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Lateral Collateral Knee Ligament Injury: Treatment & Medication
Updated: Oct 2, 2007
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
Treatment
Acute Phase
Rehabilitation Program
Physical Therapy
For grade I and II LCL injuries, the suggested treatment includes rest, ice, compression, elevation (RICE), and non–weight-bearing restriction with the use of crutches. Hinged bracing may also be helpful. Grade III injuries, those usually involving a tear of posterolateral capsular complex, are best treated with surgical intervention.4 A return to full-weight-bearing gait should be gradual over the course of 4 weeks.
Surgical Intervention
Grade III tears usually involve a tear in the posterolateral capsular complex and are best treated with surgical intervention.4
Recovery Phase
Rehabilitation Program
Physical Therapy
Physical therapy consists of early range-of-motion (ROM) exercises, particularly cycling and quadriceps-strengthening exercises.
Medication
Short-term use of nonsteroidal anti-inflammatory drugs (NSAIDs) is acceptable for treating the symptoms of LCL injury.
Nonsteroidal anti-inflammatory agents (NSAIDs)
Although most NSAIDs are used primarily for their anti-inflammatory effects, they are effective analgesics and are useful for the relief of mild to moderate pain. Any prescription-strength NSAID can be effective. For patients who cannot tolerate the early-generation NSAIDs because of gastrointestinal (GI) intolerance, they may benefit from cyclooxygenase-2 (COX-2) inhibitors (eg, celecoxib [Celebrex], Pfizer Inc, New York, NY).
Ibuprofen (Motrin, Ibuprin, Advil)
DOC for patients with mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.
Adult
800 mg PO tid q8h
Pediatric
Not established
Coadministration with aspirin increases the risk of inducing serious NSAID-related side effects; probenecid may increase the concentrations and, possibly, toxicity of NSAIDs; may decrease the effect of hydralazine, captopril, and beta-blockers; may decrease the diuretic effects of furosemide and thiazides; may increase duration of PT when the patient is taking anticoagulants (instruct patients to watch for signs of bleeding); may increase the risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; peptic ulcer disease, recent GI bleeding or perforation, renal insufficiency, or high risk of bleeding
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Category D in third trimester of pregnancy; caution in patients with congestive heart failure, hypertension, and decreased renal and hepatic function; caution in patients with anticoagulation abnormalities or who are administered anticoagulant therapy
Diclofenac (Voltaren)
Inhibits prostaglandin synthesis by decreasing activity of enzyme cyclooxygenase, which in turn decreases formation of prostaglandin precursors.
Adult
50 mg PO bid
Pediatric
Not established
Coadministration with aspirin increases the risk of inducing serious NSAID-related side effects; probenecid may increase the concentrations and, possibly, toxicity of NSAIDs; may decrease the effect of hydralazine, captopril, and beta-blockers; may decrease the diuretic effects of furosemide and thiazides; may increase duration of PT when patients are taking anticoagulants (instruct patients to watch for signs of bleeding); may increase the risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; do not administer into CNS or give to patients with peptic ulcer disease, recent GI bleeding or perforation, renal insufficiency, and those at high risk of bleeding
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Category D in third trimester of pregnancy; acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases the risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; low white blood cell counts occur rarely and usually return to normal in ongoing therapy; discontinuation of therapy may be necessary if there is persistent leukopenia, granulocytopenia, or thrombocytopenia
Sulindac (Clinoril)
Decreases activity of cyclooxygenase and in turn inhibits prostaglandin synthesis. Results in a decreased formation of inflammatory mediators.
Adult
200 mg PO bid
Pediatric
Not established
Coadministration with aspirin increases the risk of inducing serious NSAID-related side effects; probenecid may increase the concentrations and, possibly, toxicity of NSAIDs; may decrease the effect of hydralazine, captopril, and beta-blockers; may decrease the diuretic effects of furosemide and thiazides; may increase duration of PT when patients are taking anticoagulants (instruct patients to watch for signs of bleeding); may increase the risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; patients in whom aspirin, iodides or other NSAIDS induce hypersensitivity; GI bleed, and renal insufficiency
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Category D in third trimester of pregnancy; acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases the risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; low white blood cell counts occur rarely and usually return to normal in ongoing therapy; discontinuation of therapy may be necessary if there is persistent leukopenia, granulocytopenia, or thrombocytopenia; caution in patients with anticoagulation defects or who are receiving anticoagulant therapy
COX-2 Inhibitors
Although increased cost can be a negative factor, the incidence of costly and potentially fatal GI bleeding is clearly less with COX-2 inhibitors than with traditional NSAIDs. Ongoing analysis of the cost avoidance of GI bleeds further defines the populations that will find COX-2 inhibitors the most beneficial.
Celecoxib (Celebrex)
Inhibits primarily COX-2. COX-2 is considered an inducible isoenzyme that is induced during pain and inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited; thus, GI toxicity may be decreased. Seek lowest dose of celecoxib for each patient.
Adult
200 mg PO qd
Pediatric
Not established
Coadministration with fluconazole may cause an increase in celecoxib plasma concentrations because of inhibition of the celecoxib metabolism; coadministration of celecoxib with rifampin may decrease celecoxib plasma concentrations
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
May cause fluid retention and peripheral edema; caution in patients with compromised cardiac function, hypertension, conditions predisposing to fluid retention; caution in patients with severe heart failure and hyponatremia because the circulatory hemodynamics may deteriorate; NSAIDs may mask the usual signs of infection; caution in the presence of existing controlled infections; evaluate symptoms and signs that suggest liver dysfunction, or in cases in which there are abnormal liver laboratory results
More on Lateral Collateral Knee Ligament Injury |
| Overview: Lateral Collateral Knee Ligament Injury |
| Differential Diagnoses & Workup: Lateral Collateral Knee Ligament Injury |
 Treatment & Medication: Lateral Collateral Knee Ligament Injury |
| Follow-up: Lateral Collateral Knee Ligament Injury |
| References |
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References
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Further Reading
Keywords
fibular collateral ligament, LCL injury, posterolateral corner of the knee
