Updated: Jul 9, 2008
Medial collateral ligament (MCL) and lateral collateral ligament (LCL) injuries of the knee are common. In fact, injury to the MCL is the most common ligamentous knee injury.
The MCL and LCL provide restraint to valgus and varus angulation of the knee, respectively. The MCL has superficial and deep components. The superficial MCL fibers attach proximally to the medial femoral epicondyle and distally to the medial aspect of the tibia, approximately 4 cm distal to the joint line. The deep MCL fibers originate from the medial joint capsule and are attached to the medial meniscus.
The LCL is part of a complex of ligaments collectively named the posterolateral corner (PC). The structures in the PC include the LCL, the popliteofibular ligament, the popliteus ligament, the arcuate ligament, the short lateral ligament, and the posterolateral joint capsule. The LCL is separated from the lateral meniscus by a fat pad (see Image 1).1,2,3,4
Related eMedicine topics:
Collateral Ligament Pathology, Knee
Knee, Collateral Ligament Injuries (MRI)
Lateral Collateral Knee Ligament Injury
Medial Collateral Knee Ligament Injury
Related Medscape topic:
Resource Center Joint Disorders
Medial collateral ligament (MCL) and lateral collateral ligament (LCL) injuries are caused primarily by valgus and varus stress (respectively) to the knee joint. Injuries also can occur to both ligaments with excessive lateral rotation of the knee.
The annual incidence of acute knee injury in the United States is estimated to be 300 cases per 100,000 population. Collateral ligament injuries account for 25% of patients presenting to emergency rooms with acute knee injury. Peak incidence of collateral ligament injuries occurs in adults aged 20-34 years. The National Collegiate Athletic Association (NCAA) injury surveillance system reported 2.1 medial or lateral collateral injuries per 1000 player exposures in games across all NCAA sports over 1 year.5 Even noncontact sports, such as gymnastics and swimming, can lead to collateral ligament injuries.6
Medial collateral ligament (MCL) and lateral collateral ligament (LCL) injuries can in most individuals be treated successfully with conservative methods. Severe injuries may require surgical intervention and tend to have good outcomes.2,7
There is no known racial predilection for medial collateral ligament (MCL) and lateral collateral ligament (LCL) injuries.
Unlike anterior cruciate ligament (ACL) injuries, which occur at a higher rate in women, medial collateral ligament (MCL) and lateral collateral ligament (LCL) injuries occur at equal rates in men and women.6,8
Related eMedicine articles:
Anterior Cruciate Ligament Pathology
Anterior Cruciate Ligament Injury [Physical Medicine and Rehabilitation]
Anterior Cruciate Ligament Injury [Sports Medicine]
Knee, Anterior Cruciate Ligament Injuries (MRI)
Age patterns for medial collateral ligament (MCL) and lateral collateral ligament (LCL) injuries are bimodal, with the highest incidence rates found in individuals aged 20-34 years and in persons aged 55-65 years. Nonetheless, MCL and LCL injuries can occur at any age.
Listen to the patient's description of the injury event. The force vector of injury to the knee indicates the most likely site of pathology.9 For example, a football player who complains of medial knee pain after a valgus stress on the knee is likely to have an injury to the medial collateral ligament (MCL). Have the patient use the uninjured knee to explain precisely what he/she was doing when the incident occurred.
Recognize that collateral ligament injuries often are seen in association with injury to other knee structures. A comprehensive musculoskeletal knee examination should be completed to direct further diagnostic testing and therapeutic interventions. A systematic review of the available literature revealed no articles that adequately assessed the diagnostic sensitivity and specificity of a physical examination in detecting medial and lateral collateral ligamentous injuries.
Patellofemoral Syndrome
Pes Anserinus Bursitis
Rheumatoid Arthritis
Tibial Plateau Fractures
Osteochondral fracture
Extensor mechanism rupture
Osteonecrosis of the femoral epicondyle
Osteonecrosis of the tibial condyle
Inflammatory conditions (systemic disease)
All MCL 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:
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.15,16 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.17 A technique for repairing severe MCL injuries using autogenous hamstring tendons has been proposed.18
An orthopedic surgery consultation is advised for individuals with severe ligament injury.
The goal of pharmacotherapy is to reduce morbidity.
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.
DOC for patients with mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.
400 mg PO q4-6h prn; not to exceed 2400 mg/d; take with food
4-10 mg/kg PO q6-8h prn; not to exceed 50 mg/kg/d; take with food
Co-administration with aspirin increases risk of inducing serious NSAID-related side effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; history of GI bleeding
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy
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.
200 mg/d PO qd; alternatively, 100 mg PO bid
Not recommended
CYP450 2C9 substrate; co-administration with fluconazole may cause increase in celecoxib plasma concentrations because of inhibition of celecoxib metabolism; co-administration of celecoxib with rifampin may decrease celecoxib plasma concentrations
Documented hypersensitivity
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.
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.
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
Not established
Significantly decreases carbamazepine effects; cimetidine increases toxicity, risk of serotonin syndrome with co-administration of antidepressants
Documented hypersensitivity; opioid-dependent patients; concurrent use of MAOI or within 14 days; use of SSRIs, TCAs, or opioids; acute alcohol intoxication
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Can cause dizziness, nausea, constipation, sweating, and pruritus; additive sedation with alcohol and TCAs; abrupt discontinuation can precipitate opioid withdrawal symptoms; adjust dose in liver disease, myxedema, hypothyroidism, and hypo-adrenalism; pregnancy and breastfeeding; seizure; and development of tolerance or dependency with extended use
Fu FH, Harner CD, Johnson DL, et al. Biomechanics of knee ligaments: basic concepts and clinical application. Instr Course Lect. 1994;43:137-48. [Medline].
Swenson TM, Harner CD. Knee ligament and meniscal injuries. Current concepts. Orthop Clin North Am. Jul 1995;26(3):529-46. [Medline].
Young JL, Olsen NK, Press JM. Musculoskeletal disorders of the lower limbs. In: Braddom RL, ed. Physical Medicine and Rehabilitation. Philadelphia, Pa: WB Saunders; 1996:783-812.
Amiri S, Cooke D, Kim IY, et al. Mechanics of the passive knee joint. Part 2: interaction between the ligaments and the articular surfaces in guiding the joint motion. Proc Inst Mech Eng [H]. Nov 2007;221(8):821-32. [Medline].
National Collegiate Athletic Association. NCAA Injury Surveillance System. 1999-2000;[Full Text].
Yawn BP, Amadio P, Harmsen WS, et al. Isolated acute knee injuries in the general population. J Trauma. Apr 2000;48(4):716-23. [Medline].
Quarles JD, Hosey RG. Medial and lateral collateral injuries: prognosis and treatment. Prim Care. Dec 2004;31(4):957-75, ix. [Medline].
Dugan SA. Sports-related knee injuries in female athletes: what gives?. Am J Phys Med Rehabil. Feb 2005;84(2):122-30. [Medline].
El-Dieb A, Yu JS, Huang GS, et al. Pathologic conditions of the ligaments and tendons of the knee. Radiol Clin North Am. Sep 2002;40(5):1061-79. [Medline].
Pimentel L. Orthopedic trauma: office management of major joint injury. Med Clin North Am. Mar 2006;90(2):355-82. [Medline].
Strayer RJ, Lang ES. Evidence-based emergency medicine/systematic review abstract. Does this patient have a torn meniscus or ligament of the knee?. Ann Emerg Med. May 2006;47(5):499-501. [Medline].
Crotty JM, Monu JU, Pope TL Jr. Magnetic resonance imaging of the musculoskeletal system. Part 4. The knee. Clin Orthop Relat Res. Sep 1996;288-303. [Medline].
Beall DP, Googe JD, Moss JT, et al. Magnetic resonance imaging of the collateral ligaments and the anatomic quadrants of the knee. Radiol Clin North Am. Nov 2007;45(6):983-1002, vi. [Medline].
Hastings DE. The non-operative management of collateral ligament injuries of the knee joint. Clin Orthop. Mar-Apr 1980;(147):22-8. [Medline].
Bin SI, Nam TS. Surgical outcome of 2-stage management of multiple knee ligament injuries after knee dislocation. Arthroscopy. Oct 2007;23(10):1066-72. [Medline].
Wahl CJ, Nicandri G. Single-Achilles allograft posterior cruciate ligament and medial collateral ligament reconstruction: a technique to avoid osseous tunnel intersection, improve construct stiffness, and save on allograft utilization. Arthroscopy. Apr 2008;24(4):486-9. [Medline].
Medvecky MJ, Zazulak BT, Hewett TE. A multidisciplinary approach to the evaluation, reconstruction and rehabilitation of the multi-ligament injured athlete. Sports Med. 2007;37(2):169-87. [Medline].
Yoshiya S, Kuroda R, Mizuno K, et al. Medial collateral ligament reconstruction using autogenous hamstring tendons: technique and results in initial cases. Am J Sports Med. Sep 2005;33(9):1380-5. [Medline].
medial collateral ligament injury, lateral collateral ligament injury, MCL injury, LCL injury, tibial collateral ligament, fibular collateral ligament
Adam B Agranoff, MD, Physiatrist and Partner, Chelsea Back Care, Chelsea Community Hospital
Adam B Agranoff, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation and North American Spine Society
Disclosure: Nothing to disclose.
Robert J Kaplan, MD, Associate Professor, Department of Physical Medicine and Rehabilitation, University of Kansas School of Medicine and Medical Center
Robert J Kaplan, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, Association of Academic Physiatrists, International Spine Intervention Society, and Physiatric Association of Spine, Sports and Occupational Rehabilitation
Disclosure: Nothing to disclose.
Robert E Windsor, MD, FAAPMR, FAAEM, FAAPM, President and Director, Georgia Pain Physicians, PC; Clinical Associate Professor, Department of Physical Medicine and Rehabilitation, Emory University School of Medicine
Robert E Windsor, MD, FAAPMR, FAAEM, FAAPM is a member of the following medical societies: American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American College of Sports Medicine, American Medical Association, International Association for the Study of Pain, Physiatric Association of Spine, Sports and Occupational Rehabilitation, and Texas Medical Association
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.
Michael T Andary, MD, MS, Residency Program Director, Professor, Department of Physical Medicine and Rehabilitation, Michigan State University College of Osteopathic Medicine
Michael T Andary, MD, MS is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American Medical Association, and Association of Academic Physiatrists
Disclosure: allergan Honoraria Speaking and teaching
Kelly L Allen, MD, Consulting Staff, Department of Physical Medicine and Rehabilitation, Lourdes Regional Rehabilitation Center, Our Lady of Lourdes Medical Center
Disclosure: Nothing to disclose.
Consuelo T Lorenzo, MD, Consulting Staff, Department of Physical Medicine and Rehabilitation, Alegent Health Care, Immanuel Rehabilitation Center
Consuelo T Lorenzo, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation
Disclosure: Nothing to disclose.
© 1994-
by Medscape.
All Rights Reserved
(http://www.medscape.com/public/copyright)