Complications in the multiple-ligament-injured knee

Delayed or inaccurate diagnosis 

Delayed or inaccurate diagnosis of multiple-ligament knee injuries may occur during the initial medical evaluation of both low- and high-energy level injuries.1, 2, 3, 4, 5, 6, 7, 8, 9 Low-energy level injuries, such as those caused by stepping into a hole, can result in multiple-ligament knee injuries.5, 9, 10 These knee injuries are commonly misdiagnosed as contusions or sprains because the extent and severity of ligamentous disruption is not appreciated.

In high-energy trauma such as motor vehicle accidents, multiple-ligament knee injuries can be obscured by the presence of other life-threatening conditions such as head and spinal injuries, pelvic discontinuity, and long-bone fractures. These knee injuries, which commonly occur as acute dislocations, may reduce spontaneously and thereby present with no obvious limb deformity. Absence of diffuse soft-tissue swelling or joint effusion may occur from capsular disruption with resultant fluid extravasation between soft-tissue planes. Subsequently, these knee injuries may be inadvertently overlooked as attention is focused on other readily apparent conditions.

Early recognition and a high level of suspicion are important to avoid delayed or inaccurate diagnosis of multiple-ligament knee injuries. Physical examination of the knee should include the Lachman test, anterior and posterior drawer tests, hyperextension or recurvatum evaluation, posterolateral rotatory instability tests, varus and valgus stress tests at 0 and 30°, and complete neurovascular assessment. Plain radiographs and magnetic resonance images of the knee should be obtained to determine the extent and severity of ligamentous disruption and to evaluate for concomitant bony or soft-tissue injuries.11

Vascular injuries 

Multiple-ligament-injured knees have an incidence of vascular injury that ranges from 16% to 64%.6, 7, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26 Green and Allen reported popliteal artery injury in 32% of 245 patients with knee dislocations.15 Moreover, this rate increased to 40% when only posterior or anterior dislocations were considered. Posterior dislocations had a higher rate of popliteal artery injury (44%) than anterior dislocations (39%). When the popliteal artery injury was not repaired within 6 to 8 hours after the injury, 86% of the patients underwent eventual amputation and two thirds of the remaining 14% developed ischemic changes of the limb.

Popliteal artery injury is made susceptible by the anatomic constraints within the popliteal fossa where the artery is tethered proximally at the adductor hiatus and distally at the soleus arch (Fig 2). 1, 6, 7, 27, 28, 29 In anterior dislocations, injury results from traction of the popliteal artery, which may develop an intimal tear.1, 7, 27, 30 An intimal tear can precipitate late formation of thrombosis within the vessel. In posterior dislocations, injury occurs from direct transection or contusion of the popliteal artery by the posterior rim of the tibial plateau. Complete transection and damage localized to the intima can occur in posterior and anterior dislocations.7, 15, 17, 31, 32

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Fig 2. Arteriogram shows complete disruption of the popliteal artery at level of knee joint with some distal perfusion through collateral circulation. (Reprinted with permission from Wascher DC: High-velocity knee dislocation with vascular injury: Treatment principles. Clin Sports Med 19:470, 2000.)

Vascular examination of the limb should include palpation for the posterior tibial and dorsalis pedis arterial pulses. However, presence of distal arterial pulses does not absolutely exclude popliteal artery injury.17, 23, 33, 34 Doppler pressure measurements and ankle/brachial pressure ratios may be helpful. Arteriography should be used routinely in the evaluation of multiple-ligament knee injuries that occur as a result of high-energy trauma and sports (Fig 3). With high suspicion for popliteal artery injury, arteriography should be performed in the operating room, where conversion to open surgical exploration and repair can be facilitated if necessary. Evidence of limb ischemia requires immediate vascular surgery consultation for open surgical exploration and repair.

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Fig 3. Arteriogram shows an intimal flap tear of the popliteal artery in knee with normal distal arterial pulses and an ankle/brachial pressure ratio of 1. (Reprinted with permission from Wascher DC: High-velocity knee dislocation with vascular injury: Treatment principles. Clin Sports Med 19:472, 2000.)

Neurologic injuries 

Peroneal nerve injury occurs with an incidence that ranges from 14% to 40% of multiple-ligament-injured knees.6, 7, 19, 24, 28, 35, 36, 37, 38 Peroneal nerve injury usually results from excessive traction on the nerve that has a tethered course around the fibular neck. Traction injury of the peroneal nerve, which is often associated with disruption of the lateral ligament complex, can be produced by varus or medial translational force on the tibia relative to the femur.6, 7, 24, 28, 39, 40 Such force is encountered with posterior, posterolateral, and medial knee dislocations.

Peroneal nerve injury from excessive traction is often characterized by axonotmesis over a long nerve segment.6, 7, 29, 29, 36, 38, 41 Neurotemesis can occur, but usually presents as a long, stretched, and contused nerve segment (Fig 4). 6, 29 Electroconduction studies may be helpful to assess the severity of nerve injury. Peroneal nerve repair or decompression should be performed during lateral ligament reconstruction in patients with associated peroneal nerve injury. If lateral ligament reconstruction is not indicated, then peroneal nerve exploration with repair or decompression should be considered for peroneal nerve injury that has not shown evidence of functional recovery by 4 months.6 Functional recovery is generally poor because the majority of patients will continue to have residual peroneal nerve deficits.6, 7, 29, 36, 38

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Fig 4. Gross photograph shows complete transection of peroneal nerve.

Tibial nerve injury has a worse prognosis for functional recovery than peroneal nerve injury in multiple-ligament-injured knees. Nerve injury most commonly occurs with knee dislocations that result from high-energy trauma. Wascher et al reported tibial nerve injury in 5 of 40 knee dislocations (or 12.5%) caused by high-energy trauma.38 All cases of tibial nerve injury were associated with ipsilateral peroneal nerve injury.

Compartment syndrome 

Compartment syndrome with limb ischemia may develop from extensive soft-tissue injury and vascular disruption, or from soft-tissue reperfusion after vascular repair in the multiple-ligament-injured knee. Knee fracture-dislocations that involve comminuted tibial plateau fractures with associated ligament and capsular disruption have a high risk of soft-tissue and neurovascular complications. Consequently, knee fracture-dislocations must be evaluated carefully for clinical signs of compartment syndrome.

Close observation with serial neurovascular examination of the affected limb should be performed to monitor for clinical signs of compartment syndrome. If clinical signs of compartment syndrome are equivocal, then direct compartment pressure measurements should be obtained by using the Whitesides method or the Stic catheter system. Fasciotomy of all 4 compartments of the lower leg should be performed when compartment syndrome is suspected.

Open-knee dislocations 

Open-knee dislocations with multiple-ligament injuries have an incidence that ranges from 16% to 35% of all knee dislocations.7, 19, 36, 38, 42 Open-knee injuries most commonly occur with posterior and anterior knee dislocations.7, 36, 42 Open-knee injuries are often associated with extensive soft-tissue damage, multiple-ligament injuries, and neurovascular disruption because they usually result from high-energy trauma (Fig 5). Wright et al evaluated the operative results of 19 open-knee injuries in 18 patients.26 Fourteen knees were salvaged with only fair to poor function, 3 had above-knee amputation, 1 had knee arthrodesis, and 1 had total knee replacement. Nine patients (or 47%) sustained concomitant vascular or neurologic injuries. Eight patients (or 42%) developed wound complications.

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Fig 5. Gross photograph of a high-energy open-knee dislocation with extensive soft-tissue damage and multiple-ligament injuries. (Reprinted with permission from Wascher DC: High-velocity knee dislocation with vascular injury: Treatment principles. Clin Sports Med 19:467, 2000.)

Open-knee injuries require emergent surgical irrigation and debridement of foreign material and devitalized tissue to decrease the risk of infection. Repeat surgical irrigation and debridement should be performed in 48 hours. An external fixator that spans the knee joint should be applied to facilitate access to the wounds and to stabilize the multiple-ligament-injured knee. Ligamentous reconstruction should be delayed until the knee joint is closed with no signs of infection.

Fractures and dislocations 

Periarticular fractures about the knee that occur with multiple-ligament injuries often require different treatment than purely ligamentous injuries because the fractures often must be reduced and stabilized. Wascher et al identified periarticular fractures in 6 of 50 knee dislocations (or 12%).38 These fractures included 2 open tibial plateau fractures, 2 open supracondylar femur fractures, 1 closed medial femoral condyle fracture, and 1 closed lateral femoral condyle fracture. Sisto and Warren identified periarticular fractures in 4 of 19 knee dislocations (or 21%).24 These fractures included 2 closed tibial plateau fractures and 2 avulsion fractures.

Knee fracture-dislocations as described by Moore involve tibial plateau fractures with associated ligament injuries that result in joint instability.43 Fracture-dislocations are often characterized by tibial plateau fractures, ligamentous and capsular disruption, extensive soft-tissue injury, and neurovascular complications because they most commonly occur during high-energy trauma. Computed tomographs and magnetic resonance images of the knee should be obtained to define the fracture pattern and severity of ligament and soft-tissue injury, and for preoperative planning. Fracture reduction and stable fixation as well as ligamentous reconstruction are important to restore articular congruity and joint stability.

Avulsion fractures that have attached ligaments or tendons can occur with multiple-ligament knee injuries (Fig 6). Such fractures include lateral capsular Segund fractures, fibular head avulsion fractures, and bony avulsions of the anterior cruciate ligament (ACL) or posterior cruciate ligament (PCL) from the tibia. Computed tomographs may be helpful to characterize the size and location of bony avulsions. Reduction and secure fixation of avulsion fractures that have attached ligaments should be attempted before ligament reconstruction is considered.

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Fig 6. Anteroposterior radiograph of right knee shows fibular avulsion fracture and bony MCL injury. (Reprinted with permission from Hegyes MS, Richardson MW, Miller MD: Knee dislocation: Complications of nonoperative and operative management. Clin Sports Med 19:526, 2000.)

Proximal tibiofibular joint dislocations that occur with multiple-ligament injuries are often unrecognized.7, 44, 45, 46 Fallon et al reported an anterior dislocation of the proximal tibiofibular joint that was detected 1 month after closed reduction of a posterior knee dislocation.44 Open reduction and internal fixation were necessary to restore stability of the proximal tibiofibular joint. Evaluation of the multiple-ligament-injured knee should include assessment of the proximal tibiofibular joint.44, 46

Iatrogenic vascular injuries 

Careful preoperative evaluation is important to decrease the risk of vascular injury during multiple-ligament knee reconstruction. Popliteal artery occlusion with signs of limb ischemia during surgery may arise from thrombus formation at the site of pre-existing intimal flap tears (Fig 7). Intimal flap tears in the popliteal artery that have less than 50% luminal stenosis are not considered hemodynamically stable and have a 3% rate of thrombus formation.29, 47 Management of such tears with normal distal pulses is close observation for 48 to 72 hours.27, 29 However, intimal flap tears that progress to thrombus formation with popliteal artery occlusion and signs of limb ischemia require immediate vascular surgery consultation for open surgical exploration and replacement of the arterial segment that contains the thrombus with reverse saphenous vein graft.15, 20, 29, 30

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Fig 7. Arteriogram shows vascular occlusion after multiple-ligament knee reconstruction in a limb with a previously unrecognized intimal tear of the popliteal artery. (Reprinted with permission from Hegyes MS, Richardson MW, Miller MD: Knee dislocation: Complications of nonoperative and operative management. Clin Sports Med 19:529, 2000.)

Popliteal artery repairs are vulnerable to reinjury during multiple-ligament knee reconstruction. Precaution must be exercised to avoid reinjury to vascular repairs. Tourniquets should be used with careful discretion to minimize the risk of thrombosis formation in vascular repairs. If they are used during surgery, then tourniquets should be placed away from the site of vascular repairs and inflated only for the minimal amount of time required to complete the procedure. Postoperative arteriography should be used to evaluate for suspected disruption or occlusion of vascular repairs.5, 7, 14, 48 Vascular surgery consultation should be readily available during multiple-ligament reconstruction of knees with popliteal artery repairs.

Popliteal artery injury can occur from direct trauma during the transtibial tunnel technique for PCL reconstruction.5, 49, 50 In this technique, a guide wire is placed in an anterior to posterior direction in the proximal tibia until it emerges at the inferolateral aspect of the PCL insertion site. A cannulated reamer is used over the guide wire to create a transtibial tunnel. Advancement of the guide wire or cannulated reamer beyond the posterior capsule may result in popliteal artery injury.5

Risk of popliteal artery injury with the transtibial tunnel technique can be decreased by using a guide wire that has a spade tip rather than a trochar tip,5 an oscillating drill,5 and a cannulated reamer with a drill bit that is tapered rather than square.5, 51 Intraoperative fluoroscopy may be helpful to confirm the position of the guide wire and cannulated reamer in the proximal tibia.5 Fanelli et al describe a posteromedial safety incision through which the surgeon can place a finger over the extra-articular surface of the posterior capsule to monitor the position of the guide wire and cannulated reamer as they enter the posterior aspect of the knee from the proximal tibia.49, 50, 52

Popliteal artery injury also can occur from direct trauma during the tibial inlay technique for PCL reconstruction. In this technique, blunt dissection is used to isolate the medial head of the gastrocnemius muscle. Mobilization with lateral retraction of the medial head of the gastrocnemius muscle provides exposure to the posterior capsule and tibial inlay site on the posterior tibial cortex as well as coverage for the popliteal artery.53 However, scar formation from previous injury or surgery in the posterior aspect of the knee can distort the normal anatomy and predispose the popliteal artery to risk of injury.

Iatrogenic nerve injuries 

Neurologic injury during multiple-ligament knee reconstruction most commonly involves transection of the infrapatellar branch of the saphenous nerve. The infrapatellar branch courses transversely across the anteromedial aspect of the knee and innervates the overlying skin and fascia on the proximal leg. The infrapatellar branch is susceptible to injury while establishing a standard anteromedial arthroscopic portal or performing a medial approach for exposure to the medial collateral ligament (MCL). Injury to the infrapatellar branch may cause development of a painful neuroma or an area characterized by hypoesthesia. Complex regional pain syndrome in the affected limb has been associated with injury to the infrapatellar branch.5, 7, 54

The sartorial branch of the saphenous nerve is susceptible to injury during proximal dissection near the musculotendinous junction of the sartorius when harvesting the semitendinosus and gracilis tendons for graft material. The sartorial branch courses distally at the musculotendinous junction of the sartorius and innervates the overlying skin on the anteromedial aspect of the leg. Injury to the sartorial branch may result in hypoesthesia of the anteromedial aspect of the leg. Pain may localize to an area in the posteromedial thigh where the nerve is compressed by scar formation after harvesting the semitendinosus and gracilis tendons.

Peroneal nerve injury usually occurs from excessive traction while performing a lateral approach for exposure to the lateral ligament complex. The peroneal nerve follows the medial border of the biceps tendon in the popliteal fossa before it passes behind the fibular head and winds around the fibular neck. The peroneal nerve can be subject to excessive traction during manipulation and transplantation of the biceps tendon for lateral ligament reconstruction.39, 55 Peroneal nerve injury may cause hypoesthesia along the cutaneous distribution and foot-drop.

Tibial nerve injury can occur by direct trauma similar to popliteal artery injury during either tibial inlay or transtibial tunnel techniques for PCL reconstruction. Risk of neurologic injury during knee surgery can be decreased by incomplete exsanguination of the limb to allow visualization of nerves and vessels, blunt dissection between skin and joint capsule, identification and careful retraction of nerves, prevention of nerve dessication, and avoidance of nerve injury during wound closure.56

Fluid extravasation and compartment syndrome 

Compartment syndrome can develop from fluid extravasation during arthroscopic procedures for multiple-ligament knee reconstruction.5, 7, 57, 58, 59, 60, 61 Extravasation of arthroscopic fluid occurs through capsular and fascial defects in the knee and travels between fascial planes in the lower leg. Fluid extravasation between fascial planes in the lower leg may result in elevated compartment pressures.

Fluid extravasation can be minimized by delaying surgical reconstruction for 10 to 14 days to allow for capsular sealing.5 During arthroscopic procedures, fluid extravasation can be reduced by gravity inflow rather than pressure inflow created by an arthroscopic pump.5, 7, 60 A posteromedial safety incision as described by Fanelli for PCL reconstruction can be made for egress of arthroscopic fluid.3, 4, 5

Tourniquet complications 

Tourniquet complications that occur with multiple-ligament knee reconstruction are mainly time dependent and related to duration of compression.7 Other factors that may contribute to development of tourniquet complications include patient age, thigh morphology, vascular supply of the injured limb, and excessive or insufficient inflation pressure.62, 63, 64

Thrombus formation can develop from vascular stasis during tourniquet inflation.7 Moore et al showed that tourniquet inflation for 1 hour increases the risk of thrombus formation in an animal model.65 Previous vascular injury or repair increases the risk of thrombus formation during tourniquet inflation. For nonocclusive intimal flap tears of the popliteal artery, a loading dose of heparin should be administered before tourniquet inflation to decrease the risk of thrombus formation.29

Sciatic nerve injury characterized by sensory and motor deficits can develop from decrease in nerve conduction velocity associated with tourniquet inflation.66 Decrease in nerve conduction velocity may be caused by arterial ishemia or a differential pressure gradient in the nerve around the site of compression.7, 67 Rorabeck showed that the magnitude of decrease in nerve conduction velocity and the amount of recovery time needed for the nerve conduction velocity to reach baseline levels are directly related to inflation pressure and the duration of compression in an experimental model.67

Tourniquet complications may be prevented by correctly applying the tourniquet, exsanguinating the limb before tourniquet inflation, monitoring the inflation pressure during surgery, reducing the amount of time needed for tourniquet inflation, and using calibrated equipment that functions properly.5, 7, 66 Inflation pressure should be as low as possible and determined by the systolic blood pressure.67 Three hours is near the upper limit of time for safe application of the tourniquet.68, 69

Wound complications 

Wound infections occur with an incidence that ranges from 0.3% to 12.5% of open-knee reconstructions.7, 12, 58, 70 Open and high-energy multiple-ligament knee injuries are particularly vulnerable to wound infection after surgical reconstruction because they are often associated with extensive soft-tissue damage that impairs wound healing and predisposes the affected limb to wound breakdown. Other factors that may contribute to the development of wound infection include past medical history, age greater than 50 years, skin condition, history of corticosteroid use, previous open or arthroscopic knee surgery, and prolonged tourniquet time.5, 7, 38

Superficial wound infections are often managed by aggressive wound care with frequent dressing changes and oral antibiotics. For infections that do not respond, debridement should be performed. Deep wound infections usually require debridement and intravenous antibiotics. Repeat debridement should be considered in 48 to 72 hours. Graft and hardware removal may be necessary for infections that continue despite repeat debridement and intravenous antibiotics.

Wound breakdown and dehiscence can be reduced by carefully planning skin incisions and delaying surgical reconstruction until soft-tissue swelling has decreased. Surgical hazards that should be avoided to decrease the risk of wound breakdown include narrow skin bridges, undermined skin flaps, tense wound closure, hematoma formation, and postoperative infection (Fig 8). 5, 7 Prophylactic intravenous antibiotics are recommended before surgery and after surgery for 24 to 48 hours, or until drains are removed.5, 7, 12, 58, 70

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Fig 8. Gross photograph shows skin blisters from excessive traction during wound closure. (Reprinted with permission from Hegyes MS, Richardson MW, Miller MD: Knee dislocation: Complications of nonoperative and operative management. Clin Sports Med 19:533, 2000.)

Anterior knee pain 

Anterior knee pain can originate from patella tendon autograft harvest for ligament reconstruction. Other causes of anterior knee pain may include patella tendonitis, intratendinous calcification, and infrapatellar contracture. Prominent hardware over the proximal tibia and distal femur can be a source of anterior knee pain (Fig 9).

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Fig 9. Anteroposterior radiograph of a right knee shows backout of femoral screw after nonisometric posterolateral corner reconstruction. (Reprinted with permission from Hegyes MS, Richardson MW, Miller MD: Knee dislocation: Complications of nonoperative and operative management. Clin Sports Med 19:538, 2000.)

Anterior knee pain can result from persistent posterior sag after PCL reconstruction.5, 71 Persistent posterior sag causes patella baja and increased patellofemoral forces that may lead to development of patellofemoral arthrosis.5, 71 PCL reconstruction should recreate the anatomic tibial step-off with return of more normal patellofemoral forces.5, 53

Medial femoral condyle osteonecrosis 

Medial femoral condyle osteonecrosis can occur as a complication after PCL reconstruction in the multiple-ligament-injured knee. Athanasian et al reported the development of osteonecrosis in the medial femoral condyle 10 months after combined PCL and MCL reconstruction.72 Clinical evaluation reveals discomfort and tenderness over the medial femoral condyle. Radiographic evaluation demonstrates a subchondral area of radiolucency surrounded by sclerosis.

Medial femoral condyle osteonecrosis may result from disruption of the intraosseous blood supply to the medial femoral condyle during creation of the PCL femoral tunnel.5, 73 The PCL femoral tunnel should be located in the anterior portion of the native femoral insertion site 8 to 10 mm proximal to the articular surface of the medial femoral condyle. Placement of the PCL femoral tunnel closer to the articular surface may cause disruption of the intraosseous blood supply of the medial femoral condyle, which consists of a single nutrient vessel.5, 73 Extensive soft-tissue dissection over the medial femoral condyle for combined PCL and MCL reconstruction may contribute to the development of osteonecrosis.5, 73

Heterotopic ossification 

Heterotopic ossification (HO) is a frequent complication after multiple-ligament reconstruction for knee dislocations.74, 75, 76 Stannard et al reported formation of HO in 15 of 57 (26%) knee dislocations.76 Seven of the 15 knee dislocations had severe HO involving more than 50% of the joint space. Formation of HO increased with the severity of knee dislocation based on the Wascher classification.76

HO most commonly involves the posterior and medial aspects of the knee.74, 76 Pain and loss of knee motion are predominant symptoms.74, 76 Formation of HO can develop concurrently at other anatomic sites.76 Arthrofibrosis is frequently associated with HO around the knee.74, 76, 77 Formation of HO also can occur after nonoperative management of multiple-ligament knee injuries (Fig 10).

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Fig 10. Anteroposterior stress radiograph of a left knee after previous knee dislocation shows gross varus instability with lateral compartment widening. Foci of heterotopic ossification are related to avulsion of the lateral collateral ligament (straight arrow) and tear of the MCL (curved arrow). (Reprinted with permission from Potter HG: Imaging of the multiple-ligament-injured knee. Clin Sports Med 19:427, 2000.)

Prophylaxis against formation of HO with indocin or low-dose irradiation should be considered for open-knee dislocations, prior history of HO, and knees that require irrigation and debridement.76 Initial management of symptomatic HO consists of physical therapy to restore knee motion. If physical therapy does not restore knee motion, then arthroscopic lysis of adhesions is performed for mild HO involving less than 50% of the joint space.76 Surgical excision through a combined open and arthroscopic approach is usually required for severe HO.76 Low-dose irradiation should be used to prevent recurrence of severe HO.

Loss of motion 

Loss of knee motion after multiple-ligament reconstruction is a common and potentially serious complication that may result in significant functional deficit. Loss of extension greater than 5° can produce gait abnormality with quadriceps atrophy and patellofemoral pain, whereas loss of flexion greater than 110° can produce difficulty with sitting, squatting, stairclimbing, and running.78 Loss of knee motion often has a multifactorial etiology that can include improper graft placement or tensioning, fibrous adhesions and scar formation, and concomitant MCL or meniscal repair.78

Improper graft placement or tensioning during ACL and PCL reconstruction can result in loss of knee motion.5, 49, 50, 78, 79 In PCL reconstruction, the PCL graft is positioned over the anterior portion of the PCL femoral insertion site to reproduce the anterolateral PCL bundle. The anterolateral PCL bundle becomes tighter as the knee moves from extension into flexion. If the PCL graft is tensioned with the knee in extension, then the PCL graft becomes overtightened as the knee is brought into flexion, which may cause graft failure or loss of knee flexion. Hence, the PCL graft is tensioned with the knee in 70° to 90° of flexion while applying an anterior tibial drawer to eliminate the posterior sag, recreate the normal anterior tibial step-off, and minimize the loss of knee flexion.

In ACL reconstruction, the ACL graft is positioned over the anatomic ACL tibial and femoral insertion sites to reproduce the ACL graft. The ACL graft is observed as the knee is moved from flexion into extension to evaluate for graft impingement, which may cause graft failure or loss of knee extension. Causes of graft impingement include intercondylar notch scar formation, inadequate notchplasty, development of a cyclops lesion, and anterior graft placement.78, 80

Anterior graft placement may produce graft impingement with the intercondylar roof as the knee is brought into extension. If graft impingement occurs with knee extension, then the intercondylar notch should be enlarged to provide adequate clearance for the ACL graft so as to allow full extension without graft impingement. Incomplete debridement of soft tissue including the ACL remnant anterior and lateral to the tibial tunnel can lead to development of a cyclops lesion, which is a fibrous nodule of granulation tissue that can cause soft-tissue impingement and loss of knee extension.78

Concomitant MCL or mensical repair also predisposes to loss of knee motion.5, 78, 80 For MCL repair, dissection is often carried through extensively injured soft tissue, where normal tissue planes are difficult to identify and restore. Failure to restore normal tissue planes may accentuate the fibrotic response of the extensively injured soft tissue, causing proliferative scar formation that may limit knee flexion and extension. MCL plication and advancement may contribute to loss of knee motion because they do not give an isometric repair. If the MCL injury requires surgical management, then direct repair or anatomic reconstruction with graft augmentation is used to reproduce the native MCL. For mensical repair, loss of knee motion can be reduced by fastening sutures with the knee near full extension.78

Fibrous adhesion and scar formation in the suprapatellar pouch, intercondylar notch, infrapatellar fat pad, and posterior recess of the joint may result in muscle and joint contractures and significant loss of knee flexion and extension.7, 80, 81, 82, 83, 84 Causes of fibrous tissue development include hemarthrosis,5, 7, 80, 81, 82, 83, 84 capsulitis or infrapatellar contracture syndrome,7, 78, 85 and prolonged immobilization.5, 7, 83, 86 Fibrous adhesion and scar formation can be reduced by using arthroscopic procedures, initiating early postoperative range of motion, and delaying reconstruction until signs of acute injury have resolved. If loss of knee motion does not improve with rehabilitation, then arthroscopic lysis of adhesions and manipulation may facilitate restoration of motion.

Loss of knee motion after multiple-ligament reconstruction also can result from infection, myositis ossificans, and complex regional pain syndrome.5, 7, 87, 88 Older age has been associated with a higher incidence of motion loss, which may be related to connective tissue alterations such as increased stiffness and decreased elasticity.78, 80 Autograft for ACL reconstruction has been associated with a higher incidence of motion loss when compared with allograft, which may be related to donor-site morbidity.1, 7, 44, 55, 75, 78, 80 Loss of knee motion also can result from conservative nonoperative treatment of multiple-ligament knee injuries.5, 19, 25, 36

Persistent laxity 

Persistent laxity after multiple-ligament knee reconstruction occurs most commonly as residual posterior instability after PCL reconstruction.5, 7, 75, 86, 89 Causes of residual posterior instability include graft laxity and failure, improper graft placement or tensioning, and loss of graft fixation.5, 71, 90 Open kinetic chain knee flexion during early postoperative rehabilitation after PCL reconstruction also may result in residual posterior instability.5, 71, 79

Open kinetic chain knee flexion that ranges from 75° to full flexion causes posterior tibial translation from unopposed hamstring contraction and produces increased strain on the PCL.79 Open kinetic chain knee flexion in this range should be avoided during early postoperative rehabilitation to prevent overloading the healing PCL graft, which may contribute to residual posterior instability. Closed kinetic chain exercises should be used during early postoperative rehabilitation to improve quadriceps and hamstring strength while minimizing stress on the PCL graft and patellofemoral articulation.79

Failure to recognize associated posterolateral corner and MCL injuries may result in persistent knee laxity and poor functional outcome after combined ACL and PCL reconstruction. Grade I and II MCL injuries that occur with combined ACL and PCL injuries can heal without surgical repair. However, grade III MCL and PLC injuries that occur with combined ACL and PCL injuries do not heal and usually require surgical repair and reconstruction to restore joint stability.1, 5, 80, 91