September 2000

‘Jumper’s knee’ images need clinical backup

By Jill L. Cook, Ph.D., P.T., Zoltan S. Kiss, M.D., Brett D. Coleman, M.D., Bruce B. Forster, M.D., and Karim M. Khan, M.D., Ph.D.

Athletes in jumping sports such as basketball and volleyball often suffer anterior knee pain caused by “jumper’s knee,” a condition that has curtailed some promising careers and limited many more. This painful condition of the patellar tendon ranks along with the dreaded anterior cruciate ligament tear as a major fear of professional athletes.

A typical presentation is an Olympic basketball or volleyball player reporting to the team physician or therapist with pain just below the patella that is aggravated by jumping. Pain may arise after particularly arduous training, or special activities such as weight training or plyometrics. Examination reveals tenderness at the junction of the patella and the patellar tendon, and this is most evident when the knee is slightly flexed. This clinical scenario has a number of names, including jumper’s knee, patellar tendinopathy, patellar tendinosis, and patellar tendinitis. The preferred diagnostic term is patellar tendinopathy.¹

In clinical practice, MR imaging and ultrasound are the investigations of choice for the jumping athlete with knee pain. For MR imaging of the athlete with jumper’s knee, we use high-field (1.5-tesla) equipment and suggest that both knees be imaged. We obtain multiple sagittal and axial sequences using a 3-inch surface coil placed directly over the patellar tendon to obtain T1-weighted, sagittal spin-echo (SE) imaging (TR 400/TE 20), 3-mm-thick sections with no gap, 12-cm field-of-view, 256 x 256 matrix, two signals acquired, imaging time of three minutes 31 seconds.

We also use T2-weighted sagittal, fast SE imaging with fat saturation (TR 3000/TE 110), echo train length of 8, 12-cm field-of-view, 3-mm-thick sections with no gap, 512 x 256 matrix, two signals acquired, imaging time of three minutes 24 seconds. We also employ two-dimensional, T2*-weighted sagittal gradient-echo (GRE) imaging, (TR 800/TE 30), 70° flip angle, 12-cm field-of-view, 3-mm-thick sections with no gap, 256 x 256 matrix, one and a half signals acquired, imaging time of five minutes 10 seconds.

The protocol also includes two-dimensional, sagittal short tau inversion recovery (STIR) imaging (TR 4000/TE 17) with an inversion time of 140 msec, echo train length of 6, 12-cm field-of-view, 3-mm-thick sections with no gap, 256 x 192 matrix, two signals acquired, imaging time of four minutes 32 seconds; and axial, T1-weighted imaging (TR 600/TE 20), 3-mm-thick sections with no gap, 12-cm field-of-view, 256 x 256 matrix, one and a half signal acquisitions, imaging time of three minutes 59 seconds.

With this protocol, the abnormality appears as an area of abnormal signal intensity within the tendon at the junction with the patella (Figure 1). Lesions have increased signal intensity relative to the tendon on T1-weighted images and are markedly hyperintense on the GRE T2*-weighted image, the FSE T2-weighted image, and the STIR sequence (Figure 2). Generally, the maximal anteroposterior (AP) and craniocaudad (SI) lesion sizes are bigger on the sagittal GRE T2* sequence than on other MR sequences.² The STIR and FSE T2 sequences often reveal abnormal signal in the patella.² We have noted that the “magic angle” phenomenon³ will produce increased tendon high-signal intensity on GRE T2* if the tendon courses at 55° to the coil.

Ultrasound

Sonographic appearances in jumper’s knee reveal a focal hypoechoic area (Figure 3), combined with various amounts of swelling of the surrounding tendon. Hyperechoic areas represent tendinosis, not tendinitis, although the two terms are often used interchangeably.

The pathology underlying both MR and sonographic imaging appearances has been well described and is based on examination of surgical specimens. At surgery, the chronically painful patellar tendon is dull-appearing, slightly brown, and soft, in contrast with white, glistening, and firm normal tendon tissue. Under the light microscope, the area of abnormal signal on imaging represents loss of collagen continuity and an increase in ground substance, vascularity, and cellularity. Cellularity results from the presence of fibroblasts and myofibroblasts, not inflammatory cells.

Thus, in patients who have chronic overuse tendinopathies, inflammatory cells are absent. In other words, the imaging appearance on both MR and ultrasound is consistent with what could be considered “microtearing” of collagen, rather than an invasion of normal collagen by inflammation.² In histopathological terms this represents the condition of tendinosis, not tendinitis⁵ and has numerous clinical implications that are outside the scope of this review.⁶ Interestingly, the same pathological appearance is found in a number of tendons that have been subjected to overuse⁶—the Achilles tendon, the lateral elbow extensors, the rotator cuff, and the tibialis posterior.

When new imaging modalities are first used in sports medicine, symptomatic athletes are inevitably examined more closely than control subjects. This may lead investigators to draw incorrect conclusions about the significance of imaging findings and clinical symptoms in the athletic population. For example, the early cases of severe patellar tendinopathy, imaged by ultrasonography, all failed to respond to conservative management. Thus, it was concluded that a focal hypoechoic ultrasound region was not amenable to conservative management⁷ and that this radiologic finding per se was an indication for surgery.⁸

Subsequent studies have demonstrated the flaw in this assertion. The Victorian Institute of Sport researchers used ultrasound to image the patellar tendons of 160 asymptomatic elite male and female jumping athletes in sports including basketball.⁹ Hypoechoic regions were present in 22% of athletes’ tendons—more in male athletes (30%) than in females (14%). Although some would argue that this could represent the remains of previous jumper’s knee, sonographic hypoechoic regions were present in 14% of patellar tendons in athletes who had never had anterior knee pain.⁹ A study with MR also found poor correlation between regions of abnormal signal and clinical symptoms. The authors reported only 75% sensitivity and 76% specificity for MR imaging in patellar tendinopathy.¹⁰

Because patellar tendon imaging abnormalities exist in asymptomatic patellar tendons of a proportion of elite athletes, clearly this appearance cannot be used as an indication for surgery.⁹ Surgery can only be decided upon using clinical assessment together with imaging appearances.

After Surgery

Recent imaging studies of postoperative ultrasound and MR images^11,16 revealed abnormalities consistent with patellar tendinopathy (Figure 5) despite 11 of 15 (73%) subject tendons being rated clinically as either ”good” or “excellent.” Imaging modalities were unable to distinguish tendons so rated from those rated “poor” at 12 months. Even at four years postoperatively, ultrasound abnormalities persisted in now asymptomatic athletes.¹¹ There was no correlation between dimension of sonographic abnormality and either clinical rating¹⁷ or time since surgery.¹¹ Thus, clinicians ought to base postoperative management of patellar tenotomy patients on clinical grounds, rather than imaging findings. At present, there appears to be no role for routine postoperative imaging of patients recovering slowly after patellar tenotomy. This is not to suggest, however, that imaging cannot play a role in special circumstances.

After autograft surgery of the middle third of the patellar tendon for anterior cruciate ligament reconstruction, the elite athlete is prone to developing jumper’s knee. Several studies examined the ultrasound appearance of the healing donor site^14,18,19 and recent investigations provide MR and histopathologic data.¹⁹ Taken together, these studies provide further evidence that clinical progress does not correlate precisely with imaging appearance. Furthermore, the patellar donor site remains histologically abnormal even two years after surgery.

Predictability

To determine whether these findings were predictors of future symptoms in these athletes, the authors followed their progress for one to two years and discovered that there was a four times greater incidence of clinical patellar tendinopathy in those athletes with the sonographic abnormality.²¹

Yet the case for screening athletes in anticipation of symptoms of jumper’s knee remains controversial. In adult athletes, there appears to be poor correlation between sonographic abnormality and current symptoms,^9,22 and the same seems to apply when they are screened with MR.¹⁰ The few studies²³ examining whether or not sonographic abnormality can predict future symptoms found no association, but these particular studies did not use MR. On the other hand, sonographic abnormalities in 14 to 18-year-old basketball players predicted a quadrupling of risk for symptomatic patellar tendinopathy.²¹ Further studies are needed, using both ultrasound and MR.

Radiologists play an important role in educating primary care physicians and should use the terms “patellar tendinopathy” or “patellar tendinosis” when reporting the characteristic imaging appearance of jumper’s knee traditionally mislabeled “patellar tendinitis.” Radiologists should emphasize that in adults, clinical correlation with imaging is essential, and especially that the finding of a focal hypoechoic region is not necessarily an indication for surgery. Radiologists should teach clinicians that after patellar tenotomy, routine postoperative imaging is not a useful guide to management. The time for patients to recover from surgery is six to 12 months, so clinicians should not expect clinical or radiological recovery before then.

References

1. Maffulli N, Khan KM, Puddu G. Overuse tendon conditions. Time to change a confusing terminology. Arthroscopy 1998;14:840-843.
2. Khan KM, Bonar F, Desmond PM, et al. Patellar tendinosis (jumper’s knee): findings at histopathologic examination, US and MR imaging. Radiology 1996;200:821-827.
3. Erickson SJ, Prost RW, Timins ME. The ‘magic angle’ effect: background physics and clinical relevance. Radiology 1993;188:23-25.
4. Fornage BD. The hypoechoic normal tendon: a pitfall. JUM 1987;6:19-22.
5. Khan KM, Cook JL, Bonar F, et al. Histopathology of common overuse tendon conditions: update and implications for clinical management. SM 1999;27:393-408.
6. Khan KM, Cook JL, Taunton JE, Bonar F. Overuse tendinosis, not tendinitis. Part 1: A new paradigm for a difficult clinical problem. PSM 2000;28(5):38-48.
7. Myllymäki T, Bondestam S, Suramo I, et al. Ultrasonography of jumper’s knee. Acta Radiologica 1990;31(2):147-149.
8. Fritschy D, de Gautard R. Jumper’s knee and ultrasonography. AJSM 1988;16:637-640.
9. Cook JL, Khan KM, Harcourt PR, et al. Patellar tendon ultrasonography in asymptomatic active athletes reveals hypoechoic regions: a study of 320 tendons. CJSM 1998;8:73-77.
10. Shalaby M, Almekinders LC. Patellar tendinitis: the significance of magnetic resonance imaging findings. AJSM 1999;27:345-349.
11. Coleman BD, Khan KM, Kiss ZS, et al. Outcomes of open and arthroscopic patellar tenotomy for chronic patellar tendinopathy: a retrospective study. AJSM 2000;28:183-190.
12. Sandmeier R, Renstrom P. Diagnosis and treatment of chronic tendon disorders in sport. SJMSS1997;7:96-106.
13. Duri ZAA, Aichroth PM. Patellar tendonitis: clinical and literature review. KSSTA 1995;3:95-100.
14. Wiley JP, Bray RC, Wiseman DA, et al. Serial ultrasonographic imaging evaluation of the patellar tendon after harvesting its central one third for anterior cruciate ligament reconstruction. JUM 1997;16(4):251-255.
15. Fornage BD, Rifkin MD. Ultrasound examination of tendons. RCNA 1988;26:87-107.
16. Khan KM, Visentini PJ, Kiss ZS, et al. Correlation of US and MR imaging with clinical outcome after open patellar tenotomy: prospective and retrospective studies. CJSM 1999;9:129-137.
17. Visentini PJ, Khan KM, Cook JL, et al. The VISA score: an index of the severity of jumper’s knee (patellar tendinosis). JSMS 1998;1:22-28.
18. Kiss ZS, Kellaway D, Cook J, Khan K. Postoperative patellar tendon healing–an ultrasound study. AR 1998;42:28-32.
19. Kartus J, Movin T, Papadogiannakis N, et al. A radiographic and histologic evaluation of the patellar tendon after harvesting its central third. AJSM 2000;28:218-226.
20. Cook JL, Khan KM, Kiss ZS, et al. Patellar tendinopathy in junior basketball players: a controlled clinical and ultrasonographic study of 268 patellar tendons in players aged 14-18 years. SJMSS 2000;10:216-220.
21. Cook JL, Khan KM, Kiss ZS, et al. Patellar tendon ultrasound in asymptomatic elite junior basketball players: A 12-month longitudinal study in 52 tendons. JUM 2000;19:473-479.
22. Lian O, Holen KJ, Engebrestson L, Bahr R. Relationship between symptoms of jumper’s knee and the ultrasound characteristics of the patellar tendon among high level male volleyball players. SJMSS 1996; 6:291-296.
23. Khan KM, Cook JL, Kiss ZS, et al. Patellar tendon ultrasonography and jumper’s knee in elite female basketball players: a longitudinal study. CJSM 1997;7:199-206.

She’s got game

Recent advances in understanding imaging and histopathology of jumper’s knee have important implications for patient management. In one case, a basketball player who had a long history of bilateral jumper’s knee was in hard training with an Olympic basketball team when she developed a sudden, severe tearing pain at the patellar tendon attachment to the patella during a practice sprint. She was unable to walk for a few days.

Clinically, this was consistent with an acute partial tendon tear. The athlete had had an ultrasound scan before this episode, and follow-up showed no change in the size of the abnormality. Thus, rather than undergoing surgery, she was managed conservatively, and she returned to playing in two weeks. She competed at the Olympic Games four weeks later, with fewer symptoms than she had prior to the episode. Her symptoms subsequently remained at this new, lower level.

If there had been an inappropriate emphasis on sonographic morphology (the hypoechoic abnormality), this athlete could have been sent for surgery and would have watched the games on TV in a hospital. Conservatively managed, she stood instead on the dais and received her Olympic medal.