Anatomically, the posterolateral corner is a complex arrangement of muscles, tendons, and ligaments [13].

Seebacher et al. in 1982 [14] described the knee lateral structures as being composed of three distinct layers; however, there does not seem to be standardization of the layers, due to the high anatomic variability in the PLC and competing nomenclature in the literature [13, 15, 16].

It is possible to classify each component of the PLC in passive stabilizers, such as capsular and noncapsular ligaments (FCL, PFL, posterolateral joint capsule, arcuate ligament complex, and fabellofibular ligament), and dynamic stabilizers, which are the musculotendinous units and their aponeuroses (popliteus complex, iliotibial band, lateral head of gastrocnemius, and biceps femoris tendons). The PLC provides stability against posterolateral rotation and varus displacement; it plays the greater role in restricting posterolateral rotation, whereas the FCL alone is the major restraint to varus displacement of the tibia.

The majority of PLC injuries are primarily due to athletic activity participation, falls, or road traffic collisions [17]. Many specific mechanisms of injury are described in the literature [18, 19]:

Although various physical examination tests are described for the diagnosis of PLC lesions, in 72 % of cases, these lesions are not identified at their initial presentation, which shows the difficulty in both performing these tests and interpreting the results. The difficulty increases significantly when central pivot and medial collateral ligament injuries are associated [20].

In chronic lesions, a varus thrust gait due to a lateral laxity of the knee may be present, especially in patients with an underlying varus limb alignment. The varus thrust gait pattern is likely associated with a lift-off of the lateral compartment of the knee, which has been shown to increase medial compartment joint stresses [4, 21].

Several clinical tests have been developed to diagnose PLRI:

Plain anteroposterior (AP) and lateral radiographs can identify Segond fractures and fibular head avulsion fractures. Comparative varus stress AP radiographs, both at 0 and 30° of knee flexion, can be helpful to quantify the lateral joint space opening in both acute and chronic lesions [26, 27]: an increase in lateral compartment gapping of 2.7 mm indicates an isolated FLC tears, more than 4.0 mm indicates the presence of a high-grade injury [28]. All patients with chronic posterolateral knee injuries should be assessed for their limb alignment. MRI should always be performed in order to evaluate not only the posterolateral structures but also cruciate ligaments, medial collateral ligament, articular cartilage, and meniscal injuries. MRI technique was effective for identifying injuries to the FCL, popliteus tendon, popliteofibular ligament, and biceps femoris. Sensibility of MRI in identifying lesion of the FCL is 57.5 % and only 24.2 % for the popliteus muscle tendon. MRI, thus, cannot be the determining factor for surgical indication for reconstruction [29].

Arthroscopic evaluation can be a powerful diagnostic tool: a drive-through sign occurs when there is more than 1 cm of lateral joint opening when a varus stress is applied to the knee in “Figure four” position [27]. Arthroscopy is particularly helpful in identifying the location of injuries at the femoral attachment of the popliteus tendon, coronary ligament of the posterior horn of the lateral meniscus, and the popliteomeniscal fascicles.

Grading of PLC injuries can be performed as shown in Table 44.1.

Conservative management of PLC injuries is not well documented in literature. This kind of lesions is in most cases combined with injuries to one or both the cruciate ligaments, with absolute surgical indication. In our experience, in grade I-II isolated PLC lesions, conservative treatment is appropriate. Grade III lesions, isolated or associated to other ligamentous injuries, always need surgical treatment.

In the acute setting, isolated PLC injuries can be treated with direct repair or repair with augmentation. Acute injuries treated within 3 weeks from the trauma results in better outcomes than chronic injuries. Damaged structures can be directly sutured or anchored back to their bony attachments. All major structures of the posterolateral complex should be macroscopically evaluated in order to provide a complete restoration of the anatomy. The repair should be performed within the first 2–3 weeks after surgery in order to avoid retraction and arthrofibrosis.

Chronic injuries to the PLC are better managed with PLC reconstruction techniques rather than direct repair. Patients with chronic combined posterolateral knee injuries and varus alignment will first require an opening-wedge osteotomy as part of a staged procedure. In varus knee, there is a high risk of failure secondary to the stretching out of the grafts. An axial correction with a proximal opening-wedge osteotomy causes a significant reduction of posterolateral laxity. Second stage PLC reconstruction is not necessary in approximately 40 % of patients who had a previous open-wedge HTO [30, 31].

Several surgical techniques for the treatment of posterolateral knee instability have been reported, but there is still no consensus on the best technique to use. These techniques can be classified into nonanatomical fibular-based reconstructions and anatomical tibial and fibular-based reconstructions. The most widely used nonanatomical reconstruction procedure was described by Larsen et al. [32]. They found the fibular head to be isometric to the lateral femoral epicondyle, so they recommended the use of a graft passed through the fibular head and inserting into the lateral epicondyle. Larsen’s PLC reconstruction aims to restore the functions of the popliteofibular ligament and the lateral collateral ligament; it is nonanatomical because the femoral insertion lies on the lateral epicondyle and not at the anatomical insertion sites of these structures.