GC230 Knee Sport Injuries: Part 2
Continuation of knee sport injuries covering conditions such as meniscal tears, collateral and cruciate ligament injuries, and associated soft tissue damage resulting from athletic activities.
Knee Sport Injuries — Part 2: Ligament Injury (Collateral and Cruciate)
Big idea: The knee relies on four major ligaments for stability — two collateral (MCL, LCL) that are extra-articular with high healing potential, and two cruciate (ACL, PCL) that are intra-articular with poor healing potential. This fundamental anatomical difference dictates the entire management philosophy: collateral ligaments can often be treated conservatively; cruciate ligaments, once torn mid-substance, generally cannot heal and may require reconstruction. This lecture also covers knee dislocation — a limb-threatening emergency requiring at least two of the four ligaments to rupture.
Learning objectives (derived from the lecture):
- Understand the anatomy and function of all four knee ligaments
- Know the mechanism of injury, clinical presentation, and special tests for each ligament
- Classify ligament injuries by severity (Grades I–III) using stress testing
- Understand investigation and management principles for each ligament injury
- Recognize knee dislocation as an emergency with neurovascular risk
Core Concepts and Mechanisms
Ligament is a dense connective tissue composed of fibroblasts (regularly arranged spindle-shaped cells), with extracellular matrix containing 90% type I collagen and 10% type III collagen, elastin, and 60% water by total weight. [1]
The micro-architecture follows a hierarchical organization: collagen molecule → microfibril → fibril → fiber → ligament. Collagen molecules are arranged in a "head-to-tail" configuration with cross-links between them, staggered in parallel to produce the characteristic "crimp" pattern. [1]
Why does this matter? The crimp pattern explains the toe region of the stress-strain curve — when a ligament is first loaded, the crimped fibers straighten out (low stiffness), requiring little force. Once straightened, the ligament enters the linear region where it resists force more stiffly. Beyond this:
| Region | What Happens | Clinical Correlate |
|---|---|---|
| Toe region | Crimp straightening, minimal stiffness | Normal physiological loading |
| Linear region | Proportional stress-strain, collagen resisting | Normal restraint function |
| Plastic region | Micro-failure of fibrils/fibers begins | Grade I–II injury (sprain/partial tear) |
| Failure region | Ultimate load exceeded, complete rupture | Grade III injury (complete tear) |
When stress reaches the plastic region, micro-failure of some fibrils and fibers occurs → sprain/partial tear → Grade 1–2 laxity. When stress exceeds the ultimate load to failure, complete failure occurs → complete tear → Grade 3 laxity. [1]
Collateral ligaments (MCL, LCL) are extra-articular → high healing potential. Cruciate ligaments (ACL, PCL) are intra-articular → less favourable healing potential. [1]
Why? Extra-articular ligaments are bathed in a vascular soft tissue environment that supports an inflammatory healing cascade (haematoma → granulation tissue → scar → remodeling). Intra-articular ligaments are bathed in synovial fluid, which dissolves clots and washes away growth factors needed for healing. The synovial environment also lacks the periligamentous tissue scaffold. This is why a mid-substance ACL tear traditionally has no healing potential and requires reconstruction rather than repair.
1. Medial Collateral Ligament (MCL)
The MCL complex has three components: Superficial MCL (sMCL), Deep MCL (dMCL), and the Posterior Oblique Ligament (POL). [1]
Superficial MCL (2nd layer):
- Origin: outer rim of medial femoral epicondyle
- Insertion: medial proximal tibia with TWO separate tibial attachments
- Proximal attachment: primarily to soft tissues over the anterior arm of semimembranosus
- Distal attachment: bony, broad-based, located just anterior to the posteromedial crest of the tibia, approximately 6–8 cm below the joint line
- Fiber orientation: anterior fibers are parallel and vertical; posterior fibers are oblique
Deep MCL (3rd layer):
- Origin: central sulcus of medial femoral epicondyle
- Insertion: medial proximal tibia, 1 cm below joint line
- Represents a thickening of the medial joint capsule → contains meniscofemoral and meniscotibial ligaments → through these, the deep MCL is attached to the medial meniscus
- The posterior border blends with and becomes inseparable from the central arm of the POL
Why does the deep MCL attachment to the medial meniscus matter? This is why MCL injuries can be associated with medial meniscus tears — the deep MCL tethers the meniscus, so when the MCL is torn, the meniscus can also be injured. This forms part of the classic "unhappy triad" (ACL + MCL + medial meniscus).
Posterior Oblique Ligament (POL):
- Origin: distal and posterior to the adductor tubercle, posterior to the sMCL origin
- Insertion: three arms
- Central/tibial arm — thickest, inserts close to articular margin
- Superior/capsular arm — continuous with posterior capsule, blends with oblique popliteal ligament
- Inferior/superficial arm — associated with semimembranosus tendon
MCL provides stability against valgus and external rotation stress. [1]
| Structure | Primary Restraint | Secondary Restraint | Tension Behavior |
|---|---|---|---|
| Superficial MCL | Valgus stress (78% at 25° flexion, 57% at 5°) | External rotation, anterior/posterior translation | Tense on flexion, relax on extension |
| Deep MCL | — | Valgus stress (4% at 25°, 8% at 5°) | Tense on flexion, relax on extension |
| POL | Posteromedial rotatory stability; stabilizes medial meniscus | Valgus (4% at 25°, 18% at 5°) | Tense on extension, relax on flexion |
Why test at 30° flexion?
At full extension, the posterior capsule and POL are taut and contribute significantly to medial stability (18%). This means that a Grade III tear may appear less severe at 0° because the intact posterior capsule compensates. Testing at 30° knee flexion isolates the MCL by relaxing the posterior capsule, revealing the true MCL laxity. If there is valgus laxity at both 0° AND 30°, suspect combined MCL + POL + possibly cruciate injury.
MCL injury occurs from: (1) direct blow to the lateral aspect of the leg or lower thigh, or (2) noncontact injury from cutting, pivoting, or twisting. Patient presents with medial knee pain ± reactive swelling. [1]
Examination findings include: bruise along the MCL course, localized tenderness at the site of injury (femoral origin / mid-substance / tibial insertion), and joint effusion (tested by fluid shift test). [1]
Valgus Stress Test at 0° and 30°
Position: supine or sitting. Examiner holds proximal tibia with both hands, patient's ankle in the examiner's axilla. Begin at full extension → apply sustained valgus stress → repeat at 30° flexion. Compare to the normal knee. Avoid movement at the ipsilateral hip. [1]
Always examine the normal knee first! This is a universal principle — you need a baseline for comparison.
| Grade | Opening (vs normal side) | End Point | Pathology |
|---|---|---|---|
| Normal | Same as normal side, pain-free | Firm | Intact |
| Grade I (Sprain) | 0–5 mm | Firm | Pain on valgus stress; micro-tears |
| Grade II (Partial Tear) | 6–10 mm | Firm end point | Partial disruption |
| Grade III (Complete Tear) | *** > 10 mm*** | No end point | Complete rupture |
X-rays (AP and Lateral): look for avulsion fracture of MCL (acute) or Pellegrini-Stieda lesion (chronic). ± Stress views. USG to locate exact site of injury. MRI (not mandatory) to locate injury site and assess concomitant intra-articular injuries. [1]
Pellegrini-Stieda lesion = calcification/ossification near the medial femoral epicondyle, representing chronic MCL injury with heterotopic bone formation. This is a classic radiological finding.
Isolated Grade I and II: conservative treatment with bracing and protected weight-bearing for 6 weeks. Good potential to heal, though usually with residual medial laxity. [1]
Grade III: complete rupture, commonly associated with other ligament injuries. Management is controversial: (a) early open exploration + surgical repair within 2 weeks, versus (b) initial trial of bracing + protected weight-bearing for 6 weeks → delayed MCL reconstruction if persistent significant laxity. [1]
Why is conservative treatment effective for MCL? Because the MCL is extra-articular — it has a rich blood supply from surrounding soft tissues and can mount an effective healing response. Even after healing, there is usually some residual laxity, but this is often clinically tolerable.
2. Anterior Cruciate Ligament (ACL)
Intra-articular. Originates on the medial wall of the lateral femoral condyle. Runs downward, forward, and medially. Inserts into the anterior aspect along the midline of the tibial articular surface. Composed of two distinct bundles: Anteromedial (AM) bundle and Posterolateral (PL) bundle. [1]
Primary restraint: (1) Prevent excessive anterior translation of tibia relative to femur. (2) Prevent excessive internal rotation of tibia relative to femur. [1]
| Bundle | Function | Clinical Test |
|---|---|---|
| AM bundle | Controls anterior translation at 90° flexion | Anterior drawer test |
| PL bundle | Controls anterior translation at full extension AND controls internal rotation | Lachman test and Pivot shift test |
Secondary restraint: Prevent excessive valgus movement of knee. [1]
Why two bundles? The ACL is not a simple uniform band — it has fibers that tighten at different flexion angles, providing stability throughout the range of motion. This is why modern anatomic ACL reconstruction aims to recreate both bundles.
Low-energy injuries during athletic activities. (1) Direct contact injury → hyperextension or valgus stress. (2) Indirect non-contact mechanism → sudden deceleration or rotation/pivoting maneuvers (most common). [1]
High Yield — Mechanism
Non-contact mechanisms (sudden deceleration, pivoting, cutting) account for the majority of ACL injuries. This is a common exam discriminator — ACL injuries are typically low-energy sports injuries, NOT high-energy trauma (contrast with PCL injuries which are typically high-energy).
"Popping" or tearing sensation at the time of injury. Immediate or early swelling within 12 hours (acute haemarthrosis). Cannot continue the game. ± Difficulty bearing weight and instability (giving way). [1]
Why does the knee swell so quickly? The ACL is a highly vascularized intra-articular structure. When torn, blood fills the joint cavity rapidly → acute haemarthrosis within hours. This is different from a meniscus tear, which typically produces an effusion over 24–48 hours.
Physical Examination
Gross knee swelling — "acute haemarthrosis." ACL insufficiency signs: Lachman, Anterior drawer, Pivot shift. Walk with quadriceps avoidance gait. Commonly associated with concomitant MCL and meniscal injury. [1]
Quadriceps avoidance gait: The patient avoids extending the knee fully during gait because the quadriceps contraction would pull the tibia anteriorly (the ACL normally prevents this). The patient walks with a flexed knee to use the hamstrings as a dynamic stabilizer.
Position: supine, knee at 20–30° flexion. Stabilize distal femur with one hand, apply anterior pulling force on tibia with the other. Finding: excessive anterior translation compared to normal knee. Grading same as collateral ligament injury. [1]
Why is Lachman more sensitive than anterior drawer? At 20–30° flexion, the PL bundle of the ACL is taut and is the primary restraint. The menisci and posterior capsule do not provide secondary restraint at this angle, so the test isolates ACL function. At 90° (anterior drawer), the menisci and hamstrings can mask ACL insufficiency.
Position: supine, knee at 90° flexion. Stabilize distal tibia by sitting on the foot. Check hamstring relaxation. Apply anterior drawing force on proximal tibia with both hands. Finding: excessive anterior translation compared to normal side. [1]
Position: supine, knee in full extension and internal rotation. Apply valgus stress to proximal tibia. Flex the knee from full extension to 30–40°. Finding: observe for clunk or "jump" of the Gerdy's tubercle. [1]
| Grade | Finding |
|---|---|
| Grade I | "Gliding" movement |
| Grade II | Obvious "clunk" |
| Grade III | "Locked subluxation" |
What does the pivot shift actually demonstrate? In an ACL-deficient knee, the tibia is anteriorly subluxed when the knee is in extension (because PL bundle normally prevents this). As the knee is flexed past 30°, the iliotibial band transitions from an extensor to a flexor of the knee, causing the tibia to suddenly reduce — producing the characteristic "clunk." This test is the most specific for ACL deficiency and correlates best with functional instability.
High Yield — Haemarthrosis Differential
Knee aspiration in patients with acute haemarthrosis is both DIAGNOSTIC and THERAPEUTIC.
Diagnostic: Of patients with sports-related acute haemarthrosis:
- ACL deficiency: 72%
- Osteochondral fracture: 14%
- Patellar dislocation: 6%
Therapeutic: Reduces pain, improves ROM. [1]
This means that in the exam, if they describe a young athlete with acute haemarthrosis, the most likely diagnosis is ACL injury (72%). Osteochondral fracture and patellar dislocation are important differentials.
X-ray findings: [1]
- Segond fracture — avulsion fracture at the lateral proximal tibia (lateral capsular sign), strongly associated with ACL rupture. [1][2]
What the ACL imaging panel shows: lateral tibial Segond fleck; tibial-spine avulsion on lateral XR ± arthroscopy; arthrocentesis of acute haemarthrosis — XR hints, MRI/EUA confirm, blood in the joint screams “think ACL.” [1]
- ACL tibial avulsion fracture — bone fragment at the tibial ACL insertion
- Standard AP and Lateral views
MRI: Gold standard for confirming ACL injury, assessing partial vs complete tear, and identifying associated meniscal and chondral injuries.
The diagnosis of ACL injury rests on: (1) Acute haemarthrosis after knee injury proven by arthrocentesis, (2) Symptoms of instability especially during pivoting sport, (3) Signs of ACL deficiency on physical examination, (4) Radiographic evidence on MRI. [1]
ACL deficiency signs are difficult to elicit acutely because the knee is too painful → "GUARDING." Sensitivity and specificity increase 2–3 weeks after resolution of pain and swelling. [1]
| Test | Sensitivity | Specificity |
|---|---|---|
| Lachman on admission | 62.7% | 87.5% |
| Lachman on day 9 | 78.4% | 85% |
| EUA Lachman | 88.2% | 90% |
| EUA Pivot Shift | 82.4% | 100% |
| MRI | 74.5% | 85% |
Exam Trap
Note that EUA pivot shift has 100% specificity — if it's positive, it confirms ACL deficiency. Also note that MRI sensitivity (74.5%) is lower than EUA Lachman — clinical examination under anaesthesia can outperform MRI! This is a common exam discriminator.
Management
High healing potential if treated properly. Early surgery — reduction and internal fixation — is advised to preserve ACL function. [1]
Why? The ligament itself is intact; it's the bone that failed. If you fix the bone back, the ACL can resume function.
Mid-substance ACL tear traditionally has NO healing potential → surgical repair is NOT advised. Initial conservative treatment → Rule of "one third" (Noyes, 1983):
- 1/3 have no or minimal symptoms during ADL/recreational activities
- 1/3 have symptoms during recreational activity and require quitting sports
- 1/3 have deteriorating symptoms and require surgical stabilization [1]
Surgery is indicated if: (1) patient wants to return to pivoting sport (soccer, basketball, etc.), or (2) persistent instability despite giving up pivoting sport. [1]
Gold standard for mid-substance ACL tear in the 21st century. A tendon graft reconstructs the ACL at its anatomical position. Healing and remodeling takes close to 1 year. Patient advised NOT to return to pivoting sport for at least 9 months. [1]
Why reconstruction, not repair? Because the intra-articular environment prevents direct healing. Simply suturing the torn ends together fails. Instead, a graft (autograft from hamstring tendon or patellar tendon, or allograft) is placed through bone tunnels to recreate the ACL. The graft undergoes "ligamentization" — a biological remodeling process where it gradually takes on the properties of a native ligament, taking ~12 months.
3. Posterior Cruciate Ligament (PCL)
Intra-articular. Originates on the lateral wall of the medial femoral condyle. Inserts into the posterior aspect of the tibial articular surface ~1–1.5 cm below the joint line. Average length: 38 mm. 30% larger than ACL. [1]
Two bundles: Anterolateral (AL) bundle — 2× bigger than PM, more taut in flexion. Posteromedial (PM) bundle — more taut in extension. [1]
Note the naming convention is reversed compared to ACL bundles (ACL has AM and PL; PCL has AL and PM). The larger bundle in both ligaments is taut in different positions.
Primary restraint: prevent excessive posterior translation of tibia relative to femur. Secondary restraint: prevent excessive external rotation at 90° flexion, hyperextension, and varus angulation in extension. [1]
Usually results from direct high-energy trauma, such as RTA — classic "dashboard injury" with direct posterior hit on anterior proximal tibia with knee flexed. Can occur in contact sports with fall on flexed knee with foot plantarflexed. Non-contact mechanisms (forced hyperflexion, hyperextension) are less common. [1]
Dashboard Injury — Classic Mechanism
In a car crash, the front seat passenger's knee hits the dashboard. The force is applied to the anterior proximal tibia, pushing it posteriorly while the knee is flexed → PCL rupture. Always look for the "tale-telling bruise on the anterior proximal tibia."
Rarely report "popping" sensation (contrast with ACL). Swelling is mild to moderate. Pain is mild, often posterior knee. PCL-deficient patients SELDOM experience instability. Many report knee stiffness. May develop anterior knee pain or medial joint line pain years later. [1]
Why anterior knee pain years later? PCL deficiency allows the tibia to sag posteriorly. The quadriceps must work harder to compensate → increased patellofemoral contact pressure → anterior knee pain. The altered biomechanics also accelerate medial compartment wear → medial joint pain.
Physical Examination
Knee swelling. "Tale-telling" bruise on anterior proximal tibia (dashboard injury). PCL insufficiency signs: posterior sagging, loss/reduction of normal medial step-off, positive posterior drawer test. Commonly associated with PLC (posterolateral complex) injury. [1]
Position: supine, both knees flexed to 90°. Observe from the side the relationship between the anterior border of proximal tibia and distal femoral condyle. [1]
Normal: anterior border of proximal tibia should be ~1 cm anterior to distal femoral condyle. [1]
| Grade | Finding |
|---|---|
| Grade I | Posterior sagging present, but anterior tibial border REMAINS anterior to femoral condyle |
| Grade II | Anterior tibial border and femoral condyle are in the SAME plane |
| Grade III | Anterior tibial border is POSTERIOR to femoral condyle |
Position: supine, knee at 90° flexion. Stabilize tibia by sitting on foot. Check for posterior sagging FIRST — if present, reduce the posteriorly subluxed tibia before applying the test. Apply posterior pushing force on proximal tibia. Finding: excessive posterior translation compared to normal side. Same grading as posterior sagging. [1]
Critical Exam Trap — False Positive Anterior Drawer
If you don't check for posterior sagging before performing the anterior drawer test, a PCL-deficient knee with posterior subluxation may appear to have a "positive anterior drawer" when you're actually just reducing the posteriorly subluxed tibia back to neutral. This is a PSEUDO-positive anterior drawer. Always assess the resting position of the tibia first!
PCL tibial avulsion fracture — high healing potential if treated properly. Early surgery (ORIF) advised if displaced with high-grade PCL laxity. [1]
| Scenario | Management |
|---|---|
| Low-grade isolated mid-substance PCL injury (Grade I–II) | Conservative: quadriceps strengthening + functional adaptation |
| High-grade symptomatic isolated mid-substance (Grade III), especially young patient | PCL reconstruction |
| Combined PCL + PLC or multi-ligament injury | Combined PCL + PLC reconstruction ± other ligament reconstruction |
| PCL avulsion fracture — undisplaced | Conservative |
| PCL avulsion fracture — displaced | Operative ORIF |
Why quadriceps strengthening for PCL injuries? The quadriceps pulls the tibia anteriorly, dynamically compensating for the lost PCL restraint. Strong quadriceps can mask PCL deficiency functionally. This is why many patients with isolated Grade I–II PCL injuries do well without surgery.
The management flowchart adds the early positioning and timing details:
- Isolated Grade I–II acute injury: 4–6 weeks of limited activity/“relative rest.”
- Isolated Grade III acute injury: hold the knee in full extension for 4 weeks to prevent posterior tibial subluxation; consider surgery in a young athlete or a “peel-off” injury.
- Combined PCL/PLC, PCL/MCL or dislocated-knee pattern: the slide directs surgery within 2 weeks, with PCL reconstruction and acute collateral repair ± ACL reconstruction.
4. Lateral Collateral Ligament (LCL) and Posterolateral Complex (PLC)
LCL:
Origin: just posterior and proximal to the lateral femoral epicondyle. Insertion: 8 mm from the anterior border of fibular head. LCL is the primary static varus restraint for the knee. [1]
PLC:
Composed of popliteofibular ligament and popliteus tendon. The PLC functions to prevent excessive external rotation of tibia at 30° of knee flexion. [1]
Sports injuries / high energy trauma. Most common mechanism: direct blow to anteromedial tibia with knee in extension → forceful hyperextension with external rotation and varus. Also: contact/noncontact hyperextension, varus non-contact force. [1]
Pain along posterolateral knee. Swelling is often minimal. Varus thrust gait with feeling of instability approaching full extension. May be associated with common peroneal nerve injury symptoms. [1]
High Yield — Common Peroneal Nerve
LCL/PLC injuries may be associated with common peroneal nerve injury because the nerve wraps around the fibular neck, in close proximity to the LCL insertion on the fibular head. Always check dorsiflexion and sensation over the first dorsal web space in LCL injuries!
Physical Examination
Mild knee swelling. Bruise around fibular head. Laxity on varus stress test. Increased external rotation > 10° compared to normal side at 30° flexion (Dial test). ± Common peroneal nerve injury. [1]
Same technique as valgus stress test but applying VARUS stress. Test at 0° and 30°. Same grading system (Grade I: 0–5 mm, Grade II: 6–10 mm, Grade III: > 10 mm). [1]
Patient prone. Knee flexed to 30° and 90° sequentially. Passive external rotation of tibia performed at each angle. Positive if ER > 10° compared to contralateral side. [1]
| Finding | Interpretation |
|---|---|
| Increased ER at 30° but NOT at 90° | Isolated PLC injury |
| Increased ER at BOTH 30° and 90° | Combined PCL + PLC injury |
Why does 90° involvement indicate PCL injury? At 90° flexion, the PCL is the main restraint against posterior tibial translation and also contributes to rotational control. If only the PLC is injured, the intact PCL limits excessive rotation at 90°. If the PCL is also torn, there's no restraint at either angle.
Fracture of fibular head and avulsion fracture of proximal fibula are suggestive of concomitant LCL ± PLC injury. [1]
Conservative: bracing and protected weight-bearing for 6 weeks. Surgical repair may be required for: (1) Grade 3 injury, (2) avulsion fracture of fibular head, (3) as part of multi-ligament injury / knee dislocation management. [1]
5. Knee Dislocation
Knee dislocation refers to dislocation of the femoral-tibial articulation. The knee can only dislocate if there is complete rupture of AT LEAST 2 out of 4 major ligaments. Usually from high-energy trauma. The neurovascular bundle is at HIGH RISK of injury, putting the limb at risk of ischemia if not reduced promptly. [1]
Critical — Vascular Emergency
Knee dislocation is a LIMB-THREATENING emergency. The popliteal artery is tethered posteriorly and is highly vulnerable to injury. Even if spontaneously reduced, vascular injury must be excluded.
X-ray findings of a dislocated knee are UNCOMMON because spontaneous reduction occurs in most knee dislocations, resulting in a seemingly "normal" X-ray. A high index of suspicion is required. [1]
Clues to a spontaneously reduced knee dislocation:
- Report of severely deformed knee at time of injury
- Gross haemarthrosis AND severe bruise along collateral ligament course
- Detection of Grade 3 laxity in at least 2 out of 4 major ligaments confirms the diagnosis
Initial assessment: VASCULAR STATUS must be assessed. [1]
- If distal circulation is intact initially → regular monitoring within the first day
- If doubt about vascular status → URGENT angiogram
Initial management: Reduce the knee urgently and immobilize. [1]
- Vascular injury → urgent exploration + repair ± vascular reconstruction
- Nerve injury (e.g., common peroneal nerve) → exploration and repair can be done at time of vascular repair
Definitive management: Rule out need for early surgery (Grade 3 collateral injury, displaced meniscal tear). Cruciate ligament injuries managed electively. [1]
| Feature | MCL | ACL | PCL | LCL |
|---|---|---|---|---|
| Location | Extra-articular | Intra-articular | Intra-articular | Extra-articular |
| Healing potential | High | Poor (mid-substance) | Poor (mid-substance) | High |
| Primary restraint | Valgus | Anterior translation + internal rotation | Posterior translation | Varus |
| Mechanism | Valgus blow / cutting | Pivoting / deceleration / valgus | Dashboard injury / hyperflexion | Varus / hyperextension |
| Classic symptom | Medial pain | Pop + haemarthrosis + giving way | Mild pain, posterior, stiffness | Posterolateral pain, varus thrust |
| Key test | Valgus stress at 0° and 30° | Lachman, anterior drawer, pivot shift | Posterior sag, posterior drawer | Varus stress, Dial test |
| Nerve at risk | — | — | — | Common peroneal nerve |
| X-ray sign | Pellegrini-Stieda (chronic), avulsion | Segond fracture, tibial avulsion | Tibial avulsion fracture | Fibular head fracture |
| Grade I–II Mx | Conservative (brace) | Conservative → rule of 1/3 | Conservative (quads strengthening) | Conservative (brace) |
| Grade III Mx | Controversial (repair vs delayed recon) | ACL reconstruction | PCL reconstruction | Surgical repair |
| Return to sport | ~6 weeks | ≥ 9 months | Variable | ~6 weeks |
Common Traps and Discriminators
-
"Haemarthrosis after acute knee injury — most likely cause?" → ACL tear (72%). Not meniscus (meniscal tears typically cause effusion, not haemarthrosis, and delayed onset).
-
"Which is more sensitive — Lachman or anterior drawer?" → Lachman. The anterior drawer can be masked by hamstring spasm, meniscal block, and posterior capsule.
-
"MRI vs clinical exam for ACL" → EUA Lachman (sensitivity 88.2%) is more sensitive than MRI (74.5%). Don't assume MRI is always superior.
-
"Can ACL be repaired?" → No, mid-substance ACL tears cannot heal → reconstruction (not repair) is the gold standard. Only avulsion fractures can be "repaired" (ORIF).
-
"Valgus laxity at 0° and 30° — what is injured?" → MCL + posterior structures (POL, posterior capsule). Isolated MCL injury shows laxity only at 30°.
-
"Posterior drawer seems positive but actually it's..." → Pseudo-positive anterior drawer in PCL injury. Always check posterior sagging first.
-
"Dial test positive at 30° only vs both 30° and 90°" → 30° only = isolated PLC; both = PCL + PLC.
-
"Knee dislocation X-ray looks normal" → Spontaneous reduction. Diagnose clinically by Grade 3 laxity in ≥ 2 ligaments + gross haemarthrosis.
-
"First step in managing knee dislocation?" → Assess vascular status and reduce urgently. NOT imaging, NOT ligament repair first.
High Yield Summary
- Four knee ligaments — two collateral (extra-articular, heal well) and two cruciate (intra-articular, heal poorly).
- MCL is the primary valgus restraint — test with valgus stress at 30°; most injuries treated conservatively. ACL is the primary restraint against anterior translation and internal rotation — haemarthrosis in 72% of acute knee injuries is ACL; diagnose with Lachman (most sensitive), pivot shift (most specific); mid-substance tears require reconstruction (NOT repair); return to sport ≥ 9 months. PCL prevents posterior translation — dashboard injury classic; check posterior sagging before drawer test; low-grade injuries managed with quadriceps strengthening. LCL is the primary varus restraint — beware common peroneal nerve injury; Dial test differentiates isolated PLC (30° only) from combined PCL+PLC (both 30° and 90°). Knee dislocation = ≥ 2 ligaments ruptured = VASCULAR EMERGENCY — reduce urgently, assess circulation, angiogram if doubt. Segond fracture is pathognomonic of ACL injury. Pellegrini-Stieda lesion indicates chronic MCL injury.
Active Recall - Lecture Notes
GC230 Knee Sport Injuries: Part 1
Knee sport injuries encompass a spectrum of traumatic musculoskeletal conditions—including ligament tears (ACL, MCL, PCL, LCL), meniscal injuries, and patellar dislocations—commonly resulting from high-impact or pivoting athletic activities.
GC230 Knee Sport Injuries: Part 3
Knee sport injuries (Part 3) covers posterior cruciate ligament (PCL) injuries, posterolateral corner injuries, and multi-ligament knee injuries, focusing on their mechanisms, diagnosis, and surgical management in athletes.