PATELLO FEMORAL SYNDROME

PATELLO-FEMORAL SYNDROME

Patellofemoral syndrome (PFS) is characterized by a group of symptoms that are easily diagnosed and often respond to simple management.

The common presentation is knee pain in association with positions of the knee that result in increased or misdirected mechanical forces between the kneecap and femur.

PATHOPHYSIOLOGY

While theories regarding the pathophysiology of patellofemoral syndrome vary, identification of the resultant forces involved in dynamic and static knee positions has been fundamental to the research on this syndrome.

Factors believed to contribute to production of retropatellar pain include impairments affecting the patellofemoral joint interface.

Such impairments may be a consequence of an unbalanced muscle pull, malalignment between the joint surfaces, excessive knee valgus (ie, increased Q-angle) resulting in increased lateral forces, and quadriceps contractures causing production of excessive leverage forces on the patellofemoral joint surface.

Excessive use of the joint, either in frequency of loading or excessive loading, also contributes to the symptoms.

FREQUENCY

Patellofemoral syndrome is common especially among physically active persons.

MORTALITY/MORBIDITY

Morbidity associated with patellofemoral syndrome is directly proportional to the activity level of the patient.

Curtailing physical activities that place unnecessarily stressful demands upon the patellofemoral articulation may be necessary (preferably while substituting other activities into the exercise program).

SEX

Patellofemoral syndrome more frequently affects females than males.

AGE

Patellofemoral syndrome occurs most frequently in adolescents and young adults.

CLINICAL

HISTORY

• Knee pain is the most common presentation of patellofemoral syndrome.

  • The pain characteristically is located behind the kneecap (ie, retropatellar) and most often manifests during activities that require knee flexion and forceful contraction of the quadriceps (eg, during squats, ascending/descending stairs).

  • Pain may worsen in intensity, duration, and rapidity of onset if the aggravating activity is performed repeatedly.

  • Pain may be exacerbated by sitting with the knee flexed for a protracted period of time, such as while watching a movie, hence leading to the terms "theatre sign" and "movie-goer's knee." Patients with this condition often may prefer to sit at an aisle seat, where they may more frequently keep the knee extended.

• Symptoms often occur during the activity, such as playing volleyball for 30 minutes, or may occur later after the activity has been completed.

• Sometimes symptoms manifest as late as the next day.

PHYSICAL

Physical examination of a patient with patellofemoral syndrome should include examination of the musculoskeletal system, including following:

• The upper and lower body should be examined to exclude generalized diseases that make up the differential diagnoses (eg, osteoarthritis).

• The usual physical findings are localized around the knee.

• Tenderness often is present along the facets of the patella. The facets are most accessible to palpation by manipulation of the patella while the knee is fully extended and the quadriceps muscle is relaxed. Manual positioning of the patella medially, laterally, superiorly, and inferiorly allows for palpation of the respective facets.

• An apprehension sign may be elicited by manually fixing the position of the patella against the femur and having the patient contract the ipsilateral quadriceps.

• Crepitus may be present, but if present in isolation, crepitus does not allow for definitive diagnosis.

• Determine the Q-angle by measuring the angle between the tibia and femur. Use the attachment of the patella to the patellar tendon as the intersection point.

• Examination of gait may demonstrate excessive foot pronation, excessive knee valgus, or an antalgic gait pattern.

• Repetitive squatting may reproduce knee pain.

• Use the physical examination and historical details to help exclude other diagnoses.

• Examination of the contralateral limb is equally important, as the syndrome often is bilateral. However, one side usually manifests more symptoms.

• Palpation of the tibial tuberosity may detect tenderness suggesting that other impairments also are present.

• Determining the muscle bulk of the vastus medialis is possible, because it is situated superficially and has little overlying tissue. Bulk may be observed by direct visualization during contraction. The vastus medialis is believed to be the most active muscle in the last 15° of resisted knee extension, making this the best arc of movement for assessing its strength.

• Genu recurvatum and hamstring weakness may contribute to the occurrence of PFS, and therefore, identifying such impairments may aid in the choice of management.

CAUSES

The potential causes of patellofemoral syndrome remain controversial and are therefore more appropriately referred to as associated factors. Overuse, overloading, and misuse of the patellofemoral joint seem to be the cornerstone factors on which most authors agree.

DIAGNOSIS

LABORATORY STUDIES

• Laboratory studies generally are not indicated for the diagnosis of patellofemoral syndrome.

IMAGING STUDIES

• Imaging studies usually are not necessary in order for a physician to diagnose or recommend treatment for patellofemoral syndrome (PFS). Imaging studies should be considered for unusual presentations and for persons in whom the syndrome is refractory to conservative management.

  • Skyline views should be included with anterior-posterior (AP) and lateral radiographic imaging of the knee. Limited positions of flexion are available for such viewing. These radiographs provide more of an indirect observation of what is happening within the articulation.

  • Lateral patellar tilt and a high-riding patella (patella alta) may be observed.

  • Osteophytes or joint space narrowing may be identified, suggesting arthritic changes in the articular cartilage.

• Nuclear scans are less likely to be of value in defining PFS and are more useful in helping to identify other, less common conditions that may mimic PFS, as outlined in the differential diagnoses. When changes have occurred in the retropatellar cartilage, mild increases in uptake of radionucleotide may be observed. Increased uptake of radionucleotide is not limited to the patella; it may be seen in the proximal tibia, distal femur, or patella.

• Computed tomography (CT) scanning and magnetic resonance imaging (MRI)

  • CT scanning and MRI allow for imaging at various angles of flexion.

  • CT scanning with the knee in full extension has been demonstrated to more accurately detect patellar subluxation.

  • Cross-sectional viewing allows more direct visualization of the articulation between the patella and femur.

  • Schutzer et al identified 3 patterns of malalignment using CT scanning :

    • Type 1 includes patellar subluxation without tilt.

    • Type 2 is described as patellar subluxation with tilt.

    • Type 3 is patellar tilt without subluxation.

OTHER TESTS

• Serology, joint aspiration, and related tests are indicated only when alternative diagnoses are suspected. Such investigations are not likely to provide useful information in this syndrome, as it is not a disease entity but rather a group of symptoms occurring sometimes in association with multiple factors (intrinsic and extrinsic).6

PROCEDURES

• Arthroscopy

  • Arthroscopy helps to confirm the diagnosis patellofemoral syndrome (PFS) by allowing direct visualization of the cartilage surface. Arthroscopic evaluation also provides assessment of joint structures that may cause symptoms that mimic PFS when they are impaired.

  • Arthroscopy also has the ability to facilitate surgical alteration of patellar tracking (eg, lateral release). Visualization of the patella may allow for some revision of the cartilage surface. However, most authors agree that surgical treatment is rarely indicated.

TREATMENT

PHYSICAL THERAPY

The basic exercise principles for management of patellofemoral syndrome (PFS) are restoring muscle balance within the quadriceps group, improving range of motion, and restricting the offending physical activity.

Quadriceps strengthening traditionally is performed while the knee is flexed 0-30°. Controversy remains regarding the extent to which the individual muscle groups making up the quadriceps can selectively be strengthened.

Usually, the lateral forces of the vastus lateralis need to be countered better by the vastus medialis. This goal is accomplished best by strengthening all of the quadriceps.

Stretching of the quadriceps should be of long duration (20-30 seconds) and performed with low force. This technique allows for overcoming neural and connective tissue barriers to lengthening.

Exercises to stretch the iliotibial band, hip, hamstring, and calf also are important for patients with PFS. Manual stretching of the lateral retinaculum may be used as a conservative approach, partially mimicking the effect of lateral retinacular release.

Physical therapists should educate patients about home exercise programs that include stretching and strengthening exercises.

Ice packs frequently are used to decrease pain and inflammation associated with this condition, especially after completing the exercises.

Other modalities that may be useful and commonly are incorporated into physical therapy include electrical stimulation and biofeedback.

Patellar taping techniques are used in patients with PFS to reduce the friction on the patella. Many physical therapists are trained in the McConnell method of taping of the knee.

Some patients report reduction of pain when wearing the tape.

Some individuals report that the taping allows them to complete more functional quadriceps-strengthening activities without anterior knee pain. If successful, the physician or physical therapist can teach the patient self-taping techniques to use at home.

Proper footwear also is important for individuals with PFS. The physical therapist can evaluate the patient's biomechanics and recommend proper shoes and orthoses, which in turn can lessen knee pain.

Foot orthoses are often of benefit in returning the subtalar joint to a nearly neutral position; this reduces foot pronation, thereby decreasing rotational forces in the tibia that affect tracking of the patella during locomotion.

Improvement in quality of life measures has been demonstrated following provision of custom orthoses to individuals with PFS and excessive foot pronation.

By 6 weeks, patients using orthoses had experienced greater improvement than had persons using flat inserts, but the orthotic group had experienced no significant difference in improvement over patients treated with physical therapy or with a combination of orthoses and physical therapy.

By 52 weeks, a significant improvement in patellofemoral pain had occurred in all of the patient groups.

Soft knee braces may also be of benefit to patients with PFS.

Bracing involves control of the tracking position of the patella and restriction of full knee flexion. Braces vary in the manner in which the patella is restricted (eg, patellar window, patellar bar, patellar horseshoe), but they accomplish the same theoretical result.

Braces that are tightly applied directly over the patella should be avoided, because they actually increase patellofemoral pressures and may exacerbate the condition.

OCCUPATIONAL THERAPY

Recommend a change in activity level or the ergonomics of the offending activity until the symptoms of patellofemoral syndrome are under control.

Activities that require repetitive squatting are a good example. The task or sport may need to be modified to reduce the frequency of squatting, or the patient may need to choose an alternate occupation or recreational activity.

Occupational therapists can be of assistance when reviewing the ergonomics of the environment in which symptoms occur with individual patients.

RECREATIONAL THERAPY

Introducing alternative recreational pursuits and means of fitness may be of benefit in alleviating symptoms of patellofemoral syndrome when conservative measures are not effective.

Modifications in recreational pursuits may need to be only temporary measures if other conservative measures are effective.

SURGICAL INTERVENTION

Surgical intervention for patellofemoral syndrome usually is in the form of arthroscopic evaluation followed by release of the lateral attachments of the patella.

Most authors agree that surgical treatment rarely is indicated.

Arthroscopy has been cited as assisting the physician with clinical diagnoses; however, the visualization procedure, in and of itself, does not significantly help the symptoms of patellofemoral pain.

• Surgical procedures performed for patellofemoral arthritis include lateral facetectomy and patellar resurfacing.

• Follow-up evaluations long after anterior advancement of the tibial tuberosity suggest limited results with this procedure.

• Research on cartilage transplantation is being performed. Additional surgical options may be added in the future.

• Arthroscopic drilling of osteochondral defects allows healing of the defect with fibrocartilage. This procedure routinely is performed. This form of cartilage is not of the normal type but provides for an improved surface compared to an osteochondral defect.

OTHER TREATMENT

Knee pain secondary to defined degenerative changes may be relieved by injecting the joint with steroid or synthetic hyaluronic acid.

Such management of patellofemoral syndrome is rare. Injection may be used when many symptoms result from disruption of the joint surface and when all other reasonable measures have failed.

MEDICATION

Two approaches to medicating symptoms of patellofemoral syndrome are recognized. These approaches are administration of analgesic medication and administration of nonsteroidal anti-inflammatory drugs (NSAIDs).

Analgesics commonly are restricted to acetaminophen or aspirin. The choices of NSAIDs available for management of joint pain are expanding continuously. Consider tolerance of medication (which may result in epigastric distress), prior history of gastric ulceration, renal disease, possible interaction with other medications, and cost.

The NSAIDs all have similar efficacy, but changes in formulation have been made to reduce the frequency of adverse effects. Selective cyclooxygenase 2 (COX-2) inhibitors have fewer gastrointestinal adverse effects.

NONSTEROIDAL ANTI-INFLAMMATORY DRUGS

No NSAID has been found to be more effective in treating symptoms of patellofemoral syndrome than any other, although tolerances of NSAIDs vary between individuals.

Listed below are the commonly used NSAIDs. These NSAIDs are used predominantly in the adult population. Except for the COX-2 NSAIDs, most have similar adverse effect profiles, and most have the same effect on prostaglandins.

DICLOFENAC (Cataflam, Voltaren)

Inhibits prostaglandin synthesis by decreasing activity of enzyme cyclo-oxygenase, which in turn decreases formation of prostaglandin precursors.

Adult: 25 mg PO bid/tid; if well tolerated, increase by 25 or 50 mg at weekly intervals until satisfactory response is obtained or total daily dose of 150-200 mg is reached; higher doses generally do not increase effectiveness 

Pediatric: <12 years: Not established

>12 years: Administer as in adults

Pregnancy

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

Precautions

Category D in third trimester of pregnancy; acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases 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 persistent leukopenia, granulocytopenia, or thrombocytopenia occurs

ETODOLAC (Lodine, Lodine XL)

Inhibits prostaglandin synthesis by decreasing activity of the enzyme cyclo-oxygenase.

The decreased activity of cyclo-oxygenase results in decreased formation of prostaglandin precursors, which in turn results in reduced inflammation.

Adult: 200-400 mg PO q6-8h prn; not to exceed 1200 mg/d

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

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Category D in third trimester of pregnancy; acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases 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 persistent leukopenia, granulocytopenia, or thrombocytopenia occurs 

FLURBIPROFEN (Ansaid)

May inhibit cyclo-oxygenase enzyme, which in turn inhibits prostaglandin biosynthesis.

These effects may result in analgesic, antipyretic, and anti-inflammatory activities.

Adult: 200-300 mg/d PO divided bid/qid

IBUPROFEN (Motrin, Ibuprin)

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

Adult: 200-400 mg PO q4-6h while symptoms persist; not to exceed 3.2 g/d 

Pediatric: <6 months: Not established

6 months to 12 years: 4-10 mg/kg/dose PO tid/qid

>12 years: Administer as in adults

INDOMETHACIN (Indocin, Indochron ER)

Rapidly absorbed. Inhibits prostaglandin synthesis. Metabolism occurs in liver by demethylation, deacetylation, and glucuronide conjugation.

Adult: 25-50 mg PO bid/tid

75 mg SR PO bid; not to exceed 200 mg/d 

Pediatric: 1-2 mg/kg/d divided PO bid/qid; not to exceed 4 mg/kg/d or 150-200 mg/d

KETOPROFEN (Actron, Orudis, Oruvail)

For relief of mild to moderate pain and inflammation. Small dosages initially are indicated in small and elderly patients and in those with renal or liver disease.

Doses over 75 mg do not increase therapeutic effects. Administer high doses with caution and closely observe patient for response.

Adult: 25-50 mg PO q6-8h prn; not to exceed 300 mg/d 

Pediatric: <3 months: Not established

3 months to 12 years: 0.1-1 mg/kg PO q6-8h

>12 years: Administer as in adults

NABUMETONE (Relafen)

Nonacidic NSAID rapidly metabolized after absorption to a major active metabolite that inhibits cyclo-oxygenase enzyme, which in turn inhibits pain and inflammation.

Adult: 1-2 g PO qd

NAPROXEN (Aleve, Naprelan, Anaprox, Naprosyn)

For relief of mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing activity of cyclo-oxygenase, which results in a decrease of prostaglandin synthesis.

Adult: 500 mg PO followed by 250 mg q6-8h; not to exceed 1.25 g/d 

Pediatric: <2 years: Not established

>2 years: 2.5 mg/kg/dose PO; not to exceed 10 mg/kg/d

OXAPROZIN (Daypro)

For relief of mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing activity of cyclo-oxygenase, which is responsible for prostaglandin synthesis.

Adult: 600-1200 mg PO qd; not to exceed 1800 mg/d

PIROXICAM (Feldene)

Decreases activity of cyclo-oxygenase, which in turn inhibits prostaglandin synthesis. These effects decrease formation of inflammatory mediators.

Adult: 10-20 mg/d PO qd 

Pediatric: 0.2-0.3 mg/kg/d PO qd; not to exceed 15 mg/d

SULINDAC (Clinoril)

Decreases activity of cyclo-oxygenase, which in turn inhibits prostaglandin synthesis. Results in a decreased formation of inflammatory mediators.

Adult: 150-200 mg PO bid or 300-400 qd; not to exceed 400 mg/d

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

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Category D in third trimester of pregnancy; acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in 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 persistent leukopenia, granulocytopenia, or thrombocytopenia occurs; caution in those with anticoagulation defects and in those receiving anticoagulant therapy

CYCLO-OXYGENASE-2 (COX-2) INHIBITORS

Although increased cost can be a negative factor, the incidence of costly and potentially fatal GI bleeds is clearly less with COX-2 inhibitors than with traditional NSAIDs. Ongoing analysis of cost avoidance of GI bleeds will further define the populations that will find COX-2 inhibitors the most beneficial.

CELECOXIB (Celebrex)

Inhibits primarily COX-2. COX-2 is considered an inducible isoenzyme, 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/d PO qd; alternatively, 100 mg PO bid.