ACL injury has been well documented and classically involves a noncontact mechanism involving rapid deceleration in anticipation of a change of direction (i.e., pivoting motion) or landing motion.9–13 Boden and colleagues¹⁴ reported that 72% of ACL tears occurred as a result of noncontact. Most injuries are sustained at foot strike, with the knee close to full extension and with the ground reaction forces lateral to the knee joint causing a “valgus collapse^9,15”; sagittal plane motion seems to have less influence on the ACL during injury.^9,16,17 The incidence of individuals sustaining a ruptured ACL has been reported at 1 in 3000.¹²

Patients describe feeling and sometimes hearing a “pop¹⁸” and are 1000 times more likely to be participating in a sporting event.⁴ Swelling is immediate, which implicates a ligamentous injury because of its associated vascularity. Patients exhibiting instability of the knee that affects pivot shift demonstrate a positive Lachman test; positive magnetic resonance imaging (MRI) for ACL rupture should be thoroughly evaluated for surgical considerations. Functionally, these patients have difficulty performing pivoting and deceleration related to activities of daily living (ADLs) or sports. Although individuals who have sustained isolated rupture of the ACL may continue to be functional, their level of function is compromised and may require future surgical intervention because of secondary restraint pathology.^19–21 The surgeon should thoroughly evaluate the patient’s desired level of activity to ensure a successful outcome. Multiple studies have made reference to the sequelae of degenerative arthritis and potential for meniscal tears in the ACL-deficient knee.^21–25

Both anatomic and physiologic risk factors have been researched. Some of the anatomic risk factors that may predispose an individual to ACL injury include the following: hypermobility (laxity of joints), hormonal influences on hypermobility, a narrow intercondylar notch, ligament width, tibial rotation, pronated feet, and increased width of the pelvis in the female athlete.²⁶ Although some causes exist to suggest certain anatomic features, conclusive evidence has not been established between ligament failure and the anatomic risk factors. Physiologic risk factors include poor core strength, lower extremity (LE) deficits in muscular strength and coordination, and foot wear–ground interface. It may be a combination of the previously listed factors that leads to ACL injury, but women are two to eight times more likely to sustain injury than males.^13,27–29 Hormonal influences that affect ligament laxity have been explored, with evidence leaning toward this as a nonfactor. However, menstrual hormones may indirectly contribute to injury by influencing neuromuscular performance and muscle function.^29,30 Although there may be some influence on laxity, more compelling arguments point to strength and coordination differences. Many researchers have further studied the relationship of neuromuscular performance as a potential risk factor. They have identified significant differences in neuromuscular control after the onset of maturation. This deficit was observed in females landing after a jump. The neuromuscular deficit allowed migration of the knee into a valgus collapse position, placing the ACL at risk.^9,30–32 Hewett, Myer, and Ford³⁰also noted that after maturation (i.e., neuromuscular spurt) males regained their control; however, females did not make similar adaptations. The “drop jump” screening test is a useful examination to help prevent and further understand the mechanisms of an ACL injury.³³ Leetun and associates³⁴ looked at lumbopelvic (core) stability as a risk factor for LE injury in female athletes. They concluded that athletes who did not sustain an injury demonstrated better hip abduction and external rotation strength, and that hip external rotation strength was the only useful predictor of injury status.

Overall, the therapist must be aware of the potential risk factors that were present leading up to the ACL injury. In this way, the rehabilitation program can safely return the patient to the sport and prevent future injury.

The timing of when to perform reconstruction (acute versus chronic) has been a source of debate. It has been accepted that a higher risk for complications exists if surgery is performed (1) before obtaining a homeostatic environment, (2) if range of motion (ROM) is limited (especially extension), and (3) when quadriceps and hamstring contraction is inadequate (i.e., unable to perform a straight leg raise [SLR]).23,35 It is also apparent that with postponing reconstruction in an active population, the risk is higher for meniscal and chondral surface damage.^22,36–38

A topic of debate is how soon after injury should reconstructive surgery be performed. When using a bone-patella tendon-bone (BPTB) autograft, evidence exists that surgery should not occur before 3 weeks after injury to decrease the risk of arthrofibrosis.^23,39–41

Other authors propose that loss of motion is not dependent upon time when performing surgery after an injury.^42–45

Bottoni and associates also showed through a randomized controlled trial that early ACL reconstructions with a hamstring autograft can be performed and will not increase the likelihood of arthrofibrosis because long rehabilitation emphasizes extension and early ROM.⁴⁵ Sterett and associates did not find an association between incidence of motion loss and timing of surgery but used the minimal criteria of active ROM of 0° to 120°, active quadriceps control, and the ability to perform an SLR without a lag as determinants of successful outcome. In a systematic review, Smith and associates did not find a consensus for the optimal time after injury to perform reconstructive surgery to return to activity faster with limited complications.^46,47

Typically, surgeons will require the patient to achieve full extension, be able to do an SLR without a lag, and have minimal to no swelling present before operating.

Researchers have speculated about an age when reconstruction is not recommended; however, to date no literature has noted any detrimental outcomes based on the age of the patient. In fact, studies have shown no significant difference in outcomes in comparing individuals at the age breaks of 35 and 40 years.^7,48–50 Reconstruction of the skeletally immature (SI) patient remains controversial, but the current literature appears to be leaning toward performing reconstruction. Younger populations are sustaining ACL tears; although it has been generally advisable to await physeal closure before reconstruction, some surgeons are having successful outcomes.^51,52 Appropriateness for reconstruction should be evaluated based on chronologic age, Tanner stage, radiologic findings in the knee, and developmental-psychologic factors.^53,54 Drilling across the physis has not been advocated because of the risks of arresting bone growth. However, Shelbourne and colleagues⁵¹ presented information on a small group of SI patients (Tanner stage 3 or 4 with clearly open growth plates) who underwent intraarticular patella tendon graft. Surgery emphasized the importance of not overtensioning the graft and meticulous placement of the bone plugs proximal to the physes. The patients had no growth disturbances on follow-up; when confronted with the potential of new meniscal tears, recurrent instability, effusion, and pain, ACL reconstruction in the SI patient appears to be a viable option.^26,55

The anticipated functional limitations (modification of activities involving pivoting and deceleration) must be explored and explained to the patient who chooses not to have an ACL-deficient knee reconstructed. Ciccotti and associates⁵⁶ reported on nonoperative management of patients from 40 to 60 years. They found that 83% of the patients had a satisfactory result with guided rehabilitation. However, they also mentioned that surgery might be an option for individuals wishing to continue sporting and pivoting activities.

Surgical techniques to replace the deficient ACL continue to evolve. Advances in arthroscopic surgery provide surgeons with the ability to perform these reconstructive procedures using a one-incision endoscopic technique. Research continues in the search for the optimal graft, fixation technique, and surgical reconstructive procedure. In 1920, Hey-Groves⁵⁷ and Campbell⁵⁸ (in 1939) first described the use of the patella tendon as an ACL graft. Because of these original surgical descriptions, numerous procedures to repair or reconstruct the ACL have been advocated. Attempts at primary repair of the ACL with and without augmentation^59–61 were of limited success.³⁷ Extraarticular ACL reconstruction also was suggested as a technique to reconstruct the ACL-deficient knee.^62,63 However, long-term results were disappointing.^64,65 Intraarticular ACL reconstruction using various tissues, including the patellar tendon, iliotibial band, and combinations of hamstring tendons (semitendinosus, semitendinosus-gracilis), has been extensively described in the literature.^20,66–69

The biologic grafts most widely used today are the central third patellar tendon (i.e., BPTB complex) or multistrand hamstring tendon grafts. Although the hamstring graft has some advantages,^70,71 both procedures are equally successful (surgeon preference dictates choice if problems such as patella dysfunction are not present).^72–75

In general the endoscopic patellar tendon autograft reconstruction remains the most popular.^10,76–78

The selection of the appropriate graft to replace the ACL is crucial to the ultimate success of the reconstruction. Primary concerns in the selection of an autogenous graft to replace the incompetent ACL include the biomechanical properties of the graft (e.g., initial graft strength and stiffness relative to the normal ACL), ease of graft harvest and fixation, potential for donor-site morbidity, and individual patient concerns. Other factors that ultimately influence graft performance include biologic changes in graft materials over time and their ability to withstand the effects of repetitive loading and stress.79 Noyes and colleagues⁸⁰ studied the biomechanical properties of a number of autograft tissues and showed that an isolated 14-mm-wide BPTB graft has 168% the strength of an intact ACL. A graft 10 mm wide is about 120% as strong. The study also determined that a single-strand semitendinosus graft displayed only 70% of the normal ACL strength. The data show that BPTB grafts have comparable tensile strength but increased stiffness in relation to the normal ACL, whereas single-strand semitendinosus grafts have decreased tensile strength but comparable stiffness. Other researchers have shown that multiple strands of semitendinosus or semitendinosus-gracilis composite grafts are stronger relative to the normal ACL.

The graft of choice varies among surgeons. They currently include BPTB autografts and allografts; single-, double-, and quadruple-stranded semitendinosus autografts; and composite grafts using semitendinosus-gracilis autografts. The enthusiasm surrounding the use of allograft replacement of the ACL has recently declined because of the small but tangible risk of infectious disease transmission. The risk of human immunodeficiency virus transmission has been estimated to be 1 in 1.6 million using currently available bone- and tissue-banking techniques.⁸¹ Sterilization by means of fresh freezing of allograft tissue may have an advantage over gamma radiation and ethylene oxide. Fielder and associates⁸² have determined that 3 mrads or more of gamma radiation are required to sterilize HIV. Furthermore, sterilization procedures have been associated with alterations in graft properties and shown to cause a significant average decrease in stiffness (12%) and maximal load (26%),⁸³ and a marked inflammatory response with ethylene oxide use. Further studies must be conducted regarding poststerilization ACL allograft performance. Although the use of allografts as ACL replacements can diminish operative time and prevent graft harvest site morbidity, they are not recommended for routine use in primary ACL deficiency. Currently, either BPTB or multistrand semitendinosus autografts are the most widely used ACL substitutes to reconstruct the ACL-deficient knee.

Adequate fixation of the biologic ACL graft is crucial during the early postoperative period after ACL reconstruction. Fixation devices must transfer forces from the fixation device to the graft and provide stability under repetitive loads and sudden traumatic loads. Various techniques are now available for fixation, including interference screws, staples, sutures through buttons, sutures tied over screw posts, and ligament and plate washers. Kurosaka, Yoshiyas, and Andrish84 determined the interference screw to be the strongest method of fixation of BPTB grafts. Interference screw strength depends on compression of the bone plug,⁷⁹ bone quality,^79,84 length of screw thread-bone contact,⁸⁵ and direction of ligament forces.⁷⁹ Robertson, Daniel, and Biden⁸⁶ studied soft tissue fixation to bone and determined the screw with washer and the barbed staple to be the strongest methods of fixation.

Graft maturation has an influence on the patient whose goals include a return to sports, most of which require pivoting and cutting. The healing properties of autografts have been discussed in the literature.14,87–90 Although a majority of the studies we have reviewed describe the maturity of the graft at 100% 12 to 16 months postoperatively, return to sports participation in some protocols occurs at 6 months (if functional tests and isokinetics meet criteria).^91,92

The graft maturation process begins at implantation and progresses over the next 1 to 2 years. Autografts are strongest at the time of implantation. The implanted graft undergoes a process of functional adaptation (ligamentization), with gradual biologic transformation. The tendon graft undergoes four distinct stages of maturation^14,87,89:

Within the first 3 weeks after implantation, necrosis occurs in the patella tendon intrinsic graft cells. The graft consists of a collagen network that to this point has relied on a blood supply. As this blood supply is interrupted, the graft undergoes a necrotizing process. Necrosis commences immediately and generally lasts 2 weeks.^88–90 Native patella tendon (graft) cells diminish, and replacement cells can be present as early as the first week. Cellular repopulation occurs before revascularization. These cells are thought to arise from both extrinsic sources (i.e., synovial cells, mesenchymal stem cells, bone marrow, blood, ACL stump) and intrinsic sources (i.e., surviving graft cells). Early full ROM is desirable because as new collagen is formed, its formation and strength are dictated by the stresses placed on it.

As the new cells find their way to this frame and add stability to this weak structure, rehabilitation must be careful not to disrupt or stretch them. Necrosis of the graft allows the metamorphosis of the graft from tendon to ligamentous process. Necrosis of the graft is highlighted by the formation of granulation tissue and inflammation. The bone blood supply and synovial fluid nourish the graft by synovial diffusion.⁹³ Revascularization occurs within the first 6 to 8 weeks after implantation. By this time the graft is revascularized via the fat pads, synovium, and endosteum,^88–90 and the inflammatory response should be under control. Further inflammatory problems signify a delayed healing process and potential graft problems; the physician and therapist should be alert for them.^94,95

Amiel and colleagues⁹³ in 1986 described ligamentization of the rabbit patella tendon ACL graft. However, the graft never obtained all the cellular features of normal ACL tissue. Although the graft takes on many of the physical properties of the normal ACL, the cellular microgeometry of the remodeling graft does not closely resemble that of a normal ACL. The revascularization process progresses from peripheral to central.

Bone plugs incorporate into their respective bone tunnels over a 12-week period but are felt to near completion by approximately the sixth postoperative week. The comparative strength of the healed tendon-to-bone attachment versus the healed bone-plug attachment is unknown. Tendon-bone healing begins as a fibrovascular interface develops between the bone and tendon. Bony ingrowth occurs into these interfaces, which extends into the outer tendon tissue. A gradual reestablishment of collagen fiber continuity between bone and tendon occurs, and the attachment strength increases as collagen fiber continuity increases. These ACL autografts approximate 30% to 50% of the normal ACL strength 1 to 2 years postoperatively.⁸⁹

Cellular proliferation and collagen formation take place as a continuing process throughout the maturation process. The function of collagen in the ligament is to withstand tension, and certain types of catalysts are present during the healing process. Transforming growth hormone factor b1 has been isolated during the healing of the medial collateral ligament in rats. Administration of this growth hormone during the first 2 weeks after injury was found to increase strength, stiffness, and braking energy of the ligament.⁹⁰ Other catalysts of collagen formation (platelet-derived growth factor 1 [basic fibroblast growth factor]) have had equally good results in improving the tensile strength of healing ligaments. Since our last edition, more human studies are being presented with varying degrees of success.⁹⁶ With the relatively recent expansion of platelet rich plasma injections to assist in soft tissue repair, more research is coming out on its use in anterior cruciate ligament reconstruction (ACLR). Recent studies have looked at the use of platelet rich growth factor in assisting the reconstruction.⁹⁷ Future studies should be performed to validate this intervention.

During the rehabilitation program, pain and edema should dictate the speed at which the patient may progress. In clinics in which it is available, an assessment using the KT-1000 (Medmetric, San Diego) is helpful as well.^{4,23,98–102}

The procedure begins with a complete examination of the knee under anesthesia followed by a thorough diagnostic arthroscopic evaluation. The menisci, joint surfaces, and ligamentous structures are evaluated and additional injuries assessed arthroscopically. The leg is then exsanguinated, and a tourniquet is inflated with 350 mm of pressure. A medial parapatellar incision is made from the inferior pole of the patella to the tibial tuberosity. The skin is dissected down to the peritenon, and skin flaps are made superiorly, inferiorly, medially, and laterally. The peritenon is incised and the patella tendon is exposed. The width of the patellar tendon is noted (Fig. 22-1), and a 10-mm graft is measured from the midpatellar tendon. Two small incisions 10 mm apart are made in the patellar tendon and then extended superiorly and inferiorly with a hemostat. The patellar and tibial bone plugs are measured to provide graft lengths of 20 to 25 mm of patella and 25 to 30 mm of tibial bone. To facilitate bone graft harvest, the corners of the bone plugs are predrilled with a 2-mm drill to decrease stress risers. The perimeters of the bone plugs are then sawed out with a reciprocating saw to a depth of 10 to 11 mm, depending on the size of the patella and tibial tubercle. The graft (Fig. 22-2, A and B) is then taken to the back table, where it is prepared and fashioned to allow passage through the appropriate guides. The surgeon completes the graft by placing one No. 5 Tycron suture in the femoral and three No. 5 Tycron sutures into the tibial bone plugs to facilitate graft passage through the knee. The graft is preserved in a saline-moistened gauze sponge for later use.

The remnant of the ACL is resected, along with any hypertrophic tissue. Arthroscopically, the intercondylar notch is then prepared with the aid of a burr to prevent graft impingement. A site is chosen for placement of the tibial tunnel. Through the midline incision, a small area medial to the tibial tubercle is prepared with subperiosteal elevation. Using a tibial guide and under direct visualization, the surgeon drills a guide pin into the knee from the outside in, exiting within the knee at a site chosen anteromedial to the ACL insertion. The tibial tunnel is reamed to the size of the harvested graft. A curette placed over the guide pin during reaming helps protect the articular cartilage and posterior cruciate ligament from damage. The tibial tunnel must be larger than the femoral tunnel to allow passage of the graft into the knee. The tibial tunnel edges are smoothed with a rasp to prevent graft abrasion after implantation. A fenestrated plug is then placed into the tibial tunnel to prevent fluid extravasation yet allow passage of instruments.

The femoral isometric point is determined on the medial aspect of the lateral femoral condyle, usually 3 to 5 mm anterior to the posterior cortex near the superior intercondylar notch margin (over-the-top position); it is marked with a curette or burr. With the knee flexed past 90°, a fenestrated guide pin is inserted into the knee through the tibial tunnel and drilled through the femoral isometric point and out through the skin with the aid of an over-the-top guide. The femoral tunnel is then reamed to the size of the femoral bone plug to a depth of 30 mm.

The sutures from the femoral bone plug are inserted into the femoral pin and pulled out through the skin. The graft is delivered into the knee, through the tibial tunnel, and into the femoral tunnel under direct visualization. A cannulated interference screw is then inserted into the knee over a nidal guide pin and screwed into the femoral tunnel, compressing the femoral bone plug within the tunnel. Graft isometry is evaluated. The tibial bone plug within the tibial tunnel is secured with interference screw fixation. ROM and stability testing are then performed. The graft is evaluated arthroscopically to assess graft excursion and placement within the intercondylar notch.

The tourniquet is released, hemostasis is obtained, and the knee is irrigated. Loose closure of the patellar tendon is performed with the peritenon approximated to close the anterior defect. The subcutaneous tissue is approximated, and a continuous subcuticular skin closure is performed. The wounds are dressed sterilely. A light compressive wrap and continuous ice water cryotherapy system are applied, and the patient is taken to the recovery room with the knee in a knee immobilizer in full extension.

Preoperative Management (Table 22-1)

Goals:

Regardless of when surgery is scheduled, the patient almost always is evaluated and receives treatment to increase ROM, especially extension, increase quadriceps/hamstrings strength, and achieve a normal gait pattern. The evaluation commonly begins with an assessment of gait when the patient enters the premises. The patient will often exhibit a flexed-knee gait or a quadriceps avoidance pattern.¹²⁰ The patient will commonly have a rehabilitation brace locked in extension and will use two crutches. While the brace is thought to limit ROM and varus-valgus forces to the knee,¹²¹ the evidence is inconclusive that braces improve extension, and decrease pain and graft strain following ACL reconstruction.¹²² Clinically speaking, the brace is used preoperatively and postoperatively to limit external forces that may cause further damage to the knee. For example a patient before having ACL reconstruction may fall and tear their meniscus or have some osteochondral damage. Active and passive knee ROM, patella mobility, presence of edema, hamstring and gastrocnemius flexibility, quadriceps strength, and weight-bearing capacity should be assessed. During the preoperative phase, the patient’s whole kinetic chain should be evaluated. Strength, flexibility, and mobility of the foot, ankle, hip, and core should be assessed. Particular attention should be given to the mechanism of injury to start planning prevention strategies for postoperative rehabilitation. Assessing the entire kinetic chain before the surgery is easier and more comfortable for the patient than after surgery because of the amount of pain and how inflamed the knee will be. Exercises and modalities should be used to decrease inflammation and swelling, restore patellofemoral mobility and increase quadriceps strength as well as global LE strength and flexibility.

Phase 1: 0 to 4 Weeks (Table 22-2)

Goals:

Rehabilitation following ACL reconstruction can be broken down into phases. Phase 1 begins immediately after surgery and lasts 4 weeks. In this phase, emphasis is placed on decreasing pain and inflammation, protecting the healing graft, and restoring strength and ROM. While inflammation after surgery is normal, the swelling and subsequent pain must be reduced as soon as possible. Swelling can increase pain and quadriceps muscle inhibition.^123,124

Hopkins and associates showed that transcutaneous electric neuromuscular stimulation can be used to control pain and edema.¹²⁵ Jarit and associates showed that home interferential current therapy can help to reduce pain and swelling, and increase ROM following knee surgery.¹²⁶ However, the time parameters for transcutaneous electric neuromuscular stimulation¹²⁵ was 30 min/day and interferential current therapy treatment¹²⁶ was 3 sessions per day for 28 minutes per session, which may not be feasible for both the patient and treating physical therapist. Cryotherapy, whether in the form of continuous flow cold therapy, crushed ice, or commercial cold gel packs, is effective at reducing secondary hypoxia, pain, and edema.^125,127 When available, continuous flow cold therapy should be used over crushed ice.^128,129 Elevation with muscle pumping (ankle pumps, quad sets) can help the lymph system remove tissue debris and inflammatory byproducts (free-floating proteins too large to filter through the capillaries).¹²⁷ Cryotherapy with compression and elevation should occur after each treatment session, as well as up to 5 times daily for 20 minutes when pain, inflammation, and swelling are present. Girth measurements should be taken at the midpatella, as well as proximally and distally, to monitor progress of swelling reduction.

Patients will typically have two crutches and a postoperative brace locked in extension for the first week following surgery. After 1 week, the brace can be unlocked for exercise and gait. If the patient demonstrates a normal pain-free gait pattern, they may wean from two to one crutch, and then discharge them entirely. The brace will typically be discharged once the patient has approximately 100° of flexion, is able to do an SLR without a lag, and has a normal pain-free gait cycle. This process usually occurs 4 to 6 weeks after surgery. Table 22-3 shows commonly used guidelines for using and discharging the brace and crutches.

As previously stated, there should be an emphasis on early ROM following surgery. Full passive knee extension should be achieved within the first week to decrease abnormal joint arthrokinematics and prevent arthrofibrosis.^130,131 Bracing in extension^22,132 or hyperextension¹³³ can be used as a means to prevent flexion contractures. Patellar mobilizations, especially superiorly and inferiorly, should be applied to regain full mobility. Patellar immobility could result in ROM complications and difficulty recruiting quadriceps contraction.^{4,92,100,134–145}

Exercises to achieve full extension include, but are not limited to, hamstring and gastrocnemius stretching, quad sets with the heel propped under a wedge, superior patella mobilizations, a prone or supine (Figs. 22-3 and 22-4) hang, and overpressure of up to 10 lb. Remember that the ACL prevents anterior tibial translation and posterior femoral translation. With joint mobilizations, take caution with overpressure to avoid pushing the joint in the direction that the healing ACL graft limits (Fig. 22-5). The heel should also be propped up when icing and/or resting at home. You must educate the patient to avoid putting a pillow under the knee when resting at home so that the patient does not develop a flexion contracture. Tables 22-4 and 22-5 show examples of commonly used exercises to increase ROM.

Within the first 2 weeks following isolated ACL reconstruction, the patient should achieve 100° to 120° of flexion. If a concomitant meniscal repair is performed, the patient will be limited to 90° flexion for the first 4 to 6 weeks following surgery. Common causes of decreased flexion include arthrofibrosis, patella immobility (particularly with the inferior glide), posterior capsular hypomobility, decreased quadriceps flexibility, and excessive swelling. Exercises to increase knee flexion include active and active-assisted heel slides, posterior tibial and inferior patella mobilizations (in non–bone-tendon-bone autograft graft patients), and pedaling on a stationary bicycle. It is difficult to stretch the quadriceps when there is decreased knee flexion. However, the physical therapist can stretch the patient in the side-lying position with the knee flexed as much as tolerated and stretching into more hip extension. Despite conflicting evidence of long-term benefits,^146–148 the use of a continuous passive motion device may also be used at home for 4 hours per day until the patient reaches 120° flexion.

Increasing quadriceps strength is another goal of phase 1. A hallmark in the early rehabilitation process is the ability to perform an SLR without a lag. To achieve full active extension, the patient must also have full passive extension and adequate superior patella mobility. As mentioned previously, there should be minimal pain and swelling to decrease quadriceps inhibition.^{55,123,124,127}

Early initiation of quadriceps strengthening has been shown to increase ROM and quadriceps muscle torque safely.¹⁴⁹

Debate exists on the most appropriate type of strengthening. Closed kinetic chain (CKC) exercises are more functional and were previously thought to be safest for the healing graft.^92,150–155

CKC exercises can begin with isometrics (Fig. 22-6) and progress to include minisquats and the leg press in the range of 0° to 45° to minimize patellofemoral joint stress (Fig. 22-7).^47,156