Posterior cruciate ligament (PCL) tear is an injury to the strongest intra-articular ligament of the knee. The PCL extends from the medial femoral condyle to the posterior surface of the tibia and prevents posterior tibial translation. It is much rarer than ACL tear (3-20% of all knee ligament injuries) because PCL is approximately 2 times thicker than ACL. The most common injury mechanism is 'dashboard injury' — direct blow to the anterior surface of the tibia with knee in flexion (knee impacting dashboard in motor vehicle accidents). Falling on flexed knee and hyperextension are other mechanisms. On MRI, normal PCL appears as a homogeneously low-signal curved band. In tear, the ligament appears thickened, amorphous, and hyperintense. Partial tears are more common than in ACL because PCL's strong structure predisposes to partial rather than complete disruption. Isolated PCL tear is generally treated conservatively; combined ligament injuries may require surgery.
Age Range
18-50
Peak Age
30
Gender
Male predominant
Prevalence
Uncommon
The PCL is the strongest and thickest ligament of the knee (approximately 2x thicker than ACL, ~38 mm long, ~13 mm wide). It consists of two main bundles: anterolateral bundle (AL — taut in flexion, primarily controls posterior translation) and posteromedial bundle (PM — taut in extension). PCL's primary function is preventing posterior tibial translation. In dashboard injury mechanism, direct impact to the anterior tibial surface with knee at 90 degrees flexion pushes the tibia posteriorly — this force exceeds PCL's tolerance and tear occurs. Tear pattern varies by impact localization: proximal tibial avulsion (20-30%), midsubstance tear (50-60%), or femoral detachment (10-20%). In hyperextension mechanism, PCL is stressed against both posterior translation and hyperextension and tears — posterolateral corner injury and popliteal artery damage may also accompany this mechanism. The amorphous thickened appearance of PCL tear on MRI results from hemorrhage and edema penetrating between ligament fibers disrupting fiber architecture — the normal homogeneously low-signal structure is replaced by a heterogeneous hyperintense, ill-defined mass.
On sagittal PD fat-suppressed MRI, instead of PCL's normal thin curved low-signal band appearance, a thickened (>7 mm), amorphous (irregular margins), diffusely hyperintense mass is seen. This appearance reflects complete disruption of fiber architecture by hemorrhage and edema penetrating between ligament fibers. While normal PCL shows homogeneous low signal, torn PCL shows heterogeneous hyperintense signal. This finding is the most important primary MRI finding for PCL tear and is diagnostic when combined with dashboard injury history.
On sagittal PD fat-suppressed images, PCL loses its normal thin curved low-signal band appearance and appears as a thickened (>7 mm), amorphous, diffusely hyperintense structure. In complete tear, fiber continuity is completely lost and a gap filled with hyperintense edema/hemorrhage is seen. In partial tear, PCL is thickened with hyperintense signal in some fibers while other fibers remain intact and low-signal. The tibial attachment of PCL is the most common tear site.
Report Sentence
PCL is thickened, amorphous, and diffusely hyperintense with no visible fiber continuity; consistent with complete tear.
On T2 fat-suppressed/STIR sequences, bone marrow edema is seen in the proximal anterior tibia — this 'dashboard contusion' is a finding of direct impact to the anterior tibial surface. Edema is typically at the level of tibial tuberosity and proximal anterior tibial cortex. Dashboard contusion is a specific secondary finding for PCL tear with different localization from pivot-shift contusion. Additionally, bone edema in the posterior tibial fossa region may be seen — this is avulsion-related edema at the PCL tibial attachment level.
Report Sentence
Bone marrow edema consistent with dashboard contusion is seen in the proximal anterior tibia, supporting PCL injury mechanism.
On sagittal PD images, posterior position of the tibial posterior margin relative to the medial femoral condyle posterior line is measured. >7 mm posterior tibial translation indicates PCL insufficiency. In chronic PCL insufficiency, the ligament is lax and posterior tibial sag develops. The posterior sag finding is more prominent on lateral radiograph. On MRI, progressive thinning and partial visualization of PCL fibers (chronic tear finding) may be seen.
Report Sentence
Approximately ___ mm posterior tibial translation is seen on sagittal images, consistent with PCL insufficiency.
Damage to posterolateral corner structures (popliteus tendon, lateral collateral ligament, arcuate ligament, posterolateral capsule) may be seen with PCL tear. Edema, signal increase, and discontinuity are seen in these structures on T2 fat-sat/STIR sequences. When posterolateral corner injury coexists, instability significantly increases and surgical indication strengthens. Popliteal artery injury risk also increases — MR angiography evaluation may be needed.
Report Sentence
Edema and partial discontinuity in posterolateral corner structures (popliteus tendon, LCL) accompanying PCL tear is seen, suggesting combined ligament injury.
On T1-weighted sagittal images, cortical irregularity and small avulsion fragment may be seen at the PCL tibial attachment. PCL tibial avulsion fractures constitute 20-30% of all PCL injuries and can be surgically refixed (unlike midsubstance tears). The fragment is usually small (5-15 mm) and seen displaced in the posterior tibial fossa. The fragment carrying bone marrow signal on T1 is easily identified.
Report Sentence
Cortical irregularity and approximately ___ mm avulsion fragment at the PCL tibial attachment is seen, consistent with PCL tibial avulsion fracture.
Criteria
Both bundles (AL + PM) completely torn — complete loss of fiber continuity
Distinct Features
Significant posterior instability, common in combined injuries, stronger surgical indication, amorphous thickened PCL
Criteria
One bundle torn, other bundle intact — partial fiber continuity present
Distinct Features
More common (50% of all PCL tears), conservative treatment usually successful, PCL thickened but some fibers visible
Criteria
Cortical avulsion fracture at PCL tibial attachment — ligament fibers intact
Distinct Features
20-30% of all PCL injuries, surgical refixation possible (good prognosis), fragment in posterior tibial fossa
Distinguishing Feature
ACL tear is anterior ligament pathology with pivot/deceleration mechanism; PCL tear is posterior ligament with dashboard mechanism — different ligament, different contusion pattern
Distinguishing Feature
MCL injury is medial extra-articular ligament pathology; PCL is intra-articular posterior ligament — but may coexist in combined injuries
Distinguishing Feature
Isolated bone contusion can occur without ligament tear; dashboard contusion specifically indicates PCL injury
Urgency
urgentManagement
conservativeBiopsy
Not NeededFollow-up
specialist-referralIsolated PCL tear generally yields successful results with conservative treatment — quadriceps strengthening exercises, bracing, and rehabilitation. PCL has better spontaneous healing capacity than ACL because it is covered by synovial sheath with better blood supply. However, in combined ligament injuries (PCL + posterolateral corner, PCL + ACL, PCL + MCL), surgical reconstruction is indicated. In PCL tibial avulsion fracture, surgical refixation (screw fixation) is preferred with good prognosis. In chronic PCL insufficiency, posterior compartment osteoarthritis risk increases — especially medial femoral condyle and patellofemoral joint are affected. Posterolateral corner injury coexistence is the most important prognostic factor — untreated posterolateral corner injury significantly increases reconstruction failure risk.
Isolated PCL tears generally respond to conservative treatment. However, multiligamentous injuries (especially with posterolateral corner damage) require surgical reconstruction. Chronic PCL insufficiency leads to early arthropathy in the medial and patellofemoral compartments.