Lateral collateral ligament (LCL) injuries occur from a varus force to the knee (ie, a force directed at the medial side of the knee or leg).

These injuries are much less common than medial collateral ligament (MCL) injuries because the opposite leg usually guards against direct blows to the medial side of the knee. 

However, LCL injuries can occur in situations in which trauma occurs as the leg is extended in front of the body, such as when attempting to gain control of the ball from another player in soccer or rugby (eg, tackling).


The LCL is a round ligament that lies beneath the tendon of the biceps femoris muscle and runs from the lateral epicondyle, anterior to the origin of the gastrocnemius muscle, to the fibular head.

The LCL lies just posterior to mid-axial point of the knee and is the primary restraint to varus stress in the knee.



v  The mechanism of injury is the most important component of the patient history to determine the possible injured structures. Direct contact to the anteromedial aspect of the tibia is the most likely cause of injury to the LCL.

v  Ascertain whether the patient noted any effusion within a few hours following the incident. One should not expect a significant joint effusion unless there also is a cruciate ligament or meniscal tear. It is also important to determine whether the individual felt or heard a pop in the knee, as this may suggest a concomitant injury.

v  Inquire about previous knee symptoms, injuries, or surgeries.

v  Discuss and obtain the patient's age, occupation, recreational activities, lifestyle, and interests to help determine the proper course of treatment.

v  A more concerning injury is one that involves the posterior lateral complex. The most important structures in this complex include the iliotibial tract, long and short head of the biceps femoris muscle, fibular collateral ligament, posterior arcuate ligaments, and the posterior capsule. The peroneal nerve can also be injured because of its proximity to the biceps tendon; this type of injury requires extensive surgical repair because of the complex structures involved. The surgery should be individualized to each patient and his or her specific injuries.

  • Examine the injured extremity.
    • Inspect the leg for gross abnormalities, skin abrasions, and other signs.
    • Inspect and palpate the suprapatellar pouch for effusion.
    • Palpate for joint-line tenderness.
    • Perform special tests for LCL stability: Varus stress occurs at 0° and 30° of flexion. The LCL is isolated at 30°; testing at 0° also evaluates the posterolateral corner structures and cruciate ligaments.
    • Physical examination clues of posterolateral injury include footdrop, peroneal nerve injury, tenderness in the posterolateral corner, and pain with posterior-internal rotation of the tibia. 
    • Assess the cruciate ligaments and the menisci.
    • Evaluate for effusion.
    • Examine the uninvolved extremity. Compare the alignment, motion, swelling, and ligamentous stability of the affected limb with the injured extremity.
  • Grade the degree of the LCL injury according to the following :
    • Grade 1 – Interstitial injury without laxity is present, but there is pain with varus stress; only microscopic tearing has occurred.
    • Grade 2 – A 5-10 mm of joint-space opening with a distinct end point is noted; partial macroscopic tearing has occurred.
    • Grade 3 – Complete tearing (>10 mm joint-space opening) has occurred; complete macroscopic tearing is noted.


  • LCL injury is caused by a direct blow to the medial aspect of the knee or the anterior medial tibia with the foot planted and the knee in various degrees of flexion.
  • An LCL injury should not be confused with other overuse lateral knee injuries (eg, iliotibial band syndrome, biceps femoris tendinitis).


Physical Therapy

The type of physical therapy (PT) treatment indicated for a medial collateral ligament (LCL) injury depends on the severity of the injury.

Recommendations for treatment of LCL Injury include the following:

  • Grade I - Compression, elevation, and cryotherapy are recommended. Short-term use of crutches may be indicated, with weight-bearing–as–tolerated (WBAT) ambulation. Early ambulation is recommended.
  • Grade II - A short-hinged brace that blocks 20º of terminal extension but allows full flexion should be used. The patient may ambulate, WBAT. Closed-chain exercises allow for strengthening of knee musculature without putting stress on the ligaments.
  • Grade III - The patient initially should be non–weight-bearing (NWB) on the affected lower extremity. A hinged braced should be used, with gradual progression to full weight-bearing (FWB) over 4 weeks. Grade III injuries may require 8-12 weeks to heal.

All LCL injuries should be treated with early range of motion (ROM) and strengthening of musculature that stabilizes the knee joint.

Conservative measures usually are adequate, but, if the patient fails to progress with treatment, a meniscal or cruciate ligament tear is suggested.

Lateral collateral ligament (LCL) injuries heal more slowly than do MCL injuries, due to the difference in collagen density.

Recommendations for the treatment of LCL injuries include the following:

  • Grades I and II - These injuries are treated according to a regimen similar to that for MCL injuries of the same severity. A hinged brace is used for 4-6 weeks.
Grade III - Severe LCL injuries typically are treated surgically due to rotational instability, because they usually involve the posterolateral corner of the knee. Patients may require bracing and physical therapy for up to 3 months in order to prevent later instability.
Surgical Intervention
Most patients with a collateral ligament injury can be treated effectively with conservative measures.

Grade III lateral collateral ligament (LCL) tears usually involve the posterolateral complex and are associated with instability. These patients do require surgical repair.

Surgical treatment for isolated injuries of the medial collateral ligament (MCL) or LCL is a controversial topic.

The treatment plan should be based partially on the patient's pre-injury level of activity and on motivational factors.

For example, a young competitive swimmer may want surgery, followed by a comprehensive rehabilitation program to accelerate the time needed for adequate functional recovery.

A technique for repairing severe MCL injuries using autogenous hamstring tendons has been proposed. 


The goal of pharmacotherapy is to reduce morbidity.

Nonsteroidal anti-inflammatory drugs

These have analgesic, anti-inflammatory, and antipyretic activity. Their mechanism of action is not known, but they may inhibit cyclo-oxygenase activity and prostaglandin synthesis.

Other mechanisms may exist as well, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell-membrane functions.

Ibuprofen (Motrin, Ibuprin)

DOC for patients with mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.

Adult: 400 mg PO q4-6h prn; not to exceed 2400 mg/d; take with food

Pediatric: 4-10 mg/kg PO q6-8h prn; not to exceed 50 mg/kg/d; take with food

Celecoxib (Celebrex)

Primarily inhibits COX-2. COX-2 is considered an inducible iso-enzyme; it is induced by pain and inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity.

At therapeutic concentrations, COX-1 iso-enzyme is not inhibited; thus, incidence of GI toxicity, such as endoscopic peptic ulcers, bleeding ulcers, perforations, and obstructions, may be decreased when compared with nonselective NSAIDs. Seek lowest dose for each patient.

Neutralizes circulating myelin antibodies through anti-idiotypic antibodies; down-regulates pro-inflammatory cytokines, including INF-gamma; blocks Fc receptors on macrophages; suppresses inducer T and B cells and augments suppressor T cells; blocks complement cascade; promotes remyelination; may increase CSF IgG (10%).

Has a sulfonamide chain and is primarily dependent on cytochrome P450 enzymes (a hepatic enzyme) for metabolism.

Adult: 200 mg/d PO qd; alternatively, 100 mg PO bid


C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus


May cause fluid retention and peripheral edema; caution in compromised cardiac function, hypertension, conditions predisposing to fluid retention; caution in severe heart failure and hyponatremia because may deteriorate circulatory hemodynamics; NSAIDs may mask usual signs of infection; caution in the presence of existing controlled infections; evaluate therapy when symptoms or lab results suggest liver dysfunction


Pain control is essential to quality patient care. Analgesics ensure patient comfort, promote pulmonary toilet, and have sedating properties, which are beneficial for patients who have sustained trauma or injuries.

Tramadol (Ultram)

Inhibits ascending pain pathways by binding to mu-opiate receptors in CNS, thus altering perception of and response to pain. Also inhibits re-uptake of norepinephrine and serotonin.

Adult: 50 mg/d PO initially; gradually increase by 50 mg/d PO q3d to 50-100 mg PO q4-6h prn; not to exceed 400 mg/d.