Anterior Cruciate Ligament Injury

• Mechanism: usually non-contact — sudden deceleration, pivoting or landing with the knee near extension in valgus with external rotation. Female athletes have a several-fold higher incidence.
• History: an audible or felt "pop", immediate giving way, inability to continue play, and rapid knee swelling within a few hours — a haemarthrosis, which distinguishes it from the slower effusion of a meniscal tear.
• Examination:
• Lachman test — the most sensitive, performed at 20–30° of flexion.
• Anterior drawer — at 90°, less sensitive acutely because hamstring spasm guards the joint.
• Pivot shift — the most specific, often needing relaxation or anaesthesia.
• Associated injuries: the "unhappy triad" is classically ACL, medial collateral ligament and meniscus. Note that modern series find the lateral meniscus involved at least as often as the medial in acute ACL tears, despite the traditional teaching.
• Imaging: radiographs to exclude fracture (a Segond fracture — lateral tibial rim avulsion — is highly associated); MRI confirms the tear and defines meniscal and chondral injury.
• Management: reconstruction is favoured for young, active or pivoting-sport patients and where instability persists; structured rehabilitation is reasonable for lower-demand patients. Either path depends heavily on quadriceps and hamstring rehabilitation.

Mechanisms of injury

• Non-contact deceleration/pivot (the majority): planting the foot and cutting, or landing from a jump with the knee near extension, the hip adducted and internally rotated — dynamic valgus collapse. Quadriceps contraction near full extension pulls the tibia anteriorly, loading the ACL directly.
• Contact valgus ("clipping" blow to the lateral knee): produces the combined ACL–MCL–meniscal injury pattern described in the overview.
• Hyperextension / hyperflexion: skiing falls, where a fixed boot creates a boot-induced anterior drawer, or forced hyperextension in football.
• High-energy multiligament injury: knee dislocation with ACL, PCL and collateral disruption — a different, limb-threatening entity.

Non-modifiable risk factors

• Female sex: several-fold higher incidence at equivalent exposure. Contributors include a narrower intercondylar notch, a smaller ACL cross-sectional area, greater generalised ligamentous laxity, and a landing strategy that is more quadriceps-dominant with greater knee valgus.
• Increased posterior tibial slope and small notch width: both increase anterior shear on the ligament.
• Prior ipsilateral ACL tear or contralateral tear, and family history: among the strongest predictors of a subsequent tear.
• Skeletal immaturity: shifts the failure point to a tibial spine avulsion rather than a mid-substance tear.

Modifiable risk factors

• Poor neuromuscular control: low hamstring-to-quadriceps strength ratio, weak hip abductors/external rotators, and stiff, knee-valgus landing mechanics. These are the targets of prevention programmes.
• Fatigue and late-game play: proprioceptive and eccentric control deteriorate.
• Sport and playing surface: soccer, basketball, football and skiing dominate; high shoe–surface friction (cleat design, artificial turf) increases torsional load.
• Elevated BMI and inadequate pre-season conditioning.

• Anatomy dictates the exam findings: the ACL runs from the posteromedial aspect of the lateral femoral condyle to the anterior intercondylar tibia, with an anteromedial bundle (taut in flexion) and a posterolateral bundle (taut in extension). Loss of the ligament removes the primary restraint to anterior tibial translation and a secondary restraint to internal rotation.
• Why Lachman beats the anterior drawer: at 20–30° of flexion the hamstrings are relaxed and the anteromedial bundle is the dominant restraint, so translation is unmasked. At 90° the hamstrings act as dynamic secondary restraints and acute spasm guards the joint, blunting the drawer.
• Why the pivot shift occurs: with the ACL gone, the tibia subluxes anteriorly and internally rotates in near-extension. As the knee is flexed past roughly 20–30°, the iliotibial band converts from an extensor to a flexor and abruptly reduces the plateau — the palpable clunk of anterolateral rotatory instability.
• Why the swelling is fast: the ACL is vascularised by the middle geniculate artery and is intra-articular. Rupture bleeds directly into a closed synovial space, producing a tense haemarthrosis within hours, in contrast to the reactive, slower effusion of an isolated meniscal tear.
• Why it does not heal: the ligament is intra-synovial and extra-fascicular. Synovial fluid lyses the fibrin clot that would otherwise scaffold repair, so the torn ends retract and resorb rather than bridging — the reason surgery is reconstruction with a graft rather than suture repair.
• Why instability persists after pain resolves: the ACL is densely populated with Ruffini endings and Pacinian corpuscles feeding hamstring reflex arcs. Loss of this afferent input produces proprioceptive deficit and giving way on cutting, independent of static laxity.
• Why associated damage occurs: the subluxation event drives the lateral femoral condyle against the posterolateral tibial plateau (the MRI kissing contusions), shears the menisci, and may avulse the anterolateral capsule from the lateral tibial rim as a Segond fracture.

Acute symptoms

• Audible or felt "pop" at the moment of injury, from sudden ligament failure under tension.
• Immediate disability: unable to continue play, unlike the athlete who limps through a meniscal tear.
• Rapid tense swelling over 1–4 hours — haemarthrosis from the ruptured middle geniculate supply. A knee that swells the next morning is more suggestive of meniscal or capsular injury.
• Deep, diffuse pain and a sense of the knee "coming apart", reflecting the subluxation–reduction event rather than a focal tender point.

Subacute and chronic symptoms

• Giving way on pivoting or descending stairs, from combined mechanical instability and lost mechanoreceptor feedback.
• Quadriceps atrophy within weeks, driven by arthrogenic muscle inhibition — effusion-mediated reflex shutdown of the quadriceps.
• Recurrent effusions and, later, mechanical symptoms if a secondary meniscal tear develops.

Examination findings and their mechanisms

• Large tense effusion with a positive ballottement/patellar tap and reduced range of motion; guarding limits the anterior drawer acutely.
• Lachman grading: grade I 0–5 mm, II 6–10 mm, III >10 mm of translation; the quality of the endpoint (soft or absent versus firm) matters as much as the excursion.
• Pivot shift: graded from a glide to a gross clunk; frequently negative in a guarded awake patient and most reliable under anaesthesia.
• Fixed loss of terminal extension with a springy block suggests a displaced bucket-handle meniscal tear, not simply pain-related stiffness.
• Always co-examine: valgus stress at 30° for MCL, posterior sag and posterior drawer for PCL, joint-line tenderness and McMurray for meniscus, and distal pulses plus common peroneal and tibial nerve function if a multiligament injury or dislocation is suspected.

• Segond fracture: elliptical avulsion off the lateral tibial rim — near-pathognomonic for ACL rupture.
• Tibial eminence (spine) avulsion: the skeletally immature equivalent of a mid-substance tear.
• Deep lateral femoral notch sign and lipohaemarthrosis on a cross-table lateral (fat–fluid level signals an intra-articular fracture).

• Discontinuous or abnormally horizontal ACL fibres with an empty lateral wall of the notch.
• Bone marrow oedema in the lateral femoral condyle (sulcus terminalis) and posterolateral tibial plateau — the kissing contusions of the pivot event.
• Secondary signs: anterior tibial translation, buckling of the PCL, and associated meniscal, MCL or chondral injury that changes the operative plan.

Immediate/acute phase

• Protection, ice, compression, elevation, and crutches with weight bearing as tolerated; a hinged knee brace for comfort and control.
• Analgesia: acetaminophen and a short course of an oral NSAID (for example ibuprofen). Opioids are rarely needed and are discouraged for musculoskeletal pain.
• Early physical therapy focused on restoring full extension, resolving effusion and reactivating the quadriceps. This is not filler — operating on a stiff, inflamed knee is the main modifiable risk factor for postoperative arthrofibrosis.
• Urgent orthopaedic referral if there is a locked knee (displaced bucket-handle tear), a multiligament injury or suspected knee dislocation, or an open injury.

Surgical specifics

• Arthroscopic reconstruction with a graft, not primary suture repair, because the intrasynovial ligament will not heal.
• Autograft (bone–patellar tendon–bone, hamstring, or quadriceps tendon) is favoured in young athletes; AAOS notes higher graft failure rates with allograft in this population, though allograft remains reasonable in older or lower-demand patients.
• Skeletally immature patients: physeal-sparing or transphyseal techniques to avoid growth arrest and angular deformity; tibial spine avulsions are fixed rather than reconstructed.
• Return to sport is criterion-based — quadriceps strength symmetry, hop testing and psychological readiness — typically not before nine to twelve months, since earlier return correlates with re-tear.

Of the injury itself

• Post-traumatic osteoarthritis: the dominant long-term outcome, driven by the initial chondral impact (the kissing contusions), meniscal loss and altered kinematics. Reconstruction restores stability but has not been shown to abolish this risk.
• Secondary meniscal and chondral injury: repeated giving-way episodes shear the menisci — the reason a chronically unstable knee accrues damage. Signals: new locking, catching or joint-line pain.
• Chronic instability and quadriceps atrophy from arthrogenic muscle inhibition and proprioceptive loss.
• Missed multiligament injury/knee dislocation — an emergency. Popliteal artery disruption or intimal tear may present with a normal-appearing foot initially; check ankle–brachial index and obtain CT angiography if abnormal. Common peroneal nerve palsy causes foot drop.
• Acute compartment syndrome with high-energy injury — pain out of proportion, pain on passive stretch: an emergency.

Of treatment

• **Arthrofibrosis and *cyclops lesion***: fibroproliferative nodule at the graft base causing a hard block to terminal extension; risk rises with surgery on a stiff, inflamed knee.
• Graft failure/re-rupture: highest in young patients returning to pivoting sport, with allograft, and with early return. Presents as recurrent giving way with a recurrent positive Lachman.
• Donor-site morbidity: bone–patellar tendon–bone grafts cause anterior knee pain, pain with kneeling, and rarely patellar fracture or patellar tendon rupture; hamstring grafts cause residual flexion/deep-flexion weakness.
• Numbness lateral to the incision from injury to the infrapatellar branch of the saphenous nerve — common and usually benign.
• Septic arthritis — an emergency: fever, escalating pain, warm tense effusion; aspirate and take to theatre for irrigation with graft retention where possible.
• Venous thromboembolism after arthroscopy, and physeal arrest with limb-length or angular deformity in the skeletally immature.

• Haemarthrosis within hours after a non-contact pivot = ACL until proven otherwise. ACL rupture is the single most common cause of acute traumatic knee haemarthrosis; a slow effusion appearing the next day points to meniscus.
• Lachman is the most sensitive test; pivot shift is the most specific. The anterior drawer is the classic distractor — it underperforms acutely because hamstring spasm guards the joint at 90°.
• Best next step after the history and exam is a plain radiograph (guided by the Ottawa Knee Rules) to exclude fracture, then MRI to confirm the tear and stage meniscal/chondral injury. MRI is not the first step, and a normal radiograph never excludes an ACL tear.
• **The *Segond fracture* — a small avulsion off the lateral tibial rim — is the association examiners love: it is highly predictive of ACL rupture. In a child, look instead for a tibial spine avulsion**.
• Kissing bone contusions of the lateral femoral condyle and posterolateral tibial plateau on MRI are the radiologic footprint of the pivot-subluxation event.
• Unhappy triad caveat: the classic teaching is ACL + MCL + medial meniscus, but modern series find the lateral meniscus torn at least as often acutely. Know both versions.
• Posterior sag sign or a dashboard injury is PCL, not ACL — the most common wrong answer in a knee-trauma stem.
• Surgery is reconstruction with a graft, never primary suture repair, because the intrasynovial ligament cannot form a healing clot; autograft is preferred in young athletes per the AAOS guideline, and neuromuscular training programmes are the evidence-based way to prevent the injury in the first place.