken three times a day), 15 mg in the 2nd (one tablet taken three times a day), 10 mg in the 3rd (one tablet taken two times a day), and 5 mg in the 4th. In cases of severe arthrofibrosis, oral corticosteroids may be required for 2 to 3 months in an effort to avoid repeat surgery. Complications that may arise from prolonged corticosteroid intake include pituitary adrenal suppression, fluid and electrolyte disturbance, hyperglycemia, peptic ulcers, and avascular necrosis. In the most resistant cases, it is necessary to repeat oral steroid cycling on the off days to NSAIDs, which are prescribed at their maximum dosage.

GENTLE MANIPULATION UNDER ANESTHESIA

As already described, a forceful manipulation of a knee with extensive scar tissue is harmful and ineffective in treating the limitation of knee motion. A forced manipulation may tear intra-articular and extra-articular tissues and cause excessive tibiofemoral and patellofemoral compression with the risk of fracture, damage to the articular cartilage, rupture of the patellar tendon, and even femoral fracture.⁷² Therefore, any patient who has a hard-stop to knee motion (which represents a joint contracture) is treated with an arthroscopic débridement and lysis of adhesions.

A gentle manipulation under anesthesia, done with only mild pressure exerted on the distal leg, is effective if performed early after ligament surgery, within 3 to 4 weeks postoperatively. Even at 6 weeks, dense scar tissue proliferation may exist in joint soft tissues and the window of opportunity has been lost in not performing an early ranging of motion under general anesthesia. Adequate patellar mobilization must be established before flexing the knee during the procedure to prevent damage to the patellofemoral articular surface. A supervised physical therapy program is required to maintain the knee motion achieved by the manipulation, as detailed in the treatment algorithm.

OPERATIVE MANAGEMENT OF SEVERE RESTRICTION OF KNEE MOTION

Arthroscopic Soft Tissue Releases

A demonstration of an arthroscopic technique for débridement of contracted tissues in a knee with arthrofibrosis is shown in Figure 41-16. In this patient, there was a restriction in medial-to-lateral translation (glide) of the patellofemoral joint, with a contracture of the medial and lateral retinaculum. However, approximately 50% of normal patellar mobility was still present, indicating that an arthroscopic technique could be used and an open extensive technique was not necessary. There was a limitation of motion at 0°/5°/90°. The procedure was performed after tourniquet inflation.

FIGURE 41-16 A, The anterolateral portal is used to transect the lateral retinaculum 15 mm. B, The anteromedial portal is used to transect the medial retinaculum 15 mm. C, The anterolateral portal is used to place a Metzenbaum scissor beneath the patellar tendon and palpate for an infrapatellar patella–tibial band of scar tissue. The scissor is bluntly pushed posterior to the patellar tendon and through the infrapatellar band to allow fluid to pass into the fatty space behind the patellar tendon. This maneuver protects the patellar tendon during removal of the infrapatellar band, to be described. If a safe plane cannot be established and verified arthroscopically, an open débridement procedure is indicated. D, There is now sufficient patellar mobility to pass an arthroscope beneath the patella safely without damaging the patellofemoral cartilage surfaces. If this is not possible, additional medial and lateral releases are performed. The releases at this point are conservative. E, A blunt obturator or shaver is placed into the suprapatellar pouch and translated in a superior and inferior plane to reestablish a space sufficient for the initial arthroscopic débridement. A band of scar extends from the superior patella to the trochlea, and dense suprapatellar adhesions are present. Débridement of suprapatellar scar tissues is performed using an electrocuting device. F, The soft tissues and synovium over the anterior femur are not removed to leave a gliding soft tissue surface. G, A resection of scar tissue beneath the vastus medialis obliquus (VMO) and vastus lateralis obliquus (VLO) may be required because this scar can limit muscle mobility. H, The scope is placed in the superolateral portal to view the infrapatellar region and débride an infrapatellar contracture. I, An arthroscopic view through the superolateral portal shows the fat pad and instruments to remove infrapatellar scar tissue. Care is taken to not transect the anterior medial and lateral meniscus attachments. J, With the scope placed alternatively in the anteromedial and anterolateral portals, extensive synovium and scar are removed from the medial and lateral recesses and intercondylar notch. Scar tissue proliferation may block extension on the anterior aspect of the medial and lateral meniscus; this requires removal. K, The knee is placed at 30° flexion and sufficient medial and lateral parapatellar contracted tissue and retinaculum are removed to allow for a normal medial-lateral glide. This release rarely extends above the midportion of the patella. In this knee, moderate patellofemoral damage is observed. L, Notch ingrowth of tissue removed that may block extension. After completion of the arthroscopic procedure, and verification that no scar tissue remains, the tourniquet is deflated and meticulous electrocoagulation of bleeding points is performed. The decision to use a drain is based on the ability to control intra-articular bleeding. A gentle ranging of the knee with the patient under anesthesia is performed that is not aggressive in terms of the loads applied. The knee is placed into a bulky compression (cotton-Ace-cotton-Ace) dressing with an ice bladder incorporated into the dressing.

Critical Points GENTLE MANIPULATION UNDER ANESTHESIA

• Forceful manipulation of a knee with extensive scar tissue is harmful and ineffective in treating the limitation of motion.

• Patients with a hard-stop to knee motion (joint contracture) treated with arthroscopic débridement, lysis of adhesions.

• A gentle manipulation under anesthesia, done with only mild pressure exerted on the distal leg, is effective if performed within 3–4 wk postoperatively.

• Supervised physical therapy program required to maintain the knee motion achieved by the manipulation.

Open Z-Plasty, Medial-Lateral Retinacular Tissues

Figure 41-17 demonstrates the operative technique for an open Z-plasty release of the medial and lateral retinacular tissues. An arthroscopic release alone is contraindicated in this case, because the release is so extensive (extending above the proximal patella and releasing all medial and lateral soft tissues) that there would be open communication of the joint into the subcutaneous tissues. The principle shown is to preserve the function of the medial and lateral retinacular soft tissues and, as well, débride the tissues to a normal thickness. The Z-plasty open release allows an arthrotomy to thoroughly débride infrapatellar contracted tissues, protect the patellar tendon, and lengthen contracted medial and lateral patellar tissues.

FIGURE 41-17 Z-Plasty operative technique for contracted medial and lateral peripatellar tissues. A, Preoperative examination under anesthesia of a patient with established arthrofibrosis discloses a complete lack of patellar mobility, absent medial and lateral glide, and an obvious patella infera with shortening of the patellar tendon. The patient’s range of motion was 0°/0°/80°. B, Open medial Z-plasty approach. The medial retinaculum and soft tissues are split in a Z-plasty fashion to allow a loose closure and restore a normal medial patellar glide. An arthroscopic procedure was performed just prior to the open procedure to reestablish the suprapatellar pouch, remove intra-articular adhesions within the suprapatellar pouch and medial and lateral tibiofemoral gutters, and document the condition of the joint. C, Completion of medial Z-plasty release shows the medial soft tissue flaps that have been developed. A débridement of infrapatellar scar tissue was performed under direct visualization. D, A lateral Z-plasty release of contracted lateral retinacular tissues is performed in a similar fashion. E, The loose closure of the lateral Z-plasty release allows restoration of a normal medial glide. A medial and lateral Z-plasty release for contracted soft tissues represents a real key for the successful management of this type of contracture. There is restoration of normal patellar mobility, and most importantly, the joint soft tissues can be closed.

Posterior Medial-Lateral Capsulotomy

The technique for a posterior medial-lateral capsulotomy involves the same exposure as that used for a medial or lateral meniscus repair (Fig. 41-18). On the medial side, the posterior capsule is sectioned at its femoral attachment proximally. On the lateral side, the capsule is sectioned in its proximal aspect just below the attachment of the lateral gastrocnemius to the posterior capsule. The dissection and posterior capsule excision are carried directly over the posterior femoral condyles and not into the posterior intercondylar region, because scar tissue may extend to the neurovascular structures. It is often impressive how dense the posterior capsular structures are, and with their release, further gains in knee extension are possible on the operating table. The remaining posterior intercondylar tissues are easily stretched with the overpressure program. The posterior capsule releases are also accompanied with an arthroscopic procedure to remove any tissue that has grown into the notch producing an anterior impingement that would also block extension.

FIGURE 41-18 Operative photographs of a patient with arthrofibrosis (0°/15°/80°) requiring an arthroscopic lysis of adhesions, parapatellar releases, and posterior medial and lateral capsulotomy for the 15° flexion contracture. A, An arthroscopic lysis of adhesions, removal of scar tissue, and parapatellar releases is performed, as already described. All scar tissue from the notch region is removed and a notchplasty performed as required so that these tissues do not block extension. B, The medial joint line is marked. C, A posteromedial incision is made. D, The approach reflecting the sartorius is used as described for an inside-out medial meniscus repair (see Chapter 28, Meniscus Tears: Diagnosis, Repair Techniques, and Clinical Outcomes). E, A vertical posteromedial capsulotomy is made directly behind the superficial medial collateral ligament (MCL). Operative photograph: The surgeon uses a headlamp and the femoral insertion of the posteromedial capsule is identified and transected millimeter by millimeter to the edge of the medial femoral condyle, but not beyond to avoid the neurovascular structures. F, The posterolateral approach for a capsular release uses the same approach as that for a lateral meniscus repair (see Chapter 28, Meniscus Tears: Diagnosis, Repair Techniques, and Clinical Outcomes) with a skin incision just distal to the joint line as shown. G, The posterolateral capsule anterior to the gastrocnemius tendon is identified. H, The posterolateral capsule is carefully incised under direct visualization to the edge of the lateral femoral condyle, avoiding the neurovascular structures. I, A finger is placed into the posteromedial and posterolateral incisions and the central neurovascular structures can be palpated. The central posterior capsule anterior to the neurovascular structures is not released. The finger palpation confirms that the capsule directly posterior to the medial and lateral femoral condyles has been incised, removing this block to extension as the knee is extended. J and K, The posterior capsular releases. The remaining posterior capsular tissues are gently stretched with the overpressure program to achieve extension. This is a limited cosmetic approach that does not disturb other posterior soft tissues and removes only the contracted posterior capsule as shown by the dotted line.

IN-PATIENT PHYSICAL THERAPY PROGRAM

An in-patient physical therapy program, supplemented with a continuous epidural anesthetic, femoral nerve block, or appropriate analgesics may be used for 3 to 4 days in resistant patients who do not respond to other interventions or in whom limitations of knee motion return after manipulation or arthroscopic débridement. The epidural is regulated to block pain and sensory input, with the goal to retain muscle motor control to allow active knee motion and the overpressure program. The block requires close supervision by an anesthesiologist for levels and medication dosage. The catheter is replaced under fluoroscopy control if the patient expresses insufficient pain relief. If the repeat block fails, pain relief is obtained with a femoral nerve block and analgesics. A skin care and protection program is performed by nursing personnel. The block is maintained for a minimum of 72 hours in order to allow a gradual overpressure program to stretch contracted soft tissues.

The following measures are taken in order to avoid deep venous thrombosis and pulmonary embolism. First, a careful analysis is done to detect patients at increased risk, including diabetics, obese individuals, or those with venous insufficiency, prior history of phlebitis, or venous clots or embolism. These patients are not appropriate candidates for the epidural program owing to the associated inactivity and bedrest. When the epidural is in place, the patient remains mobile and is encouraged to be out of the bed intermittently throughout the day. Antiembolism stockings are worn and ankle pumps are done for 5 to 10 minutes hourly. The extremity is monitored daily and a calf venous compression device is used. Aspirin (600 mg daily) is prescribed. The patient is monitored for calf tenderness or leg edema and an ultrasound examination of both lower extremities is obtained if any suggestion of a deep venous thrombosis exists.

The in-patient overpressure program is contraindicated in patients with open growth plates or disuse osteopenia owing to the increased risk of a fracture. The patient is taught before the epidural how to perform the program, and the patient uses the amount of tension applied to the foot-calf stocking for achieving knee flexion. It is important that other individuals such as the family not assist in the overpressure flexion, because this would involve a flexion manipulation by untrained personnel.

The overpressure extension (Fig. 41-19) and flexion (Fig. 41-20) exercises are described in Table 41-7. The authors recommend an active range of motion program performed by the patient instead of use of a continuous passive motion machine. As well, the patient should continue with leg lifts and isometric exercises while in the hospital. It is imperative to control soft tissue inflammation and avoid a hemarthrosis. If soft tissue swelling persists, or thigh muscle pain occurs owing to excessive stretching, an NSAID or steroidal dose pack should be considered. After the epidural, it is routine to obtain a venous ultrasound to exclude venous clot disease.

FIGURE 41-19 In-patient extension overpressure exercises include hamstring stretching (A) and hanging weights (B).

FIGURE 41-20 In-patient flexion overpressure exercises include rolling stool (A) and figure-four with a towel or strap in which the heel is brought up to a predetermined mark on the anterior thigh of the opposite extremity (B).

TABLE 41–7 In-Patient Overpressure Extension and Flexion Program

	Exercises
Extension (perform first, before flexion)	1 Determine weight to be used and pain limits before epidural is begun. 2 Use 15-20-25 lb of weight over the knee with the foot and ankle supported. Progress as tolerated. 3 Use lowest amount of weight to achieve 3° hyperextension at the 3rd day.

Flexion

1 Perform release of contracted tissues that produce a hard-stop to flexion before the overpressure program, protect patellofemoral joint. Expect soft-stop to gradually release over 72 hr, producing significant gains in flexion.

2 Mark the affected heel height on the opposite thigh before the epidural is begun to determine the extent of contracture and starting point.

3 Limit the amount of flexion gained over the first 24 hr to prevent muscle and tissue tearing.

4 Perform patellar mobilizations to avoid patella overpressure with knee flexion.

5 Figure-four position in bed, place and hold strap or towel using approximately 15–20 lb of pull on the ankle. Monitor heel-thigh mark on the opposite thigh to determine the gain in flexion.

6 Perform flexion overpressure program every 30 min for 5 min while awake. Goal is to achieve heel-height above patella.

7 Physician performs flexion overpressure test to determine whether soft or hard resistance is present and measures knee flexion angle daily.

8 Continue the overpressure program after discharge at home, eight times every 24 hr, using pain control to achieve flexion gained under the epidural.

Upon completion of the in-patient program, the exercises must be continued at home eight times a day. Close supervision by the physical therapist is required, because the gains in knee flexion and extension may be reduced rapidly if the regimen is not maintained or if pain and swelling prohibit the patient’s ability to perform the exercises.

Critical Points IN-PATIENT PHYSICAL THERAPY PROGRAM

• An in-patient physical therapy program—supplemented with either a continuous epidural anesthetic, femoral nerve block, or appropriate analgesics—may be used for 3–4 days in resistant cases who do not respond to other interventions or in whom limitations of knee motion return after manipulation or arthroscopic débridement.

• Contraindicated in patients with open growth plates or disuse osteopenia owing to the increased risk of a fracture.

• Block maintained at least 72 hr to allow a gradual overpressure program to stretch contracted soft tissues.

• Take appropriate measures to avoid deep venous thrombosis.

• Patient is taught before the epidural how to perform the overpressure program.

• Recommend active range of motion program by the patient, not continuous passive motion machine.

• Leg lifts, isometric exercises performed while in the hospital.

• Exercises must be continued after discharge at home eight times a day, along with supervised therapy program.

DEVELOPMENTAL PATELLA INFERA

Critical Points DEVELOPMENTAL PATELLA INFERA

• Occurs secondary to contracture of peripatellar and infrapatellar scar tissues and quadriceps weakness.

• May result in permanent shortening of the patellar tendon, patellofemoral arthritis, and severe functional limitations.

• Prevention: voluntary quadriceps contraction by 2nd postoperative day, knee motion, patellar mobilization.

• Serial lateral radiographs to measure patellar height in patients with limited patellar mobility, early arthrofibrotic response detected.

• Treatment of established patella infera: preoperative muscle strengthening, rehabilitation. Operative removal of contracted and scarred tissues.

• Final functional limitations based on residual motion deficits, joint arthritis.

The senior author has reported on the complication of developmental patella infera (Fig. 41-21) that occurs after major knee injury or surgery, secondary to contracture of peripatellar and infrapatellar scar tissues and quadriceps weakness.^105,¹⁰⁶ This condition may result in permanent shortening of the patellar tendon, patellofemoral arthritis, and severe functional limitations. To prevent this problem, the steps previously described to prevent arthrofibrosis are taken before and after surgery. In addition, the patient is instructed preoperatively on the importance of achieving a voluntary quadriceps contraction as soon as possible after surgery, which is expected to occur by the 2nd postoperative day. Patellar mobility is assessed weekly by the therapist to detect any early contracture. Serial lateral radiographs are taken to detect any decrease in patellar height for patients demonstrating limited patellar mobility or in whom an early arthrofibrotic response is detected (Fig. 41-22). The differences in criteria for determining the presence of patella infera according to published techniques are shown in Table 41-8.

FIGURE 41-21 Pathomechanics for developmental patella infera, quadriceps insufficiency, patellar tendon shortening, and arthritis.

(From Noyes, F. R.; Wojtys, E. M.; Marshall, M. T.: The early diagnosis and treatment of developmental patella infera syndrome. Clin Orthop 265:241–252, 1991.)

FIGURE 41-22 Treatment recommendations for avoiding developmental patella infera syndrome. (From Noyes, F. R.; Wojtys, E. M.; Marshall, M. T.: The early diagnosis and treatment of developmental patella infera syndrome. Clin Orthop 265:241–252, 1991.)

TABLE 41-8 Published Values for Patellar Height: Normal, Alta, Infera

For patients who present with an established patella infera, the treatment algorithm is shown in Figure 41-23. The first principle of treatment is the preoperative preparation of the patient to establish quadriceps muscle function, rehabilitation, and training to avoid a quadriceps shutdown after the surgical procedure. Second, to remove the contracted and scarred tissues by either arthroscopic or open surgery, as already discussed. A number of months of intensive therapy are then required. The final functional limitations are based on residual motion deficits and joint arthritis that are present. A majority of patients with established patella infera have functional limitations.¹⁰⁶ The patients do not desire any further surgery and are willing to live with these limitations, understanding that an eventual arthroplasty procedure may be required. A small percentage of patients with a remaining patella infera and minimal patellofemoral arthritis who have symptoms of anterior knee pain and stiffness may be candidates for restoration of a normal patellotrochlear relationship.

FIGURE 41-23 Treatment algorithm for established patella infera.

AUTHORS’ CLINICAL STUDIES

Two studies were conducted by the authors to determine the effectiveness of the postoperative rehabilitation program and early diagnosis and treatment of knee motion limitations after ACL reconstruction in preventing arthrofibrosis. In the first study,¹⁰² a group of 207 knees that underwent an ACL bone–patellar tendon–bone (B-PT-B) allograft reconstruction were followed for at least 1 year postoperatively to determine the final amount of knee flexion and extension obtained and document the necessity of treatment interventions. Sixty-nine patients received the operation for an acute ACL rupture, and 138 for chronic ACL deficiency. Of the 207 knees, 90 had the ACL reconstruction alone, 52 had a concurrent iliotibial band extra-articular procedure, 52 had a concurrent meniscus repair, and 13 had a concurrent MCL repair.

The investigation found that 189 of the knees (91%) regained normal motion without requiring additional treatment intervention. The remaining 18 required extension casting, gentle manipulation under anesthesia, or (in only 3 knees) arthroscopic débridement and lysis of adhesions (Table 41-9). There was a correlation between concurrent procedures and the incidence of patients requiring addition treatment, because 4% in the ACL alone subgroup, 10% in the iliotibial band extra-articular subgroup, 12% in the meniscus repair subgroup, and 23% in the MCL subgroup required intervention. The timing of surgery had no effect on the necessity for treatment intervention.

TABLE 41-9 Patients Requiring Treatment Intervention for Knee Motion Limitations after Anterior Cruciate Ligament Allograft Reconstruction

Critical Points AUTHORS’ CLINICAL STUDIES

ACL, anterior cruciate ligament; B-PT-B, bone–patellar tendon–bone; FCL, fibular collateral ligament; MCL, medial collateral ligament.

Extension casts were applied to 6 knees between 4 and 12 weeks postoperatively and all regained normal extension. A gentle manipulation under anesthesia was performed in 9 knees between 3 and 13 weeks postoperatively. All achieved full flexion and all but 2 achieved full extension; two knees lacked 5° of extension at follow-up. Arthroscopic débridement was done in 3 knees; the details and results are shown in Table 41-10. At follow-up, full knee motion was present in 98%, 1% had a 5° limitation of extension, and 1% had a permanent contracture.

TABLE 41-10 Results of Arthroscopic Débridement for Arthrofibrosis after ACL Allograft Reconstruction

The authors conducted a second study ¹⁰¹ comprising 443 knees that underwent ACL B-PT-B autograft reconstruction. The operations were performed for acute/subacute ACL ruptures in 161 patients and for chronic ruptures in 283 patients. All were followed an average of 25 months (range, 12–86 mo) postoperatively. Concurrent procedures done in 224 knees included meniscus repairs in 194 knees, proximal advancement of the posterolateral structures in 32 knees, an autograft reconstruction of the fibular collateral ligament (FCL) in 4 knees, a repair or reconstruction of the MCL in 9 knees, and a proximal patellar realignment in 17 knees.

No correlation existed between concurrent procedures and the incidence of patients requiring addition treatment in this study. The percentage of patients requiring additional treatment intervention was 6% in the ACL alone subgroup, 5% in the FCL reconstruction/posterolateral advancement subgroup, 8% in the meniscus repair subgroup, 18% in the proximal patellar realignment subgroup, and 22% in the MCL subgroup. The timing of surgery had no effect on the necessity for treatment intervention.

The investigation found that 98% of the knees regained normal motion and 2% had mild losses of extension of 5°. In 23 knees, treatment intervention was required (Table 41-11), which was successful in treating the limitation of knee flexion or extension (Table 41-12). The 2% (7 knees) who had mild losses of extension refused treatment intervention.

TABLE 41–11 Patients Requiring Treatment Intervention for Knee Motion Limitations after Anterior Cruciate Ligament Bone–Patellar Tendon–Bone Autograft Reconstruction

TABLE 41-12 Results of Treatment Intervention

Extension casts were applied to 9 knees an average of 13 weeks postoperatively. All of these knees regained normal extension. A gentle manipulation under anesthesia was performed in 9 knees a mean of 6.4 weeks postoperatively, and all achieved full knee motion. Arthroscopic débridement was done in 3 knees, which also successfully restored normal knee motion. There was no statistically significant increased risk for knee motion problems for six variables studied including gender, injury chronicity, condition of the articular cartilage at reconstruction, location of physical therapy, whether prior surgery had been performed, and whether a prior ACL reconstruction had been performed.

The data from the two investigations on 650 knees showed that 6% of the patients required and agreed to treatment intervention for a knee motion problem. At the final follow-up evaluation, 2% lacked normal knee motion (9 knees lacked 5° of extension and 2 had permanent contractures). An extension cast was applied in 2%, gentle manipulation under anesthesia was done in 3%, and arthroscopic débridement was performed in less than 1%. The percentage of all 650 knees requiring additional treatment intervention was 5% in the ACL alone subgroup, 5% in the FCL reconstruction/posterolateral advancement subgroup, 10% in the meniscus repair subgroup, 10% in the extra-articular subgroup, 18% in the proximal patellar realignment subgroup, and 23% in the MCL subgroup.

OTHER AUTHORS’ CLINICAL STUDIES

Several authors have reported on the outcome of the treatment of arthrofibrosis after ACL reconstruction (Table 41-13).* These studies help identify risk factors for a limitation of knee motion, discussed previously. In general, the surgical débridement procedures were done an average of 1 year after the reconstruction, which in the opinion of authors of this chapter, is too late. In many of the series, patients were referred from other centers and the treating surgeon was unable to perform the débridement earlier. Although many authors reported that significant gains were obtained in knee motion, most found that the majority of patients had permanent residual losses of flexion and extension and more complaints of pain and limitations compared with patients who did not suffer from this complication. Table 41-13 also shows other studies of the treatment of arthrofibrosis after fractures, infection, meniscectomy, and other knee ligament reconstructions.^1,^73,^149,¹⁵¹ These studies report even poorer results in terms of restoration of normal knee motion and function.

TABLE 41-13 Clinical Studies Treatment of Arthrofibrosis

Illustrative Cases

Case 1

A 42-year-old woman presented 7 months after an open reduction internal fixation of a patellar fracture and 4 weeks of immobilization with a severe patella infera, marked by a Linclau ratio of 60% of the left knee (compared with 97% on the opposite knee; Fig. 41-24A). She complained of muscle weakness, pain, and limitations with activities of daily living. She had a range of motion of 0°/10°/95° and a significant decrease in patellar mobility in both medial-lateral and superior-inferior directions. Physical examination showed an obvious patella infera, with mild patellofemoral crepitus. An isokinetic evaluation revealed a 75% deficit in quadriceps peak torque compared with the contralateral side. She underwent 2 months of rehabilitation owing to this severe quadriceps muscle weakness.

FIGURE 41-24 Case 1. A, Preoperative lateral radiographs demonstrate patella infera. B, Preoperative appearance of the left knee. The skin mobility was sufficient and did not contraindicate surgery. C, The line for the incision of the Z-plasty lengthening of the patient’s patellar tendon. D, Extensive resection of infrapatellar scar tissue was required. E, Appearance of the femoral trochlea shows intact articular cartilage. An extensive medial Z-plasty release was performed. F, Placement of a central patellar tunnel for later passage of semitendinosus and gracilis tendons from a distal-to-proximal direction. G, Final appearance of patellar tendon reconstruction. The patient’s patellar tendon was reapproximated after the Z-plasty lengthening. The semitendinosus and gracilis tendons were passed from the inferior to the superior pole and brought distally along the medial retinaculum to further augment the medial portion of the patellar tendon. In this case, the advantage of using the patient’s own patellar tendon added significant soft tissues so that further augmentation was not required. H, Postoperative radiograph shows three internal fixation wires that provide stabilization and allow immediate range of motion. I, Radiograph shows restoration of normal patellar height after removal of internal fixation wires. The patient was asymptomatic with activities of daily living and able to perform light recreational activities. The final range of motion was normal (0°/0°/135°).

The patient was then treated with an open release of scar tissue, which completely obliterated the suprapatellar pouch. Dense scar was present in the medial and lateral gutters, the medial and lateral joint lines, and the intercondylar notch. After the procedure, the patient underwent 3 days of in-patient physical therapy on the epidural overpressure program described previously. Her knee motion improved to 0°/0°/100°.

Two months later, the patient continued to have symptoms and minimal improvement. Therefore, the decision was reached to perform a patellar lengthening procedure. Figure 41-24B-G demonstrates the tendon lengthening. A Z-plasty lengthening of the patient’s patellar tendon was performed along with an augmentation using a four-strand semitendinosus-gracilis autograft. Internal fixation with wire was used to initiate immediate knee motion. The procedure was successful in restoring a normal patellar height (see Fig. 41-24H and I). The goal is to buy time until the patient eventually requires a patellofemoral arthroplasty, which is possible with normal patellar height.

Case 2

A 33-year-old woman presented with severe patellar infera (Linclau ratio, 29%) 4 months after resection of a ganglion cyst, which was growing under her patellar tendon. A portion of the patellar tendon was damaged in the procedure and the patient was treated with 5 weeks of plaster immobilization, which resulted in severe quadriceps atrophy and severely contracted peripatellar and joint soft tissues. This represented a salvage knee condition because the patient had significant loss of function of the lower extremity. The range of motion was 0°/10°/75°. She underwent 6 weeks of intense preoperative rehabilitation for muscle strengthening and then a skin expansion procedure (Fig. 41-25A and B). Because this patient had no remaining patellar tendon to use in a Z-plasty fashion to incorporate into the reconstruction, she underwent a combined allograft-autograft patellar tendon lengthening procedure (see Fig. 41-25C-G). The patient required intensive rehabilitation for 6 months.

FIGURE 41-25 Case 2. A, Preoperative appearance of skin contracture. It is necessary to obtain more normal skin and soft tissue prior to the patellar tendon–lengthening procedure. Otherwise, there would be an increased risk of a complication of skin breakdown and infection. B, Placement of the skin expansion system at surgery. The expansion system may be placed either through the prior incision or through limited medial and lateral incisions using two balloons to avoid the primary incision. C, Appearance of expanded skin over the anterior aspect of the knee joint after 4 wk of skin expansion. The balloon was removed through a small incision before the operative procedure. Extra redundant skin and subcutaneous tissue is shown and a scar revision was performed. D, Operative photograph shows an Achilles tendon allograft for reconstruction of the patellar tendon. The bone portion of the graft is fixated at the tibial tubercle. The two arms of the graft are placed through separate patellar tunnels and sewn into the quadriceps tendon proximally. E, A semitendinosus and gracilis autograft harvest is performed. The tendons are passed beneath the tibial tubercle and the Achilles tendon–bone allograft. F, Placement of two patellar tunnels. G, Final tendon-lengthening construct. The Achilles tendon has been secured both proximally and distally. The semitendinosus-gracilis autograft tendons are placed through the proximal tibia adjacent to the tibial tubercle. Both tendon arms are passed medially and laterally and secured to the peripatellar tissues to augment the allograft tendon reconstruction. Two wire loops are placed through the tibial tubercle to the midpoint of the patella. A third wire is crossed from the tibial tubercle over the superior portion of the patella and passed beneath the quadriceps tendon patella insertion as a tension band. The height of the patella is adjusted to the normal opposite side using intraoperative fluoroscopy. H and I, Postoperative lateral radiographs of both knees show retention of the normal height of the patella in the left knee (H) compared with the right knee (I).

At the most recent follow-up evaluation, 2 years postoperative, the patient had equal Linclau ratios of 85% (see Fig. 41-25H and I) and a range of motion of 0 to 120°. She has no symptoms with activities of daily living or swimming and, while pleased with her condition, realizes that in the future a patellofemoral arthroplasty may be required.

Authors’ comment: The salvage procedure of lengthening the patellar tendon was performed in this young patient to buy time before an anticipated total knee replacement. The benefit of reestablishing the normal patellar height (see Fig. 41-25H and I) allowed a return of moderate lower limb function, with the added benefit at the time of the total joint procedure of retaining patellofemoral joint function.

Case 3

A 42-year-old woman sustained an acute ACL rupture to the right knee that was treated 4 weeks later with an anterior tibialis allograft reconstruction. Before surgery, the patient had achieved 0°/0°/100° of knee motion. Postoperatively, she experienced significant problems with quadriceps muscle atrophy and failed to gain more than 100° of knee flexion. A manipulation under anesthesia was performed 2 months postoperatively in which 0°/0°/120° was achieved; however, the patient gradually reverted to 0°/0°/90° of motion.

The patient presented to our center 5 months postoperatively with complaints of stiffness, tightness, failure to achieve past 90° knee flexion, and a flexed knee gait. On physical examination, she had a stable knee with negative Lachman and pivot shift tests. There was significant muscle atrophy, and the patient was unable to actively perform an isometric quadriceps contraction. She ambulated with limited knee flexion. The patellofemoral joint was markedly restricted, with no medial or lateral glide and an obvious patella infera position.

Standing posteroanterior radiographs showed a decrease in the height of the patella and osteopenia (Fig. 41-26A). Lateral radiographs with the knee flexed showed an obvious patella infera, with a 68% Linclau ratio on the involved side (see Fig. 41-26B) compared with the opposite side of 87% (see Fig. 41-26C). The patient underwent Z-plasty lengthening of the medial and lateral retinacular structures to restore patellar mobility, an arthroscopic suprapatellar débridement to open the synovial pouch, and removal of infrapatellar contracture. The patellar tendon shortening was permanent. The patient underwent 3 months of intensive rehabilitation, muscle strengthening, and gait retraining and achieved 0°/0°/125° of motion, with restoration of patellar mobility.