Schematic illustration of the femoral attachment of the PCL bundles 
The tibial footprint lies in an upright oval on the posterior tibia that sits between the posterior horns of the menisci and passes from the posterior tibial shelf distally (Fig. 9.2).
9.1.2 Posterolateral Corner
The posterolateral corner (PLC) is complex and probably the least well-understood region of the knee. The major components of the PLC are the iliotibial band (ITB), lateral collateral ligament (LCL) and the popliteus complex, which has both static and dynamic components. The static components are the popliteofibular ligament (PFL), popliteotibial and popliteomeniscal fascicles. The dynamic component is the popliteus muscle-tendon unit. The other structures comprising the PLC are the patellofibular ligament (popliteofibular ligament), posterolateral joint capsule, arcuate ligament, lateral coronary ligament and posterior horn of the lateral meniscus (Fig. 9.3). Cadaveric studies have found some of these structures to be more variable than others. Sudusna and Harnsiriwattanagit found the PFL to be present in 98 % of 50 cases, the FFL in only 68 % and the thin membranous arcuate ligament in 24 % . Watanabe et al. examined 155 cadavers and found seven different anatomical variants depending on the presence or not of the PFL, arcuate ligament and FFL. The LCL and popliteus were found in all and the PFL was found in 94 % of cases [3, 4].
Illustration of the anatomy of the posterolateral corner
The femoral insertions of the LCL and the popliteus tendon sit either side of the lateral epicondyle. The LCL femoral attachment is extra-capsular and sits 1.4 mm proximal and 3.1 mm posterior to the lateral epicondyle [5, 6].
The popliteus muscle originates from the posteromedial aspect of the proximal tibia and is obliquely orientated in its course as it gives rise to the popliteus tendon at the lateral one third of the popliteus fossa in the PLC. It continues proximally through the popliteal hiatus in the coronary ligament, where it is intra-articular and inserts into the lateral femoral condyle. Its insertion point is 18.5 mm anteroinferior to the femoral insertion of the LCL, on the anterior one fifth of the popliteus sulcus on the femur . The popliteus is a dynamic internal rotator of the tibia and contributes to dynamic stability of the lateral meniscus.
The PFL arises from the musculotendinous junction of the popliteus tendon and forms a “Y” configuration to anchor the popliteus to the fibula. The anterior division inserts 2.8 mm distal to the anteromedial aspect of the tip of the fibular styloid process and medial to the LCL. The posterior division is larger and is typically reconstructed in PLC surgery. It originates from the popliteus tendon and inserts 1.6 mm distal to the tip of the fibular styloid process on its posterior medial downslope. Its insertion site is just anterior to the fabellofibular ligament.
The blood supply to this area is mainly from the lateral superior geniculate artery. There is also some supply from the posterior tibial recurrent artery and directly from the popliteal artery.
The innervation of the PLC arises from the posterior articular nerve from the posterior tibial nerve, the popliteal plexus and the lateral articular nerve.
The primary function of the PCL is to resist posterior translation of the tibia throughout flexion. It has a secondary function of resisting varus when the knee is externally rotated, especially between 90° and 120° of knee flexion [6–8].
Various biomechanical studies have shown that an isolated tear of either PCL bundle results in a clinically meaningful increase in posterior tibial translation .
Studies that have previously looked at the forces within the individual bundles have contradicted each other as to which flexion angle of the knee produced the largest forces in each bundle. Fox et al. reported the in situ forces increasing in both bundles as the flexion angle increased during applied posterior tibial loads ; Harner et al. found the posteromedial bundle (PMB) graft of a double bundle reconstruction experienced its largest load at 30° of flexion . However, both studies were working on the principle that each bundle was independent of the other (superposition). The work by Kennedy et al. shows that the bundles are interdependent and therefore using the superposition principle may not be valid .
Kennedy et al. have measured direct anterolateral bundle (ALB) and posteromedial bundle graft forces in double-bundle reconstructions. They reported that the Anterolateral bundle graft force peaked during mid flexion and the posteromedial bundle graft force peaked at both full extension and deep flexion during a posterior tibial load from 0° to 120° of knee flexion .
Complete sectioning of the PCL leads to a significant increase in posterior tibial translation throughout the knee’s range of motion (0–120°) but a significant increase in internal rotation only between 90° and 120° of knee flexion . A sectioned PCL results in significantly increased internal and external rotation when subjected to rotational torques . The literature supports that the PCL has more of a role in rotational stability than previously thought and therefore it is important to examine for internal and external rotational stability when assessing a PCL injury. In biomechanical studies, there is a significant increase in external rotation after PCL resection under an applied posterior tibial load [12, 13].
The primary function of the PLC is to resist varus, external rotation and posterior translation of the tibia [14–16]. The relative importance of the LCL, popliteus and PFL has been demonstrated in studies that sectioned them in combination with the PCL [14–19].
The LCL is a primary static restraint to varus opening in the initial 0–30° of flexion [14–16]. It has an ultimate tensile strength of 295 N (Newtons).21 An isolated tear of the LCL causes a mild (1–4°) increase in varus angulation that is maximal at 30° of knee flexion. It also shows loading response at all angles of knee flexion, but a greater response at 30° than at 90.
The PCL is a secondary restraint to varus opening and if sectioned with the PLC intact, varus opening is unaffected [14, 16]. If the PLC is sectioned with an intact PCL, the maximal increased varus occurs at 30° of flexion as well as maximal external rotation and posterior tibial translation.
The PLC is a primary restraint to external tibial rotation at all angles [14, 16]. If the PLC is sectioned, with the knee flexed to 30°, 13° of external rotation is present but with the knee flexed to 90°, the external rotation was only 5.3°. Sectioning the PCL in isolation had no effect but if the PCL and PLC were both sectioned, the external rotation at 90° of flexion was 20.9° . This is because of the strongest fibres of the PCL becoming taut at 90° of flexion allowing them to form a secondary restraint against a varus moment or external rotation torque. These studies form the basis for the rationale behind the dial test [20, 21].
LaPrade et al. found that when the knee was externally rotated both at full extension & 30° of knee flexion, the LCL load response was higher than the responses of popliteus & PFL . However, in 60° of knee flexion, the load responses of popliteus and PFL to external rotation (ER) were higher. They concluded that LCL, popliteus tendon and PFL perform complimentary roles as stabilizers to ER. While the LCL assumes a primary role at lower knee flexion angles, the popliteus complex does so at higher degrees of knee flexion.
Isolated sectioning of PLC increased posterior tibial translation at all angles with the maximum in early flexion. Isolated sectioning of the PCL produces increased posterior tibial translation at all angles of flexion with the maximum effect (11.4 mm) occurring at 90° of knee flexion. While the PCL is the dominant restraint to posterior tibial translation, the PLC is very important at near full extension [16, 23].
Combined sectioning of the PLC and PCL produces a significant increase in posterior tibial translation (21.5 mm) at 90° of knee flexion compared to a normal knee or isolated sectioning of the PLC. It also leads to increased varus and external rotation at all degrees of knee flexion [14, 16, 18].
The popliteus is a static and a dynamic stabilizer [17, 19–24]. The popliteal tendon attaches to the lateral meniscus via anteroinferior and posterosuperior popliteomeniscal fascicles . These provide dynamic stability to the lateral meniscus and prevent medial entrapment of the lateral meniscus with functional varus forces to the knee . The PFL is a static stabilizer resisting varus, external rotation and posterior tibial translation. It is relatively isometric and remains functional throughout a full range of motion. In contrast, the area from the posterolateral corner of the tibia to the lateral femoral epicondyle is only tensioned near full extension. An intact popliteus muscle belly will usually tension this portion of the popliteus tendon.
A competent posterolateral corner is important in protecting a cruciate graft. When the PLC is sectioned in a knee that has had an ACL reconstruction, there is an increased load on the ACL grafts during varus and varus-internal rotation moments . This puts the grafts at risk of failure in these patients. For patients with a PCL reconstruction, a deficient posterolateral corner causes the forces on the PCL graft to be increased by 22–150 % [27–29].
In a combined PCL/PLC injury, a combined reconstruction is recommended. Sekiya et al. found that when both structures were reconstructed, the knee kinematics were nearly normal .
9.2 Clinical Assessment
9.2.1 Injury Mechanisms
Historically, 50 % of isolated PCL ruptures were the result of a flexed knee hitting a dashboard in a head-on motor vehicle accident. Since the widespread use of seatbelts, this is now an uncommon cause. In sporting injuries, isolated PCL injuries can be caused by the impact of a flexed knee onto the ground pushing the tibia back on the femur as well as hyperflexion or hyperextension injuries. Unlike the pop reported by patients at the time of ACL injuries, patients with an acute PCL rupture tend to report vague symptoms of unsteadiness or discomfort. In the chronic cases, symptoms include vague anterior knee pain, pain with deceleration and descending hills or stairs and pain when running at full stride .
In the trauma setting, PCL injuries are associated with ACL injury in 46 %, MCL in 31 % and the PLC in 62 % of cases .
The natural history of an untreated PCL injury is for medial compartment and patellofemoral wear which has been corroborated by in vitro PCL sectioning studies showing increased contact pressures in these areas. However, much like in the ACL literature, there is no evidence that reconstruction changes the natural history of degenerative disease.
An isolated injury to the posterolateral corner is uncommon (<2 % of all acute ligamentous knee injuries) because it tends to occur in combination with a cruciate or multiligament injury [32, 33]. There was a 16 % incidence of grade III PLC injuries in a consecutive series of 187 patients with an acute knee injury and complete ACL and/or PCL ligament tear on MRI .
The force causing an injury to the posterolateral corner is usually a posterolateral blow to the anteromedial proximal tibia at near full or full knee extension. This causes hyperextension and combined with a varus moment, disrupts the posterolateral structures [33, 35–37]. This can be a non-contact hyperextension and rotation twisting injury, a direct blow to the flexed knee or a high-energy trauma such as a motor vehicle accident or a fall.
The combined PCL/PLC injury can be caused by an impact to the medial side of the knee with the knee extended and the foot planted. The result is a varus force combined with hyperextension. Another common cause is landing heavily from a jump or mogul in skiing.
If there is associated sagittal plane laxity then a knee dislocation with multiligament injury must be considered. The knee may have spontaneously reduced. In all these injuries including the PLC, the status of the peroneal nerve must be checked.
In cases of chronic PLC laxity, patients can complain of joint line pain as well as posterolateral pain. Their functional instability is often in extension with their knee giving way into hyperextension on stairs, slopes or pivoting/cutting manoeuvres.
The aims of the examination are to diagnose all ligamentous and associated intra-articular injuries, rule out neurovascular pathology and then assess for anatomy or pathology that may interfere with the success of future reconstruction. For an overview of a full knee examination, see Chap. 1 (clinical assessment) but the following points are specific to assessing PCL and PLC injuries.
The patient must be evaluated for varus malalignment or hyperextension with varus thrust during stance phase [21, 38]. In chronic PCL injuries, they may walk with slight flexion in mid-stance phase to avoid posterior capsule stress .
Tenderness and ecchymosis in the posterolateral area is often present especially if there is a segond or arcuate fracture. An abrasion, laceration or ecchymosis over the tibial tubercle should raise the suspicion of a PCL injury .
The PCL should be tested with the well-described clinical tests:
Patient supine with hip flexed at 45° and knee flexed to 90°
After assessing for sag, a posterior force is applied to the proximal tibia and the grade of injury as well as an end point is assessed.
Patients can develop an end-point in a chronic rupture as the PCL scars down .
Quadriceps active test 
Place the knee at 90° of flexion and hold the foot in place against the examination table. Instruct the patient to try and slide the fixed foot anteriorly along the table.
The resultant quadriceps contraction causes a posteriorly subluxed or sagging tibia to be drawn anteriorly. Anterior movement of the tibia >2 mm is a positive test for a PCL tear.
Reverse pivot shift test 
Be aware that this test has been shown to be positive in up to 35 % patients under anaesthesia with no PCL/PLC pathology .
The foot is externally rotated with the knee in 90° of flexion. A valgus load is applied to the knee which is then extended to assess for reduction of the posteriorly subluxed tibia at 20–30° of flexion.
The PLC should be tested with the following specific tests. The grading of the injury follows this section:
Varus stress at full extension and 30° of flexion
Varus opening at full extension signifies a severe PLC injury
Dial test (posterolateral (PL) rotation test for external rotation)
>10° side to side difference
If positive at 30°, only the PLC is injured.
If positive at 90°, both the PCL and PLC are injured.
It has been validated with biomechanical studies for assessment of medial and posterolateral knee injury [16, 18, 47].
Its clinical diagnostic accuracy has been questioned .
Same patient position as the posterior drawer
Externally rotate the tibia 15° and apply a posterior force to the proximal tibia similar to a posterior drawer.
Positive if the lateral tibial plateau rotates posteriorly and externally relative to the medial tibial plateau.
In assessing a knee with ligamentous rupture, the clinician should always be suspicious of a relocated knee dislocation. The vascular examination must be thorough with popliteal artery injury a significant risk. An ankle-brachial index should be measured with a cut-off of <0.9 for further investigation with arteriography. Selective arteriography is now accepted as a non-flow limiting intimal flaps rarely become occlusive. In the presence of a normal examination and ABIs, 48 h of observation and serial physical examination is sufficient.
PCL injuries are usually classified according to Clancy and Sutherland . The normal femorotibial step-off is 10 mm with the anterior medial tibia plateau lying in front of the anterior medial femoral condyle with the knee at 90°. Applying a posterior drawer test:
Grade I injury demonstrates 0–5 mm of posterior tibial translation but the tibia is still anterior to the femur.
Grade II injuries are where the tibia translates 5–10 mm and the anterior surfaces of the two bones are now in line.
Grade III injury is where there is at least 10 mm of posterior translation. It is important to check for an end point and critical in grade III injuries to check for a PLC injury.
PLC grading is less well defined. The dial test has been discussed but while a side-to-side difference of >10° indicates a PLC injury, there is no reliable classification system to indicate the degree of injury.
The grading system of Hughston is the most commonly used, but does not evaluate rotational instability . It defines LCL injuries as:
Grade I with varus opening of 0–5 mm
Grade II with 6–10 mm
Grade III is >10 mm, which signifies associated cruciate ligament tears.
Fanelli and Larsen addressed rotational instability with their grading system .
Type A – An isolated rotational injury to popliteofibular ligament and popliteus complex. Increase in external rotation with minimal or no varus component.
Type B – Rotational injury plus mild varus instability with firm end point at 30°.
Type C – Significant rotational and varus components without a firm end point at zero degrees and 30° of knee flexion with varus stress. This occurs secondary to complete disruption of the PFL, Popliteus complex, LCL, lateral capsule and cruciate ligaments.
Stress radiographs can be used but there are unresolved issues surrounding consistency of set-up, stress application and interpretation.
Standard radiographic imaging of the knee is essential, not only to rule out associated pathology such as tibial plateau fractures but also injuries specific to the PCL and PLC such as avulsion fractures. For further details on imaging, see Chap. 2.
PCL avulsion fractures tend to occur from the tibial insertion. Radiographs should be examined closely for a ‘peel-off’ lesion in the intercondylar notch. Other signs to look for are the medial capsule avulsion fracture or ‘medial Segond fracture’.
The more commonly seen fractures in PLC injuries are the fibular head avulsion fracture, known as the arcuate sign, and an avulsion of Gerdy’s tubercle. The arcuate sign is caused by popliteofibular and fabellofibula ligament avulsions and produce a small fragment (1–8 mm) which is different from a fibular head fracture or an LCL avulsion which have a larger fragment (15–25 mm).
The laterally based capsular avulsion ‘Segond’ fracture is pathognomic for an ACL rupture which in the presence of a PCL and or PLC injury should increase suspicions for a spontaneously reduced knee dislocation.
In chronic injury, weight-bearing X-rays may demonstrate degenerative or post-traumatic arthritis, especially in the medial and patellofemoral compartments. Finally, standing alignment films may be needed to rule out varus malalignment that can threaten future reconstructions. Varus is defined as the mechanical axis of the leg falling medial to the medial tibial spine on a weight-bearing alignment film.
A magnetic resonance imaging (MRI) scan is essential in all cases to confirm diagnosis and rule out associated intra-articular pathology such as meniscal or chondral injury.
Signs of a complete PCL tear include complete non-visualization of the PCL, diffuse amorphous high signal on T-2 weighted imaged throughout the PCL and visualization of PCL fibres but with full thickness fibre disruption. If there is high signal change within the PCL or disrupted fibres but not to the level of these three criteria then a partial tear is diagnosed.
It has been reported that the most important criterion among the sonographic findings is an AP diameter of the PCL increased from the normal 6 mm to >7 mm. This is clearly visible on the MRI scans [55, 56].
In chronic PCL injuries, continuity is regained in three quarters of observed cases. Therefore, the only sign on an MRI of a chronic injury may be a lax ligament. This may change with the more widespread use of 3 T MRI scanners.
As with ACL grafts, the revascularization that occurs in the first 2 years can lead to ongoing intra-graft high signal during that time period.
The standard MRI sequences will enable evaluation of LCL, popliteus, biceps, gastrocnemius and iliotibial band (ITB). Coronal, oblique thin slices of fibula head and styloid make evaluation of the PFL, arcuate and FFL easier. Using oblique MRIs, the PFL is seen in 53–68 % of cases [57–59], the arcuate ligament in 46 % and the FFL in 48 %. This compares to 8 %, 10 % & 34 % respectively using standard coronal imaging .
While identifying all the components of the PLC is not always possible, if there is a bone contusion to the anteromedial femoral condyle, a PLC injury should be looked for with great care. A ruptured LCL will have a serpiginous contour and have lost continuity. The popliteus complex may demonstrate muscle oedema and heamorrhage on T-2 weighted and PD images. The tendon itself can be ruptured in severe injuries. An arcuate ligament injury may be suggested by oedema posterior to the popliteus tendon on sagittal or axial images. There may just be disproportionate oedema in the expected anatomical course of the other PLC structures. There may also be a lack of a joint effusion due to the disruption of the posterolateral capsule .
Ultrasonography can produce real time evaluation of the components of the posterolateral corner. However, this requires significant expertise on the part of the operator .
9.3.1 Isolated PCL
The need for surgery is dependent on the severity of the injury and the associated lesions that mandate surgical intervention. The PCL has an intrinsic ability to heal after injury although this often occurs in a lax or attenuated position [62–64].
Therefore isolated partial, grade I or grade II PCL injuries are usually managed non-operatively [62, 65, 66]. Grade III PCL injuries need to be examined with a high index of suspicion for an associated PLC or multiligament injury and need surgical management.
The evidence for outcomes after non-operative management of PCL injuries varies between isolated and combined PCL tears.
Torg et al. published in 1989 that patients with isolated PCL tears that were treated non-operatively had favourable outcomes with a follow up of 5.7 years. However, if the pattern of injury included associated ligament tears, there was a higher incidence of fair or poor outcomes and osteoarthritic progression . Some studies that have focused on isolated PCL injuries report good subjective functional scores and a healed appearance of the PCL on MRI at short term follow up (1.7–2.6 years) but less than satisfactory objective scores [34, 64–66, 68]. The conclusion was that the PCL healed in an attenuated fashion.
There is increased radiographic progression of osteoarthritis and decreased functional outcomes as the time from injury increases if treated non-operatively [66, 68]. Radiographic evidence of arthritic changes were reported in 23 % at 7 years and 41 % at 14-year follow up. However, at 14 years, only a minority had moderate or severe osteoarthritis (11 %) and the majority had good strength and subjective outcome scores .
Jacobi et al. reported that, treating isolated acute PCL with a dynamic brace for 4 months reduced the posterior sag significantly (7.1 mm), which improved at 12 months (2.3 mm) and was maintained at 24 months (3.2 mm). Ninety five percent had MRI PCL continuity restored at 6 months. There was no clinically significant decrease in Lysholm scores at 12 & 24 months .
Non-operative treatment uses an extension brace with a pad behind the upper tibia for a period of 6 weeks. Most patients with isolated PCL injuries do well with non-operative treatment with 80 % returning to their normal level of sport within 4 months. The key to the rehabilitation is a quadriceps-based programme to create a favourable quadriceps to hamstrings ratio. Most patients do not complain of subjective instability.
There is a relative indication for surgery in patients with a grade III, isolated PCL injury, who have not responded well to rehabilitation or in those with associated meniscal or major chondral injuries that require treatment. In patients with associated ligamentous injury then, early reconstruction is advised. When assessing the outcomes of isolated PCL injuries it is critical to ensure that poor outcomes were not due to missed, associated PLC injuries.
Prior to any surgery for PCL injury, it is vital to assess for associated ligamentous injury, especially of the PLC. An assessment of any varus malalignment is also mandatory. Along with incorrectly placed tunnels, failure to address these two factors are the most common causes for a failure of PCL reconstruction [31, 69, 70].
The indications in acute injuries are a PCL tear in conjunction with a dislocated knee or a grade III injury as assessed clinically or on stress radiographs or if there is a grade II injury with an associated repairable meniscal tear. For chronic PCL injuries, indications can include functional limitation including deceleration, difficulty descending stairs and hills while clearly assessing for post-traumatic arthritis.
Surgery is best performed within the first year or two from injury to prevent the development of fixed deformities. An osteotomy should be considered in the presence of a varus malalignment or medial joint disease (see Chap. 14). Reconstruction can then be carried out at the same time or staged should secondary instability persist.
The ruptured PCL may appear normal at arthroscopy in both acute and chronic cases. This is because many tears are found in the lower third obscured by the ACL, fat and synovial tissue. It is important to make the diagnosis clinically and from MRI imaging rather than use arthroscopy as a diagnostic tool.
There are multiple surgical techniques for PCL injury including bony re-attachment, local repair, microfracture, synthetic augmentation, single tunnel, double tunnel and tibial inlay techniques. These can be performed open or arthroscopically.
There is a lack of consensus on many surgical decisions in PCL surgery, including whether open or arthroscopic procedures should be used, the degree of laxity at which the surgery should be performed, the type of fixation and the rehabilitation protocol. This demonstrates that there is no good, reproducible method for reconstructing the PCL as there is with the ACL.