Updated: Sep 8, 2008
Patellar pain is common in both athletic and nonathletic individuals. Among athletes, men tend to present with more patellofemoral injuries, including traumatic dislocations, than women. In the nonathletic population, women present more commonly with patellar disorders.
Patellofemoral problems are mainly diagnosed by obtaining a thorough history and performing a physical examination. Imaging studies help confirm the diagnosis. Plain radiography is not as sensitive as magnetic resonance imaging (MRI), but it is the least expensive and most readily available modality.
Patellofemoral syndromes are usually the result of biomechanical imbalances of the kinetic chain, with each individual having an optimal joint-loading limit that is dependent on his or her unique skeletal and muscular anatomy, combined with his or her unique neuromuscular patterning. As this limit is surpassed, the patient is at risk for either acute injury, such as patella dislocation, or chronic injury, such as patellofemoral pain syndrome. Therefore, the goal of a rehabilitative treatment program must be to guide the patient toward performing functional activities without surpassing his or her optimal joint-loading limit. Therapy techniques need to be designed around this principle.
In general, surgery is more effective in preventing recurrences of dislocation because skeletal and muscular components of the patellofemoral joint and extensor mechanism are realigned; however, surgery also has risks. In a patient with normal anatomy, surgery should be considered an option after all conservative treatment modalities are unsuccessful. Patients with anatomic abnormalities may benefit from earlier surgical consideration.
Traditionally, several different systems have been used to classify patellofemoral dysfunction. Some were developed from a functional perspective, whereas others were developed from an anatomic viewpoint. This latter perspective was held by Insall and Merchant, who classified patellofemoral dysfunction according to anatomy.
In 1972, Insall proposed a method of classification based on cartilage damage. The 3 categories in his system are normal, damaged, and variably damaged cartilage. In 1986, Fulkerson and Schutzer developed a system based on measuring arthralgias against joint instability to determine the necessity for surgical intervention. In 1988, Merchant created a system of 5 categories for patellofemoral dysfunction, which included acute trauma, dysplasia, idiopathic chondromalacia, osteochondritis dissecans, and synovial plicae.
No standardized and widely accepted method of patellofemoral dysfunction classification applicable for all specialties has been developed. However, for the purposes of rehabilitation medicine, patellofemoral disorders may be loosely divided into 3 categories. These are soft-tissue abnormalities, patellar instability due to subluxation and dislocation, and patellofemoral arthritis.
Also, for excellent patient education resources, visit eMedicine's Foot, Ankle, Knee, and Hip Center and Breaks, Fractures, and Dislocations Center. Also, see eMedicine's patient education articles Knee Pain and Knee Injury.
Related eMedicine topics:
Joint Reduction, Patella Dislocation
Knee Dislocations
Patellar Tendon Rupture
Patellofemoral Arthritis
Patellofemoral Joint Syndromes
Related Medscape topics:
Resource Center Arthritis
Resource Center Exercise and Sports Medicine
Resource Center Joint Disorders
Specialty Site Orthopaedics
Knee Complaints Seen in General Practice: Active Sport Participants Versus Non-Sport Participants
Joint Loading in the Lower Extremities During Elliptical Exercise
Osteoarthritis: What We Have Been Missing in the Patellofemoral Joint
Pain of the patellofemoral joint secondary to patellofemoral dysfunction is the most common disorder of the knee. A 5-year study published in 1984 revealed that 25% of all knee issues in a sports injury clinic were of patellofemoral origin. Another study similarly revealed that 1 in 4 runners is afflicted by patellofemoral pain. Whether related to sports or not, 1 of every 4 painful knees has been reported to be the result of patellofemoral dysfunction.
Patellar injury and dislocation are more prevalent in individuals who participate in certain sports and activities. Anterior knee pain is the most common initial manifestation. In order of descending prevalence, soccer players, weight lifters, runners, and shooters regularly report acute knee pain. In addition, studies show soccer players and weight lifters have the most potential for long-term knee pain.
One study reported 52% of 31 soccer players, 31% of 29 weightlifters, 21% of 28 long-distance runners, and 17% of 29 shooters reported knee pain at least once per month.1 Thijs et al evaluated gait-related intrinsic risk factors for patellofemoral pain in 102 novice recreational runners.2 The authors findings suggested an increased risk for patellofemoral pain may be due to excessive impact shock during heel strike and at the propulsion phase of running. In addition, Thijs et al believe their results do not support the theory that those at risk for this condition show an altered static foot posture relative to those who are unaffected.2
Swimming also places the athlete at risk for knee pain.3 On the other hand, sports such as tennis are not associated with knee pain. In summary, factors that cause knee pain include the type, amount, and duration of sports activity.
In addition to activity-specific variance, patellofemoral pain displays some variation between the sexes. A study revealed that in the general population, the female-to-male ratio for patellofemoral dysfunction is 2:1. However, in the athletic population, more men than women experience such syndromes. Further, the study revealed acute dislocation occurred more frequently in males and that recurrent dislocation may be more common in individuals whose initial dislocation occurred when they were younger than 15 years.
Patellofemoral disorders are more likely the result of inappropriate activity duration and type as opposed to genetic factors. Aoyagi et al examined the higher prevalence of joint pain of female Japanese individuals living in rural Japan versus female Americans of Japanese descent living in Hawaii.4 Despite the similar genetic stock, significant differences in prevalence of joint pain were noted. The researchers postulated that environmental factors influencing activity levels and types were responsible.
Similarly, Zhang et al found that Chinese women in Beijing have a higher prevalence of knee osteoarthritis versus American women in Framingham, Massachusetts.5 Again, this was thought to be the result of the lower activity levels of women living in the United States. In the same study, men from Beijing were found to have a similar incidence of knee osteoarthritis compared with their Framingham counterparts.
Nietosvaara et al studied the annual incidence of acute patellar dislocations in Finnish children younger than 16 years.6 They found an annual incidence of 43 cases per 100,000 children. Over a 2-year period, 72 children revealed patellar dislocations. Of these, 28 (39%) of the knees had associated osteochondral fractures. Of the 28 osteochondral fractures, 15 had capsular avulsions of the medial patellar margin, and another 15 had intra-articular fragments from the patella and/or lateral femoral condyle.6
Soft-tissue elements that affect the patella are the stabilizing capsular and ligamentous structures within which the patella lies. Some ligaments of the knee are continuous with the fibrous capsule surrounding the patella. When injuries occur, all structures are simultaneously affected. These ligaments hold the patella in place during static and dynamic phases.
The synovial capsule, a separate structure, lies deep to the fibrous capsule and may often be damaged.
The regional anatomy of the knee soft tissues is as follows:
Pain may develop in these periarticular soft-tissue structures as a result of patellofemoral dysfunction, or vice versa. All these structures operate as a functional unit to optimize weight-bearing capacity. These structures decrease joint-reaction forces (JRFs) and form a base of support for the upper body. If one of these structures is altered, a greater risk of patellar injury and dislocation can develop.
The patellofemoral mechanism is very complicated. Patellofemoral malalignment, abnormal patellar configuration, and a previous history of instability increase the risk for anterior knee pain, patellar dislocation, and recurrent dislocations. The risk for symptoms increases when a combination of factors exists.
Excluding acute patellar trauma, patellar injury and dislocation are the end result of patellofemoral force imbalances. These force imbalances may also result in less dramatic presentations of patellofemoral pain. Deformities of cartilage resulting from arthritis; congenital variants of the patellofemoral joint; imbalances in lower extremity muscular strength and/or firing pattern; skeletal imbalances at the hip, knee, ankle, or foot; and changes of the patellar stabilizing capsular and ligamentous elements may also contribute to the development of patellofemoral pain and/or dislocations.
The patella is the largest sesamoid bone in the body, and it resides within the complex of the quadriceps and patellar tendons, superiorly and inferiorly, respectively. The patella assists in coordinating the forces of these tendons and functions as both a lever and a pulley. As a lever, the patella magnifies the force exerted by the quadriceps during knee extension. As a pulley, the patella redirects the quadriceps force as it undergoes normal lateral tracking during flexion.
The greater the anteroposterior length of the patella, the greater the angle between the quadriceps and patellar tendons, thus decreasing the force generation needed by the quadriceps to support the upper body at any particular angle of knee flexion. One study demonstrated that the patella most significantly increases the moment arm of the quadriceps at 20° of knee flexion. After patellectomy, the moment arm of the quadriceps is obliterated. After patellectomy, one study demonstrated the effectiveness of the quadriceps-patellar moment arm to be reduced by 31% at 0° of flexion, 22% at 30°, 13% at 60°, 12% at 90°, and 10% at 120°.
The quadriceps tendon and the patellar tendon are continuous with each other and work in cooperation. Muscular forces are transmitted in differing proportions to each tendon over the changing angle of the knee as it flexes and extends. At different angles of knee flexion, the quadriceps and the patellar tendons appear to alternate the role of being the primary force transmitter. From 0-20° of knee flexion, the consensus among researchers is that tension in the patellar tendon is greater than in the quadriceps tendon. From 20-50° of flexion, which tendon has more tension is controversial among research findings. From 50° to full flexion, tension in the quadriceps tendon is greater than in the patellar tendon. Theoretically, isolated development of either the quadriceps tendon or the patellar tendon is accomplished by appropriately limiting knee flexion in exercise programs.
The chondral surface of the patella has several divisions. The 3 transverse ridges create 3 roughly equal-sized upper, middle, and lower groups. Two vertical ridges are found on the chondral surface of the patella. The prominent median vertical ridge separates the medial and lateral facets. The facets are at an acute angle to each other, with the prominent ridge acting as their adjoining corner.
These structures form a V-shaped wedge along the transverse plane for the purpose of better insertion into the depression formed by the trochlear groove. The lateral facet is larger in most individuals. The medial facet is further separated into medial and lateral surfaces by a less prominent vertical ridge. The medial surface of the medial facet is sagittally oriented and only makes contact with the femur when the knee is flexed past 90°. Pain at this range of motion (ROM) that is associated with a compressive mechanism, such as increased JRFs, is suggestive of lesions on the chondral surface.
In full extension, the patella does not fit into the trochlear groove but lies over the smooth synovial tissue that overlies the supratrochlear tubercle. The lateral aspect of the tubercle has a smooth, continuous transition with the trochlear groove. The medial aspect of the tubercle is sharply elevated in regard to the trochlear groove. In normal motion, the patella moves superolaterally, riding the lateral aspect of the supratrochlear tubercle so that it makes a smooth translation from the groove to the tubercle.
The cartilage of the patella contacts the trochlear cartilage of the femur to reduce friction during motion of the patellofemoral joint. Gross normal joint motion is along a sagittal plane. This is why examination of the joint at the transverse plane reveals a congruent articulation, whereas the joint along the sagittal plane is incongruent. Good contact at the transverse plane promotes medial/lateral stability, whereas the incongruent sagittal articulation provides more free space for superior/inferior movement.
Compared with the femoral cartilage, the patellar cartilage is thicker, more pliant, and more permeable. In fact, the cartilage of the inner patella at the prominent median vertical ridge is normally the thickest cartilaginous structure in the body, suggesting its role in counteracting tremendous JRFs. These characteristics of the patellar cartilage allow it to sit deeper in the trochlear groove and conform to its shape, allowing for better articulation and distribution of JRFs. However, these actions place a burden on the collagen-proteoglycan matrix of the patellar cartilage and may be the reason for the higher prevalence of patellar cartilaginous lesions compared with femoral trochlear cartilaginous lesions.
JRFs at the patellofemoral joint are directly related to the contraction of the quadriceps.
The stress at the patellofemoral joint can be mathematically defined as the sum JRF divided over the surface area of force distribution. From 0-60°, the surface area of the patella contacting the femur enlarges with increased knee flexion. This provides a larger contact surface area over which to distribute the load as the load is increasing. Beyond 60° of flexion, anatomic studies regarding the contact area have been inconclusive.
The location of contact for the patella and femur vary with different degrees of flexion and joint load. At 0°, no contact occurs; in early flexion, the distal patella contacts the proximal trochlea; at 90° of flexion, the superior aspect of the patella contacts the femur; when flexion is greater than 90°, the contact area returns to the center of the patella; and when the knee is fully flexed, the inner border of the medial femoral condyle is in contact with the small vertical ridge of the medial facet.
Lateral tracking of the patella leads to decreased efficiency of the quadriceps extensor mechanism and increased patellofemoral joint stress. A lateral patellar subluxation of only a few millimeters results in a decreased contact surface area between the patellar and trochlear surfaces as the lateral facet moves closer to the lateral side of the trochlear groove and the distance between the medial facet and the medial side of the trochlear groove increases. The total JRF, initially distributed over both patellar facets, is now completely transmitted to the lateral patellar facet. This increases lateral facet stress and may result in pain, chondromalacia, and the development of arthritic changes.
A summary of forces on the patellofemoral joint follows. They maintain the physiologic positioning of the patella dynamically within the trochlea and extensor mechanism and provide for patella stability and proper tracking.
A summary of risk factors for patella subluxation and dislocation is as follows:
Kinetic chain models
JRFs of the patellofemoral joint are different when studied under closed and open kinetic chain models. When the kinetic chain is closed (eg, leg press, squats), the JRF increases when the knee is flexed 0-90°. To counteract this load, a greater surface area of the patella comes into contact with the femur, effectively dissipating the forces. However, the contact area does not increase as much as the reaction force. Therefore, forces on the contact areas increase during flexion to 90°. Further flexion greater than 90° causes a leveling off or a decrease in the JRFs. After 90° of flexion, the contact of the quadriceps tendon with the trochlear groove further diffuses the load. Irrespective of the cause, JRFs decrease when the knee is flexed 90-120°.
The open-chain model encompasses lower extremity non – weight-bearing exercises such as leg curls and extensions. When the leg is at 0° flexion, the reaction forces of the patellofemoral joint are low because the patella does not contact the femur when the leg is in full extension. Studies have shown widely varying results from 5-25° of flexion. With the knee flexed to 90°, the JRFs increase and the contact area decreases, resulting in very high patellofemoral stress. A study of knee flexion-extension with a 0.9-kg ankle weight showed JRFs are greatest at 36° of flexion. JRFs are lowest at 90° of flexion.
Closed-chain exercises are most protective for the patellofemoral joint when performed at 0-45° of flexion. Open-chain exercises should be performed from 0-5° of flexion and from 90° to full flexion. JRFs should be limited as much as possible during repetitive motion to avoid chondrosis and chondromalacia. In strengthening or rehabilitative exercises for the quadriceps, programs should be designed with open and closed kinetic chain models in mind.
Anatomic variants
When evaluating patients with patellofemoral disorders, the physician needs to consider anatomic variants, which often manifest as bone deformities and would include bipartite patellae. Additionally, the knee joint may be affected by congenital anomalies. Many genetic syndromes involve the knee joint, including congenital patellar aplasia, nail patella syndrome, small patella syndrome, Meir-Gorlin syndrome, RAPADILINO syndrome (RA for radial, PA for absent/hypoplastic patellas and cleft/high-arched palate, DI for diarrhea/dislocated joints, LI for little size/limb malformations, NO for long, slender nose/normal intelligence), and genitopatellar syndrome. A 2005 article by Bongers et al reviews genetic anomalies in greater depth.11
Obtaining a thorough history of the patient's symptoms is important when establishing a diagnosis of patellar injury or dislocation.
Anterior Cruciate Ligament Injury
Medial Collateral Knee Ligament Injury
Meniscus Injuries
Patellar Injury and Dislocation
Patellofemoral Joint Syndromes
Bipartite patella
Chondromalacia
Osteochondritis dissecans
Patella fracture
Patellofemoral arthritis
Soft tissue and capsular injury
During the acute phase of a patellar injury or dislocation, the immediate goals are to reduce inflammation, relieve pain, and stop activities that place excessive loads on the patellofemoral joint. Patients with an acute patella dislocation typically have been evaluated in an emergency department, with radiographic evaluation, and have often had a consultation with an orthopedist to assess for intra-articular pathology. Acute phase management should apply the PRICE principle: protection of the injured joint, relative rest, ice, compression, and elevation to control inflammation.
A study by Mãenpãã and Lehto suggested that a period of immobilization may be beneficial. In their study of 100 acute dislocations, patients were divided into 3 treatment groups: plaster cast, posterior splint, and patellar bandage/brace.19 At long-term follow-up, fewer redislocations were noted in the posterior splint group and the cast group than in the patellar bandage group. The first 2 groups had a period of immobility, whereas the bandage group did not. The mechanism of benefit is thought to be the time to heal the disrupted medial structures. The best outcomes were noted in the group initially treated with a posterior splint. The plaster cast group had a longer period of immobilization, and the authors suggested limiting the period of immobilization to 3 weeks to avoid muscle atrophy, knee joint restrictions, and retropatellar crepitation.19
Quadriceps strengthening is initiated during the acute phase. In the event of acute patella dislocation, these should be static exercises initiated during the period of immobilization. Quadriceps electrical stimulation is an option for muscle reeducation if the patient has difficulty activating the muscle secondary to pain. Electrical stimulation may also play a role in the management of knee joint effusion. When dolor, calor, rubor, and edema resolve, the patient may progress to the recovery phase of rehabilitation.
Therapy should also include a protocol for hamstring muscle stretching. Tight hamstring muscles functionally counteract their agonist group, the quadriceps.
In the acute phase, surgical interventions are reserved for complicated dislocations with associated fractures. The most common site of cartilage injury to the patella occurs as osteochondral fractures of the medial patellar facet or cracks in the central dome of the patella. Cartilaginous injuries are also frequently seen on the lateral femoral condyle. Arthroscopy can repair or remove fracture fragments. However, acute surgical interventions are unnecessary in most cases of patellofemoral syndromes.
If conservative management is not effective and the patient still experiences symptoms, consult an orthopedic surgeon. Particular attention should be paid to symptoms of an intra-articular foreign body, such as clicking, locking, or persistent intra-articular knee pain. These may be signs of an occult loose body within the knee.
Therapeutic theory goals of nonoperative management of patellar injury and dislocation are to improve patellar tracking. The VMO is an important medial stabilizer of the patella. Inappropriate synergy patterns between the VMO and the VL have been theorized for lateral patellar tracking. The VL is a much larger muscle than the VMO. By overpowering the VMO, the VL may contribute to lateral tracking.
The prevailing theory has been that lateral patellar tracking is associated with VMO weakness. However, research has been inconclusive for VMO weakness as a direct causative mechanism of lateral patellar tracking. A study by Mohr et al examined timing differences between the VMO and VL in patients both with and without patellofemoral pain.23 The authors concluded that the timing differences noted and their relationship to the gait cycle suggest overall quadriceps weakness rather than specific, focal VMO weakness. As such, Mohr et al recommended overall quadriceps strengthening as the basis of rehabilitation strengthening programs. Other authors have also noted that general quadriceps strengthening has demonstrated reductions in lateral tracking irrespective of the mechanism.
The patient should be educated about correct posture and joint preservation at this time. Supportive adjuncts such as taping and bracing are common treatment modalities. Exercises to strengthen the quadriceps muscle (focusing on VMO activation) include quadriceps-setting exercises and straight-leg raises.
Quadriceps-setting exercises are performed with the patient in the supine position. The contralateral hip and knee are flexed to approximately 45° to protect the low back, and the ipsilateral leg is kept in extension. The quadriceps muscle in the extended leg is contracted, and the contraction is held for 5 seconds. The patient then relaxes the quadriceps and repeats the contraction. (Repetitions and sets are gradually increased.) The ankle of the exercising leg must be actively dorsiflexed during the contraction.
Straight-leg raises are performed with the patient in the supine position and the contralateral hip and knee flexed to approximately 45°. The extended leg (the leg to be strengthened) is raised 8-12 inches from the table and is held at that level for 10 seconds. (Repetitions and sets are gradually increased.)
Additional strengthening exercises must be performed for the hip adductors, hip abductors, and hip flexors. Hip adductors are strengthened with the patient lying on his or her side. The leg against the exercise mat is lifted away from the mat and is held for 10 seconds, followed by relaxation. Hip abductors are strengthened with the patient lying on his or her side. The leg away from the exercise mat is lifted away from the mat and is held for 10 seconds, followed by relaxation. Hip flexors are strengthened with the patient in a seated position. Both the knee and hip are held at 90° of flexion, and the leg to be exercised is lifted off the ground and is held for 10 seconds. (Repetitions and sets are gradually increased for all exercises.)
Any physical therapy program for patellofemoral problems must address tightness of the lower-extremity musculature. Reduced flexibility of the hamstrings, hip abductors, and iliotibial band all can increase patellofemoral pain. Additionally, tight gastrocnemius muscles can increase patellofemoral pain.
Medial patellar gliding exercises may loosen lateral retinacular tightness in this stage. Medial patellar gliding exercises are performed with the leg extended. The patient manually pushes the patella medially and holds for a count of 10 seconds.
An important concept in the rehabilitation of patellar dislocation and patellofemoral pain is knee flexion. Initially, any activity that requires greater than 40-45° of knee flexion causes symptoms. Initial rehabilitation programs start with the isometric open kinetic chain exercises described earlier. Early rehabilitation programs should limit all activities that require quadriceps firing with the knee flexed greater than 45°.
Once isometric open kinetic chain exercises are tolerated without discomfort, the rehabilitation program advances to closed kinetic chain exercises (eg, mini squats, lunges, stair climbing). The rectus femoris, VMO, and VL are all strengthened by the mini squats (repetitions and sets modified to the tolerance of the patient). Earl et al found that when isometric hip adduction is performed in conjunction with mini squats, the strength in these muscles increased significantly compared with the control group performing conventional squats.24
Important goals are to restore ROM in the joint, mobilize soft tissues, and strengthen the surrounding musculature. Lunges and bike riding allow strengthening through a controlled ROM. The patient becomes more active in this phase, and the clinician must screen the patient for exacerbations of symptoms. If symptoms reemerge, the optimal loading zone of the knee and the activity level must be reevaluated. The patient learns activity limits in this phase. Once pain has resolved sufficiently to complete daily activity requirements without exacerbations, the patient can advance to the final phase of rehabilitation.
Advanced rehabilitation programs progress to jogging, running, plyometrics, and sport-specific exercises. Patients must be monitored and must always follow proper technique, as well as learn to properly fire the VMO.
Surgical intervention may be appropriate in 2 different patient populations: (1) those with normal anatomy who experience recurrent dislocation or pain and (2) those with an anatomic abnormality who may benefit from surgical intervention either upon initial acute dislocation or later with recurrence of dislocation or subluxation. In general, following acute patella dislocation, patients with normal lower extremity anatomy and without radiographic indications of intra-articular injury are best served by conservative treatment.
Buchner et al compared conservative treatment with surgical repair in patients with acute patella dislocation25 ; patients with radiologic signs suggestive of a predisposition to redislocation were excluded from the study. Results indicated no significant difference between surgically treated and conservatively treated groups in terms of redislocation rate, reoperation rates, level of activity, or functional or subjective outcomes.
Operative choices may be classified into distal, proximal, and combined procedures. Some authors suggest that rigid, distal procedures are associated with increased rates of progressive retropatellar arthrosis but lower rates of redislocation and that dynamic proximal procedures are associated with a lower incidence of arthrosis but a higher risk of redislocation.Distal procedures
Postsurgical rehabilitation closely follows nonoperative conservative treatment. All surgical procedures are at risk for complications such as medial tracking, arthrofibrosis, reflex sympathetic dystrophy symptoms, hemarthrosis, and rupture of the quadriceps tendon.
If the conservative management is not effective and the patient still experiences symptoms, consult an orthopedic surgeon.
The final phase of rehabilitation emphasizes developing an independence program for the patient. The patient learns how to stretch appropriately, conduct training routines, modify activity, and apply ice after activity routines. Returning the patient to the preinjured functional state often requires progressive functional activity. The rate of progression is limited by the patient’s tolerance. The patient should work toward single-leg standing, deep squatting, and jumping. Once patients are able to adjust activity routines within their optimal loading zones, they are ready to be discharged and only require routine follow-up treatment.
If the conservative management is not effective and the patient still experiences symptoms, consult an orthopedic surgeon.
Manipulation
Wu treated patients who had anterior knee pain, tenderness, quadriceps imbalance, and patellar subluxation with Chinese manipulation.36 The diagnosis was determined by a plain radiography protocol, and his patients were treated with a combination of manipulation and an exercise program. Although his treatment was successful in alleviating symptoms of patellofemoral dysfunction, Wu's study is limited by not having control groups that received either only manipulation or exercise alone. Future studies should take this into account. His manipulation techniques included the following:
Bracing and taping can be of benefit for symptoms of patellofemoral dysfunction, as discussed in Acute Phase, Other treatment.
Medications used to treat patellar injury and dislocation include nonsteroidal anti-inflammatory drugs (NSAIDs), acetaminophen, and pain medicines. Allergies, contraindications, and adverse effects should be reviewed before prescribing these medicines.
Related eMedicine topics:
Toxicity, Acetaminophen
Toxicity, Narcotics
Toxicity, Nonsteroidal Anti-inflammatory Agents
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NSAIDs have analgesic, anti-inflammatory, and antipyretic activities. The mechanism of action of NSAIDs is not known, but they may inhibit cyclooxygenase (COX) 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.
For the relief of mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing the activity of COX, which results in a decrease of prostaglandin synthesis.
500 mg PO followed by 250 mg q6-8h; not to exceed 1.25 g/d
<2 years: Not established
>2 years: 2.5 mg/kg/dose PO; not to exceed 10 mg/kg/d
Coadministration with aspirin increases the risk of inducing serious NSAID-related adverse effects; probenecid may increase the concentrations and, possibly, the toxicity of NSAIDs; may decrease the effect of hydralazine, captopril, and beta-blockers; may decrease the diuretic effects of furosemide and thiazides; may increase PT duration when 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
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
Acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with preexisting renal disease or compromised renal perfusion risk acute renal failure; leukopenia occurs rarely, is transient, and usually returns to normal during therapy; persistent leukopenia, granulocytopenia, or thrombocytopenia warrants further evaluation and may require discontinuation of the drug.
DOC for patients with mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.
200-400 mg PO q4-6h while symptoms persist; not to exceed 3.2 g/d
<6 months: Not established
6 months to 12 years: 4-10 mg/kg/dose PO tid/qid
>12 years: Administer as in adults
Coadministration with aspirin increases the risk of inducing serious NSAID-related adverse effects; probenecid may increase the concentrations and, possibly, the toxicity of NSAIDs; may decrease the effect of hydralazine, captopril, and beta-blockers; may decrease the diuretic effects of furosemide and thiazides; may increase PT duration when 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; high risk of 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 patients with congestive heart failure, hypertension, and decreased renal and hepatic function; caution in the presence of coagulation abnormalities or during anticoagulant therapy
For the relief of mild to moderate pain and inflammation. Small dosages are indicated initially in small and elderly patients and in those with renal or liver disease. Doses >75 mg do not increase therapeutic effects. Administer high doses with caution and closely observe patients for response.
25-50 mg PO q6-8h prn; not to exceed 300 mg/d
<3 months: Not established
3 months to 12 years: 0.1-1 mg/kg PO q6-8h
>12 years: Administer as in adults
Coadministration with aspirin increases the risk of inducing serious NSAID-related adverse effects; probenecid may increase the concentrations and, possibly, the toxicity of NSAIDs; may decrease the effect of hydralazine, captopril, and beta-blockers; may decrease the diuretic effects of furosemide and thiazides; may increase PT duration when 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
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 patients with congestive heart failure, hypertension, and decreased renal and hepatic function; caution in the presence of coagulation abnormalities or during anticoagulant therapy
Pain control is essential to quality patient care. Analgesics ensure patient comfort and have sedating properties, which are beneficial for patients who have sustained trauma or who have sustained injuries.
DOC for pain in patients with documented hypersensitivity to aspirin or NSAIDs, with upper GI disease, or who are taking oral anticoagulants.
325-650 mg PO q4-6h or 1000 mg tid/qid; not to exceed 4 g/d
<12 years: 10-15 mg/kg/dose PO q4-6h prn; not to exceed 2.6 g/d
>12 years: 325-650 mg PO q4h; not to exceed 5 doses in 24 h
Rifampin can reduce the analgesic effect; coadministration with barbiturates, carbamazepine, hydantoins, and isoniazid may increase hepatotoxicity.
Documented hypersensitivity; known G-6-PD deficiency
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
In long-term alcoholism, hepatotoxicity is possible following various dose levels; severe or recurrent pain or high or continued fever may indicate a serious illness; acetaminophen is contained in many OTC products and combined use with these products may result in cumulative doses that exceed the recommended maximum dose.
Indicated for the treatment of mild to moderate pain.
30-60 mg/dose PO based on codeine content q4-6h or 1-2 tab q4h; not to exceed 4 g/d of acetaminophen
0.5-1 mg/kg/dose PO based on codeine q4-6h; 10-15 mg/kg/dose based on acetaminophen content; not to exceed 2.6 g/d of acetaminophen
The toxicity of codeine increases with CNS depressants, TCAs, MAOIs, neuromuscular blockers, phenothiazines, and narcotic analgesics; rifampin can reduce the analgesic effects of acetaminophen; coadministration with barbiturates, carbamazepine, hydantoins, and isoniazid may increase the hepatotoxicity of acetaminophen.
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
Caution in patients who are dependent on opiates because this substitution may result in acute opiate withdrawal symptoms; caution in patients with severe renal or hepatic dysfunction; hepatotoxicity with acetaminophen is possible following various dose levels in those with long-term alcoholism; severe or recurrent pain or high or continued fever may indicate a serious illness; acetaminophen is contained in many OTC products, and combined use with these products may result in cumulative doses that exceed the recommended maximum dose.
Patients with patellar injury and dislocation may return to play after (1) all symptoms and episodes or exacerbations have resolved and (2) full ROM and preinjury strength have been achieved in the affected limb. The timeline for return to play varies from patient to patient. In a 2000 study, Atkin et al found that at 6 months, 58% of their study population still reported deficits in function.38
Some variability exists in the time required to return to play, and it depends on multiple factors, including the underlying anatomy and physiology, whether conservative or surgical treatment was used, and the type of surgical treatment performed. In a review article in 2003, Hinton et al suggested that following surgical correction of a patellar injury or dislocation, return to sports can be anticipated to occur 4-6 months after the procedure.39
The prognosis for patellofemoral dysfunction and dislocation has been studied and reports of outcomes vary. Overall, conservative treatment for acute patellar dislocations yields a 30-50% chance of continuing to have long-term symptoms of instability or pain.
See Prevention.
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patellar injury and dislocation, patellofemoral dysfunction, patellofemoral dislocation, patella subluxation, patellofemoral joint dysfunction, patellofemoral joint syndrome, patellofemoral pain, patellofemoral pain syndrome, PFPS, patellofemoral stress syndrome, PFSS, kneecap injury, dislocated kneecap, knee pain, knee injury, knee dislocation, dislocated knee, patella fracture, knee fracture
Gerard A Malanga, MD, Founder and Director, New Jersey Sports Medicine Institute; Director of Pain Management, Overlook Hospital; Director of Sports Medicine, Sports Medicine Fellowship Director, Mountainside Hospital; Clinical Chief, Rehabilitation Medicine and Electrodiagnosis, St Michael's Medical Center; Medical Director, Consultant, Horizon Healthcare Worker's Compensation Services, Blue Cross and Blue Shield Worker's Compensation
Gerard A Malanga, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Physical Medicine and Rehabilitation, American College of Sports Medicine, North American Spine Society, and Physiatric Association of Spine, Sports and Occupational Rehabilitation
Disclosure: Nothing to disclose.
Brian F White, DO, Staff Physician, Department of Physical Medicine and Rehabilitation, Kessler Institute for Rehabilitation, University of Medicine and Dentistry of New Jersey
Brian F White, DO is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Osteopathic Association, and Wilderness Medical Society
Disclosure: Nothing to disclose.
Wah Sang Lee, DO, MS, Staff Physician, Department of Physical Medicine and Rehabilitation, New Jersey Medical School/Kessler Institute of Rehabilitation
Wah Sang Lee, DO, MS is a member of the following medical societies: American Osteopathic Association
Disclosure: Nothing to disclose.
Thomas Agesen, MD, Assistant Clinical Professor, Department of Physical Medicine and Rehabilitation, UMDNJ, New Jersey Medical School; Consulting Staff, Mountainside Hospital, Summit Overlook Hospital
Thomas Agesen, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American College of Sports Medicine, and Physiatric Association of Spine, Sports and Occupational Rehabilitation
Disclosure: Nothing to disclose.
Andrew L Sherman, MD, MS, Associate Professor of Clinical Rehabilitation Medicine, Vice Chairman, Chief of Spine and Musculoskeletal Services, Program Director, SCI Fellowship and PMR Residency Programs, Department of Rehabilitation Medicine, Leonard A Miller School of Medicine, University of Miami
Andrew L Sherman, 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 College of Sports Medicine, American Medical Association, American Paraplegia Society, American Spinal Injury Association, and Association of Academic Physiatrists
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.
Russell D White, MD, Professor of Medicine, Department of Community and Family Medicine, University of Missouri-Kansas City School of Medicine, Truman Medical Center Lakewood
Disclosure: Nothing to disclose.
Jon B Whitehurst, MD, Clinical Instructor of Surgery, University of Illinois College of Medicine; Partner and Executive Board Member, Rockford Orthopedic Associates; Orthopedic Chairman, Rockford Memorial Hospital
Jon B Whitehurst, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Society for Sports Medicine, and Arthroscopy Association of North America
Disclosure: Nothing to disclose.
Craig C Young, MD, Professor, Departments of Orthopedic Surgery and Community and Family Medicine, Medical Director of Sports Medicine, Sports Medicine Fellowship Director, Medical College of Wisconsin
Craig C Young, MD is a member of the following medical societies: American Academy of Family Physicians, American College of Sports Medicine, American Medical Society for Sports Medicine, Phi Beta Kappa, and Wilderness Medical Society
Disclosure: Nothing to disclose.
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