|
October 2009 Case of the Month
Compiled by: MasoodA. Siddiqui, D.O.
History: A 17-year-old female with medial knee pain for one week withweight-bearing. The knee gives out. Patient is a volleyball player.
Exam: Long- and short-axis fat- and water-weighted images were obtained without intravenous contrast administration.
Findings: As on the previous MRI dated two years ago (Figure 1), there is edema in the inferior pole of the patella extending to the proximal patellar tendon with injection of Hoffa's fat pad. (Figure 2)
Figure 1

Figure 2
 |
Diagnosis: Recurrent"jumper’sknee"
Discussion: "Jumper's knee” (also known as patellar tendinopathy, patellar tendinosis, or patellar tendinitis) commonly occurs in athletes who are involved in jumping sports such as basketball and volleyball. Patients report anterior knee pain, often with an aching quality. The symptom onset is insidious. Rarely is a discrete injury described. Usually, involvement is infrapatellar at or near the infrapatellar pole, but it may also be suprapatellar.
Depending on the duration of symptoms, jumper's knee can be classified into one of four stages, as follows:
- Stage 1 – Pain only after activity, without functional impairment
- Stage 2 – Pain during and after activity, although the patient is still able to perform satisfactorily in his or her sport
- Stage 3 – Prolonged pain during and after activity, with increasing difficulty in performing at a satisfactory level
- Stage 4 – Complete tendon tear requiring surgical repair
Physical examination may reveal the following findings:
- Point tenderness at the inferior patellar pole, superior patellar pole, or tibial tuberosity
- Hamstring and quadriceps tightness
- Normal ligamentous stability of the knee during testing
- Normal knee range of motion
- Normal neurovascular examination
- Normal hip and ankle examination
- Intra-articular effusion of the knee (rare)
The cause of jumper's knee remains unclear.
Histologic specimens are devoid of inflammatory cells; therefore, the disease process probably rarely involves a true tendinitis. Histologic studies have found increased numbers of mast cells associated with vascular hyperplasia, as well as an increased number of apoptotic cells.
Biomechanical research has shown that a greater tensile load is borne by the anterior fibers. This observation contradicts the theory that jumper's knee is caused by repetitive tensile loading, given that the proximal posterior patellar tendon is routinely affected.
The degenerative "tendinosis" rather than inflammatory "tendinitis" model has prevailed since the 1970s. Hamilton and Purdam have proposed an adaptive model, whereby compressive rather than tensile loads occur at the proximal posterior aspect of the tendon, resulting in structural changes from altered biomechanical forces. This model is said to account for the presence of the routinely found asymptomatic lesions, and perhaps the absence of inflammatory cells in histologic specimens.
Almekinders, et al., suggested that stress shielding by the anterior fibers may lead to degenerative change or tendon wear of the posterior ones due to compressive forces.2They also proposed that such stress shielding and/or compressive forces, rather than repetitive tensile loads, may be more important etiologic factors in insertional tendinopathy.
Imaging Studies:
- Radiographic imaging is not necessary to make the diagnosis of jumper's knee. Such imaging may be helpful for excluding other potential maladies.
- Certain imaging findings do support the diagnosis. For instance, ultrasonography may show thickening and hypoechogenicity of tendon fibers. Signs of hypervascularity may be seen with color Doppler ultrasonography. Plain x-ray may show a radiolucency at, or elongation of, the involved pole.
Jumper’s knee is seen on MRI as thickening of the proxima patellar tendon, with high signal in and around it on T2W images.
Treatment:
1. Acute Phase 2.RehabilitationProgram
3. Physical Therapy
Most patients with jumper’s knee (patellar tendinopathy, patellar tendinosis, patellar tendinitis) respond to a conservative management program, such as the one suggested below.
- Activity modification: Decrease activities that increase patellofemoral pressure (such as jumping or squatting). Possibly initiate gentle eccentric loading activities.
- Cryotherapy: Apply ice for 20-30 minutes, four to six times per day, especially after activity.
- Joint motion and kinematics assessment: Evaluate hip, knee, and ankle joint ranges of motion.
- Stretching: Stretch (1) flexors of the hip and knee (hamstrings, gastrocnemius, iliopsoas, rectus femoris, and adductors); (2) extensors of the hip and knee (quadriceps and gluteals); (3) the iliotibial band; and (4) the patellar retinaculum.
- Strengthening: Strengthen muscles using closed-kinetic chain and eccentric exercise (for example, single-leg squat descents). Jonsson and Alfredson found eccentric quadriceps strengthening on a decline board superior to concentric strengthening in terms of pain, treatment satisfaction, and return to play. Kongsgaard, et al.,,demonstrated that eccentric squats on a decline board of 25 º increases patellar tendon loading as compared to standard eccentric squats on a level surface.
- Sport-specific proprioceptive training and plyometrics.
Ultrasonography or phonophoresis may decrease pain symptoms. A patellofemoral brace with a patellar cutout and lateral stabilizer or McConnell taping may improve patellar tracking and provide stability through augmentation of proprioception. Provide arch supports or orthotics to correct foot malalignments.
Stage I
The treatment of jumper's knee is often specific to the degree of involvement. Stage I, which is characterized by pain only after activity and no undue functional impairment, is often treated with cryotherapy. The patient should use ice packs or ice massage after terminating the activity that exacerbates the pain and later again that evening. If aching persists, a course of regularly prescribed anti-inflammatory medications should be administered for ten to 14 days.
Often, cryotherapy and anti-inflammatories suffice in the first stage, although some cases relapse once the course of anti-inflammatories is completed. Long-term use of anti-inflammatories should be avoided in the young athlete. Local corticosteroid injections are not advised in stage I treatment. In addition, most competitive athletes do not agree to rest and immobilization, given that the condition does not affect their performance at this point. For this reason, use of a counterforce strap has been suggested to relieve some of the tension on the affected area and thereby ameliorate the symptoms.
A comprehensive physical therapy program should include aggressive quadriceps and hip flexor stretching along with progressive strengthening. Begin with closed kinetic strengthening exercises, such as lunges, leg presses, and squats. Focus is given to the eccentric phase with each activity. Strict attention to proper technique is important to reduce stress on the patellofemoral joint and patellar tendon and to allow for progressive strengthening.
The strengthening program should progress to proprioceptive and plyometric exercises. Plyometrics include activities, such as jump roping, within the patient's pain tolerance. A good warm-up activity before stretching and strengthening is important to increase blood flow and tissue compliance. An exercise bicycle can be used to perform aerobic warm-up exercises. If significant anterior knee pain occurs, the seat should be adjusted slightly higher to eliminate excessive and repetitive knee flexion loading.
Stage II
In stage II, the patient has pain both during and after activity, but is still able to participate in the sport satisfactorily. The pain may interfere with sleep. At this point, activities that cause increased loading of the patellar tendon (such as running or jumping) should be avoided.
A comprehensive physical therapy program, as discussed above in stage I, should be implemented. For pain relief, the knee should be protected by avoiding high loads to the patellar tendon, and cryotherapy should continue. The athlete should be instructed in alternative conditioning.
Once the pain improves, therapy should focus on knee, ankle, and hip joint ranges of motion; flexibility; and strengthening. Eccentric strengthening (perhaps on a decline board) should be emphasized because eccentric contractions allow for a greater generation of force and simulate landing in many sports. Advanced therapy should include plyometrics and sport-specific training, as tolerated.
If the pain becomes increasingly intense and if the athlete becomes more concerned about his or her performance, a local corticosteroid injection may be considered. The physician should explain that the steroid could cause further tendon degeneration, and perhaps even rupture, if the athlete begins loading the tendon too quickly once the symptoms improve.
Stage III
In stage III, the patient's pain is sustained and performance and sport participation are adversely affected. Although discomfort increases, therapeutic measures similar to those described above should be continued, along with abstinence from the inciting activity. Relative rest for an extended period (for example, three to six weeks) may be necessary in stage III. The athlete should avoid only those activities that incite the pain to prevent deconditioning, and he or she should be encouraged to continue an aggressive alternative cardiovascular and strength-training program. If the pain is refractory to these measures, the options are limited. One can either abandon participation in jumping sports and/or consider surgery. In a randomized controlled trial, Bahr, et al., demonstrated no difference in outcome between surgical and nonsurgical treatment for patients with stage III tendinopathy.24The authors advocated 12 weeks of eccentric quadriceps strengthening before considering tenotomy. Only approximately half of athletes in both the surgical and nonsurgical treatment groups were well enough to return to sports within one year.
Stage IV
Stage IV involves tendon rupture that requires surgical repair.
References:
1. Blazina ME, Kerlan RK, Jobe FW, Carter VS, Carlson GJ. “Jumper's knee.” Orthop Clin North Am, Jul. 1973; 4(3):665-78. 2.Almekinders LC, Vellema JH, Weinhold PS. “Strain patterns in the patellar tendon and the implications for patellar tendinopathy.”Knee Surg Sports Traumatol Arthrosc, Jan. 2002; 10(1):2-5.
3. Basso O, Amis AA, Race A, Johnson DP. “Patellar tendon fiber strains: Their differential responses to quadriceps tension.” Clin Orthop Relat Res, Jul. 2002; 400:246-53. 4. Cook JL, Kiss ZS, Khan KM, Purdam CR, Webster KE. “Anthropometry, physical performance, and ultrasound patellar tendon abnormality in elite junior basketball players: A cross-sectional study.” Br J Sports Med, Apr. 2004; 38(2):206-9. 5.Cook JL, Khan KM, Kiss ZS, Purdam CR, Griffiths L. “Reproducibility and clinical utility of tendon palpation to detect patellar tendinopathy in young basketball players.” (Victorian Institute of Sport Tendon Study Group). Br J Sports Med, Feb. 2001; 35(1):65-9. 6. Cook JL, Khan KM, Kiss ZS, Purdam CR, Griffiths L. “Prospective imaging study of asymptomatic patellar tendinopathy in elite junior basketball players.” J Ultrasound Med, Jul. 2000; 19(7):473-9. 7. BuschMT. “Sports medicine in children and adolescents.” In: Morrissy RT, eds. Lovell and Winter's Pediatric Orthopaedics. Philadelphia, PA: Lippincott-Raven; 1990: 1091-1128. 8. Ferretti A, Ippolito E, Mariani P, Puddu G. “Jumper's knee. “ Am J Sports Med, Mar.-Apr. 1983; 11(2):58-62. 9. Helms, C, et al. Musculoskeletal MRI. Saunders, 2nd ed., 2008. |