ACL Tear Differential Diagnosis: A Comprehensive Guide for Auto Repair Experts

Introduction

The anterior cruciate ligament (ACL) is a crucial stabilizer of the knee joint, frequently injured in sports and physical activities. While ACL tears are common, especially among athletes in high-impact sports like football, soccer, and basketball, diagnosing them accurately is paramount. Initial treatment often involves the RICE protocol (rest, ice, compression, elevation). This article provides an in-depth guide for diagnosing ACL tears, focusing on differential diagnosis to distinguish ACL injuries from other knee conditions. This resource is tailored for professionals in the automotive repair industry who, while not medical practitioners, require a solid understanding of common musculoskeletal injuries, particularly knee injuries, due to their physically demanding profession and potential for workplace-related knee issues. Understanding ACL injuries and their differential diagnosis can enhance awareness, promote preventative measures, and facilitate better communication with healthcare providers when injuries occur.

Anatomy and Biomechanics of the ACL

The ACL, one of two cruciate ligaments in the knee, is vital for joint stability. This robust band of connective tissue and collagen fibers originates from the tibial plateau’s anteromedial intercondylar region and extends posterolaterally to the medial aspect of the lateral femoral condyle. Key anatomical landmarks at the femoral attachment include the lateral intercondylar ridge, marking the ACL’s anterior boundary, and the bifurcate ridge, separating the two ACL bundles. The ACL averages 32 mm in length and 7 to 12 mm in width, comprised of two functional bundles: the anteromedial (AM) and posterolateral (PL).

The AM bundle is taut in knee flexion and primarily responsible for anterior tibial translation stability (approximately 85%). The PL bundle tightens in extension, providing secondary restraint and crucial medial-lateral and rotational stability. The ACL boasts a tensile strength of around 2200 N. Working synergistically with the posterior cruciate ligament (PCL), the ACL forms a cross-like structure within the knee, preventing excessive anterior and posterior tibial movement relative to the femur during knee motion. Histologically, the ACL is predominantly type I collagen (90%) with 10% type III collagen. Blood supply comes mainly from the middle geniculate artery, and innervation is via the posterior articular nerve, a branch of the tibial nerve.

Etiology of ACL Tears

Most ACL tears in athletes result from non-contact injuries, particularly pivoting motions where the tibia shifts anteriorly while the knee is slightly flexed and in valgus. Direct blows to the lateral knee can also cause ACL rupture. Athletes at high risk for non-contact ACL injuries include skiers, soccer players, and basketball players, while football players are more susceptible to contact-related ACL injuries.

Acute ACL ruptures can be accompanied by various intra-articular and extra-articular injuries. Meniscal tears are common, with lateral meniscus injuries occurring in over half of acute ACL tears, and medial meniscus injuries being more prevalent in chronic cases. Injuries to the PCL, lateral collateral ligament (LCL), and posterolateral corner (PLC) can also occur with ACL tears. Chronic ACL deficiency can lead to further knee damage, including chondral injuries and complex meniscal tears like bucket handle tears of the medial meniscus.

Epidemiology of ACL Injuries

ACL injuries are the most frequent ligament injury in the knee, accounting for nearly half of all knee injuries. The annual incidence in the United States is roughly 1 in 3,500 people, with approximately 400,000 ACL reconstructions performed annually. However, due to the lack of standardized surveillance, these figures might not fully represent the actual incidence.

While ACL injuries do not show a strong age or gender bias overall, studies suggest women have a higher risk of ACL injury due to several factors. In athletes, the female-to-male ACL injury ratio can be as high as 4.5:1. Female athletes tend to experience ACL ruptures at a younger age and more often in their supporting leg, whereas males more frequently injure their kicking leg.

Several factors contribute to the increased risk in females. Some studies propose that females may have weaker hamstrings, leading to quadriceps dominance and preferential quadriceps recruitment during deceleration. Quadriceps activation while slowing down increases stress on the ACL, as these muscles are less effective at preventing anterior tibial translation compared to hamstrings. Additionally, females often exhibit weaker core stability than males.

Landing biomechanics in females may also elevate ACL injury risk, characterized by increased knee valgus angulation and extension. Video analysis has shown female athletes are more prone to placing their knees in valgus when changing direction suddenly, increasing ACL stress, along with reduced hip and knee flexion and decreased fatigue resistance.

Other risk factors include anatomical factors such as higher body mass index, narrower femoral notch, notch impingement, smaller ACL size, hypermobility, joint laxity, and previous ACL injuries. Specific sports like soccer and basketball are associated with increased risk in females and males, respectively.

Hormonal fluctuations may also affect coordination, particularly during the preovulatory phase of the menstrual cycle. Oral contraceptive pill (OCP) use may mitigate this effect. Estrogen’s influence on ligament strength and flexibility is hypothesized to play a role in injury predisposition, but this remains a debated topic. Genetic factors, such as collagen production genes (like COL5A1), have been linked to lower injury risk in females.

History and Physical Examination for ACL Tears

History

Obtaining a detailed history is crucial in diagnosing ACL tears. Patients often report injury during sports or activities involving sudden directional changes, abrupt stops while running, or awkward landings from jumps. Key historical points include the injury mechanism, timing, patient’s ability to bear weight immediately post-injury, and perceived joint stability.

A classic symptom is hearing or feeling a distinct “pop” at the time of injury, accompanied by intense knee pain. Approximately 70% of patients develop rapid knee swelling due to hemarthrosis. Other common complaints include the knee “giving way,” difficulty walking, and restricted knee range of motion.

Physical Examination

Inspection: Observe the patient’s gait. A quadriceps avoidance gait, where the patient avoids active knee extension, is suggestive of ACL injury. Note any varus knee malalignment, as it increases ACL re-rupture risk and may necessitate knee realignment osteotomy during ACL reconstruction.

Palpation: Palpate the knee for swelling (hemarthrosis) and joint line tenderness, which may indicate a meniscal tear.

Movement: Assess knee range of motion. Locking may occur due to meniscal injuries. Evaluate other knee ligaments and menisci.

Provocative Maneuvers: Several clinical tests assess ACL integrity:

Lachman Test: The most sensitive test for ACL rupture (95% sensitivity, 94% specificity). Performed with the patient supine, knee flexed to about 30 degrees. Stabilize the femur and pull the tibia anteriorly. A positive test shows increased anterior tibial translation without a firm endpoint, indicating ACL rupture. Grading is based on anterior tibial translation: Grade 1 (3-5 mm), Grade 2 (5-10 mm), and Grade 3 (> 10 mm). Always compare to the uninjured knee. Be aware that a PCL tear can cause a false positive Lachman due to posterior tibial subluxation.
Anterior Drawer Test: Patient supine, knee flexed 90 degrees, foot planted. Stabilize the foot. Grip the proximal tibia and pull forward. Excessive anterior tibial translation indicates a positive test. Less sensitive than Lachman in acute injuries but 92% sensitive and 91% specific in chronic injuries. Compare to the unaffected knee.
Pivot Shift Test: Mimics knee giving way. Internally rotate tibia, apply valgus stress, and move knee from extension to flexion. In ACL-deficient knees, the anteriorly subluxated tibia reduces with a “clunk” around 20-30 degrees flexion due to iliotibial band (ITB) tension. Requires intact ITB and MCL, and no knee flexion contracture. Highly specific (98%) but insensitive (24%) due to patient guarding and pain.
Lever Sign Test: Place a fulcrum (e.g., fist) under the proximal calf of a supine patient, apply downward force to the distal thigh (quadriceps). If the ACL is intact, the heel rises off the couch. If torn, the heel remains down.
KT-1000 Arthrometer: Quantifies anterior knee laxity with the knee slightly flexed and externally rotated.

It is crucial to evaluate for associated injuries, such as MCL, LCL, PCL, or meniscal injuries, during the physical exam.

Image alt text: Anatomical illustration of interior ligaments of a left knee, highlighting the anterior cruciate ligament, posterior cruciate ligament, medial meniscus, and lateral meniscus, providing a visual reference for knee joint structures relevant to ACL injuries.

Diagnostic Evaluation of ACL Tears

While clinical examination can strongly suggest an ACL tear, imaging, particularly Magnetic Resonance Imaging (MRI), is often used to confirm the diagnosis.

MRI: The primary imaging modality for ACL pathology, with 86% sensitivity and 95% specificity. MRI confirms ACL tears and identifies associated injuries. Normal ACL fibers appear continuous and steeper than the intercondylar roof. ACL tear signs are primary and secondary.

Primary MRI Signs:
- Sagittal View: Direct ligament injury signs. Increased T2-weighted or proton density signal within the ACL (edema), fiber discontinuity or absence, and altered ACL course (flattened fibers compared to Blumensaat’s line/intercondylar roof). Flattened appearance is common in chronic tears where the ACL scars to the PCL. Tears typically occur in the mid-portion, showing hyperintense signal changes.
- Coronal View: “Empty notch sign” (fluid against the lateral notch wall) or fiber discontinuity.
Secondary MRI Signs: Bone marrow edema (contusion) in over half of ACL tears, typically in the middle third of the lateral femoral condyle and posterior third of the lateral tibial plateau (“ACL bone bruising”). Other signs include Segond fracture, MCL injury, anterior tibial translation > 7mm (lateral view), and tibial spine avulsion fracture.

Radiographs (X-rays): (AP, lateral, skyline/merchant/sunrise views) are not diagnostic for ACL tears but rule out fractures or other bony injuries. They may show effusion or tibial eminence avulsion in younger patients. Non-specific radiographic signs include:

Segond Fracture: Avulsion fracture of the anterolateral proximal tibia at the lateral capsular ligament (anterolateral ligament – ALL) attachment site.
Arcuate Fracture: Proximal fibula avulsion fracture at the LCL/biceps femoris tendon attachment.
Deep Sulcus Terminalis Sign: Depression on the lateral femoral condyle.
Joint Effusion.
Deep Lateral Sulcus Sign: Notch on the lateral femoral condyle (>1.5 mm depth).

Computed Tomography (CT): Not routinely used for ACL diagnosis, CT is only accurate in detecting intact ACLs. CT is valuable for evaluating bone stock in ACL revision surgery planning and is highly sensitive for assessing bone loss from tunnel widening and osteolysis.

Knee Arthroscopy: Can diagnose ACL tears, differentiating complete, partial, and chronic tears. Arthroscopy is highly accurate but invasive and requires anesthesia, making it less common as an initial diagnostic step.

Arthrography: Considered the gold standard (92-100% sensitive, 95-100% specific) but rarely used initially due to invasiveness.

Image alt text: Anatomical drawing of the head of the right tibia, illustrating menisci and ligament attachments, including the anterior cruciate ligament, posterior cruciate ligament, medial meniscus, and lateral meniscus, essential for understanding ACL injury context.

ACL Tear Differential Diagnosis

Accurate diagnosis of ACL tears requires differentiating them from other knee conditions that present with similar symptoms. The differential diagnosis of ACL tears includes:

Posterior Cruciate Ligament (PCL) Injury: PCL injuries can also result from knee trauma, causing pain and instability. However, the mechanism of injury and physical exam findings differ. PCL injuries often occur from direct anterior knee trauma (dashboard injury). The posterior drawer test is positive in PCL tears, while the Lachman and anterior drawer tests are more specific for ACL tears. MRI can clearly distinguish between ACL and PCL injuries.
Medial Collateral Ligament (MCL) Injury: MCL injuries are typically caused by valgus stress to the knee. Patients present with medial knee pain and tenderness. Valgus stress testing is positive in MCL injuries, and the knee may be stable to anterior drawer and Lachman tests unless there is a combined ACL/MCL injury.
Lateral Collateral Ligament (LCL) Injury: LCL injuries result from varus stress and cause lateral knee pain. Varus stress testing is positive. Similar to MCL injuries, ACL tests may be negative unless combined injury.
Meniscal Tear: Meniscal tears, especially medial meniscus tears, can cause pain, swelling, and locking, mimicking ACL tear symptoms. However, meniscal tears typically do not cause gross instability. McMurray’s test and joint line tenderness are more indicative of meniscal injuries. MRI is helpful in differentiating meniscal tears from ACL tears and often reveals both in combined injuries.
Osteochondral Fracture: These fractures involve cartilage and underlying bone damage, often from trauma. Symptoms can include pain, swelling, and sometimes locking. Radiographs might show fractures, and MRI is highly sensitive in detecting osteochondral lesions and differentiating them from ligamentous injuries.
Patellar Dislocation: Patellar dislocation, usually lateral, presents with acute knee pain and deformity. The patella may be visibly displaced. Reduction often occurs spontaneously or with minimal manipulation. Exam findings are distinct from ACL tears, although patellar dislocation can sometimes cause ACL injury.
Tibial Plateau Fracture: Fractures of the tibial plateau are significant bony injuries resulting from high-energy trauma. They cause immediate pain, inability to weight-bear, and swelling. Radiographs and CT scans are essential for diagnosis. While fractures can coexist with ligament injuries, bony injury is the primary concern in tibial plateau fractures.
Epiphyseal Fracture of Femur or Tibia (in children/adolescents): In skeletally immature patients, epiphyseal fractures around the knee can mimic ligament injuries. These fractures involve the growth plate and require careful diagnosis to avoid growth disturbances. Radiographs are crucial in this population.
Tibial Spine Fracture: Avulsion fractures of the tibial spine, where the ACL attaches, are more common in children and adolescents. These can present similarly to ACL tears with positive anterior drawer and Lachman tests. Radiographs can often visualize the avulsed bone fragment. Arthroscopy or MRI may be needed for definitive diagnosis and to assess associated soft tissue injuries.

Image alt text: Arthroscopic view of tibial eminence fracture reduction and internal fixation, demonstrating suture-based fixation of an avulsed tibial spine fragment, illustrating a surgical approach to a differential diagnosis of ACL tears, particularly relevant in pediatric cases.

Treatment and Management of ACL Tears

ACL management is individualized, considering patient factors like age, activity level, sports participation, and associated injuries. Both operative and non-operative treatments are viable options.

Acute Management

Initial treatment follows the “RICE” protocol: Rest, Ice, Compression, and Elevation. Patients should avoid weight-bearing and may need crutches or a wheelchair. Pain can be managed with over-the-counter NSAIDs, as directed by a physician.

Non-operative Management

Non-operative treatment is suitable for patients with low ACL laxity, low physical demands, or partial ACL tears. It involves physiotherapy and lifestyle adjustments. Treatment includes acute symptom management followed by 12 weeks of supervised physical therapy, focusing on range of motion, quadriceps, hamstring, hip abductor, and core strengthening. Serial assessments monitor progress. Functional braces have not shown superior functional stability.

However, non-operative management increases the risk of meniscal and cartilage damage due to recurrent knee instability episodes, especially with high-demand activities (heavy labor, cutting/pivoting sports).

Operative Management

Surgical options are ACL repair or reconstruction.

ACL Reconstruction: Indicated for complete ACL ruptures in active patients (younger or older >40 years). The goal is anatomical ACL reconstruction to restore anterior and rotational knee stability, reducing secondary meniscal or chondral injury risk. Preoperative rehabilitation to regain full range of motion minimizes postoperative arthrofibrosis risk. Reconstruction is also indicated in pediatric cases and for partial ACL tears with functional instability. Return to sports depends on demographic, functional, and psychological factors.

Surgical Technique: Arthroscopically assisted. Graft bed preparation involves complete native ACL remnant removal or stump preservation for tunnel guidance and healing augmentation. Single-bundle reconstruction remains the most common, though double-bundle reconstruction may improve knee kinematics and stability.

Tunnel Placement:

Femoral Tunnel: Transtibial or tibia-independent techniques (inside-out or outside-in). Sagittal plane placement should be within 1-2 mm of the posterior femoral cortex. Coronal plane aims for a more horizontal graft to reduce rotational laxity (2 o’clock position for left knee, 10 o’clock for right knee). Anteromedial and far medial drilling portals facilitate proper positioning. Drilling in >70 degrees flexion prevents posterior wall blowout.
Tibial Tunnel: Sagittal plane landmarks include tunnel center 10-11 mm anterior to PCL anterior border, 6 mm anterior to median eminence, and 9 mm posterior to anterior intermeniscal ligament. Coronal trajectory <75 degrees from horizontal, achieved by starting point midway between tibial tubercle and posterior medial tibial edge.

Graft Fixation: Graft preconditioning reduces stress relaxation. Tensioning at 20 or 40 N shows no clinical outcome differences. Fixation is ideally in 20-30 degrees flexion. Options include aperture/compression fixation (interference screws) and suspensory fixation (cortical buttons, screws, washer posts, staples).

ACL Repair: Resurgence in repair techniques, especially in pediatrics, including dynamic intraligamentary stabilization (DIS), internal brace ligament augmentation (IBLA), and biological enhancement like bridge-enhanced ACL repair (BEAR). 2-year outcomes are comparable to reconstruction in select cases.

ACL Revision: Indicated for failed reconstructions with instability. Identify re-rupture etiology and missed concomitant injuries. Consider stronger grafts (quadriceps tendon, hamstrings, allografts). Allografts in primary reconstruction have a higher re-rupture risk than in revisions. Reharvesting bone-patellar tendon-bone (BPTB) autograft is contraindicated. Combined fixation (aperture and suspensory) may be considered. Bone grafting and staged procedures are needed for significant tunnel dilation (>15mm) or compromised tunnel trajectory. Anterolateral ligament reconstruction or lateral extra-articular tenodesis for added stability is debated. Conservative rehabilitation is crucial post-revision.

Graft Selection:

Quadrupled Hamstring Autograft: Common for primary reconstruction. Contralateral harvest for revisions. Autologous, avoids immune reaction/infection risk. Small incision, less pain, no anterior knee pain like BPTB. Strong graft (~4000 N failure load). Reported decreased peak flexion strength at 3 years and hamstring weakness in females, increasing re-rupture risk. Complications include hamstring weakness, paresthesia (saphenous nerve injury). “Windshield wiper” effect with suspensory fixation can cause tunnel dilation.
Bone-Patellar Tendon-Bone (BPTB) Autograft: Gold standard, autologous, faster bone-bone healing. ~2600 N failure load (intact ACL ~1725 N). Higher anterior knee pain incidence (10-30%), especially kneeling. Patella fracture/tendon rupture risk. Higher re-rupture risk in <20-year-olds and grafts <8 mm.
Quadriceps Tendon Autograft: Incision away from kneeling pressure areas. Physeal sparing in pediatrics. ~2185 N failure load. Pure soft tissue or with patella bone block. Disadvantages similar to hamstring grafts with suspensory fixation.
Allografts: Useful in revisions, no donor site morbidity. More expensive, slower incorporation, disease transmission risk (HIV, hepatitis, etc.).

Graft Processing: Fresh-frozen allografts have lower re-rupture rates than chemically treated or irradiated grafts. Radiation >3 Mrads sterilizes but reduces graft strength. Deep freezing and chlorhexidine gluconate damage cells without affecting graft strength.

Timing of ACL Reconstruction:

Timing depends on multiple factors and associated injuries.

Meniscal Tears: Address concurrently with ACL reconstruction. Meniscal repair during ACL reconstruction has high healing rates.
Chondral Injury: Managed during ACL reconstruction, staged procedures may be needed based on injury and modality. Chondral injuries can compromise long-term outcomes.
MCL Injury: Grade I/II (stable to valgus stress) managed non-operatively pre-ACL reconstruction. Grade III or unstable Grade II requiring repair/reconstruction can be addressed concurrently with ACL reconstruction. Untreated high-grade MCL injury with valgus instability compromises ACL reconstruction, increasing failure rates.
PCL/PLC Injury: Reconstruct concomitantly or staged. Untreated PCL/PLC injuries cause varus instability and ACL graft overload.
Realignment Osteotomy: Limb malalignment (coronal/sagittal) corrected before or during ACL reconstruction. Unmanaged malalignment increases ACL failure risk.

Pediatric ACL Injury and Reconstruction:

Non-operative management for low-demand, compliant children with isolated injuries. Partial ACL tears without instability can be non-operatively managed. Complete tears with instability require surgery. Menarche is a key skeletal maturity indicator in females. Physis is open in children <14 years.

Reconstruction Techniques in Pediatrics: Physeal sparing (all intra-epiphyseal), transphyseal (males ≤13-16, females ≤12-14), or partial transphyseal (leaving one physis undisturbed). No significant growth disturbance differences between techniques. Combined intra- and extra-articular reconstruction for males ≤12, females ≤11. Adult-type reconstruction for males ≥16, females ≥14. Soft tissue grafts in transphyseal approach rarely cause growth issues. Large tunnel diameter (>12mm, >7-9% physeal area) is the most significant physeal injury risk. Other risks: oblique tunnel trajectory, high-speed reaming, aperture fixation, dissection near perichondral ring of LaCroix, suturing near tibial tubercle, lateral extra-articular tenodesis. Overall physeal disruption without growth disturbance reported in ~10% cases.

Prognosis of ACL Tears

ACL-deficient knees are at higher risk of osteoarthritis progression due to further chondral and meniscal injuries. ACL reconstruction effectively restores knee kinematics and enables high rates of return to sports.

Complications of ACL Reconstruction

Complications can be intraoperative or postoperative.

Intraoperative:

Graft Tunnel Mismatch: E.g., BPTB graft too long, causing tibial bone plug prominence and fixation issues. Avoidable with accurate tunnel measurement and graft tailoring.
Tunnel Malpositioning: Femoral vertical tunnel (coronal plane) causes rotational instability. Sagittal anterior misplacement tightens knee in flexion, posterior misplacement tightens in extension. Tibial anterior misplacement tightens flexion and roof impingement, posterior misplacement causes graft impingement on PCL.
Posterior Wall Blowout: Managed with redrilling or suspensory fixation with interference screw.

Postoperative:

Graft Failure: Hardware failure, inadequate fixation, small graft diameter.
Infection/Septic Arthritis: S. epidermidis most common pathogen. Vancomycin graft soaking may reduce risk. Graft contamination during handling is a risk factor. Managed with incision and drainage, antibiotics. Graft retention more likely with S. epidermidis.
Stiffness/Arthrofibrosis: Most common complication, often from preoperative ROM limitations. Prevent with pre-hab, surgery after swelling resolves, precise tunnel placement, cryotherapy, aggressive PT. Lysis of adhesions and manipulation under anesthesia if persistent.
Infrapatellar Contracture Syndrome: Uncommon stiffness cause.
Patella Tendon Rupture: Radiographic patella alta evidence.
Complex Regional Pain Syndrome.
Patella Fracture: BPTB/quadriceps tendon grafts with bone plug. Usually 8-12 weeks post-op.
Tunnel Osteolysis: Observation unless graft laxity or instability occurs.
Osteoarthritis (long-term): Related to associated meniscal injuries. Higher incidence in ACL reconstruction patients >50 years old.
Saphenous Nerve Irritation: Hamstring autograft harvest.
Cyclops Lesion: Fibroproliferative tissue block, click in terminal extension.

Postoperative and Rehabilitation Care

Immediate Postoperative Care: Extensive cryotherapy, weight-bearing as tolerated to reduce patellofemoral pain. Early full passive extension is crucial, especially with MCL injury/patella dislocation.

Early Rehabilitation: Exercises avoiding excessive graft stress. At 3 weeks: eccentric quadriceps strengthening, isometric hamstring/quadriceps contractions, active knee ROM (35-90 degrees), core/gluteal strengthening, closed chain exercises (squats, leg press). Avoid isokinetic quadriceps strengthening (15-30°), open chain quadriceps, leg extensions.

Return to Play: Controversial, no definitive criteria. Historically, no earlier than 9 months post-op. Requires sport-specific activity demonstration and functional test completion (hopping, jumping). Dynamic valgus increases re-rupture risk. Re-rupture rates higher with premature return. Joint decision between surgeon and patient for return to play timing.

Injury Prevention: Neuromuscular training, plyometrics, landing technique training (less valgus, more knee flexion), hamstring strengthening (reduce quadriceps dominance) for female athletes especially.

Advanced Rehabilitation Updates:

Neuromuscular Electrical Stimulation (NMES): 2-6 sessions/week with standard rehab improves quadriceps strength in 4-12 weeks post-op.
Open Kinetic Chain Exercises: No significant differences compared to closed chain exercises in knee laxity, strength, function.
Structured Rehab (In-person vs. Home-based): No superiority of in-person over home-based structured rehab.
Knee Bracing: Not advantageous for knee laxity and function post-ACLR.
Preoperative Rehabilitation: 3-6 weeks of strengthening/neuromuscular stability training improves short-term outcomes but not return to sports.
Cryotherapy with Cold Compression: In first 24-48 hours post-ACLR reduces pain and analgesic use.
Other Interventions (limited evidence): Psychological interventions, whole-body vibration, protein supplements, blood flow restriction training, neuromuscular control exercises, continuous passive motion (low to very low evidence for benefit).

Pearls and Other Issues

Return to activity is variable, typically 6-12 months post-reconstruction, potentially up to 18 months for full graft incorporation. Premature return increases re-injury risk.

Enhancing Healthcare Team Outcomes

Optimal ACL management involves an interprofessional team: ED clinicians, orthopedic surgeons, sports clinicians, nurses, and physical therapists. Initial treatment is RICE. Management can be non-operative or operative. Orthopedic surgeon referral and physical therapy are essential. Orthopedic nurses coordinate care and provide patient education. Recovery takes 3-9 months of intensive PT with good overall outcomes.

Review Questions

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References

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Disclosures: