Patellar Tendinosis Acute Patellar Tendon Rupture and Jumper's Knee

Transcription

Patellar Tendinosis Acute Patellar Tendon Rupture and Jumper's Knee
The Physician and Sportsmedicine: Patellar Tendinosis
Patellar Tendinosis
Acute Patellar Tendon Rupture and Jumper's Knee
Michael James DePalma, MD; Robert Harrison Perkins, MD
THE PHYSICIAN AND SPORTSMEDICINE - VOL 32 - NO. 5 - MAY 2004
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In Brief: Patellar tendinopathy (jumper's knee) may affect athletes who engage in explosive
lower-limb movements. An eccentric contraction of the quadriceps when landing after a jump
may lead to acute patellar tendon rupture, the end-stage of patellar tendinopathy. Plain x-rays
will usually confirm the diagnosis. Treatment centers around reducing the stress placed on the
patellar tendon. Postoperative functional restoration and preventive measures must address
biomechanic abnormalities that may predispose patients to disruptive patellar tendon strain. As
this case report shows, counseling patients who have early-stage tendinopathy on appropriate
flexibility and plyometric exercises may prevent more serious damage.
Patellar tendinopathy, or jumper's knee, is a relatively common condition in patients who
engage in sports that involve explosive lower-limb movements. It is characterized by localized
collagen degeneration and subsequent fibrosis at the bone-tendon junction of the inferior
patellar pole1-5 (figure 1).
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The Physician and Sportsmedicine: Patellar Tendinosis
Jumper's knee may also be viewed as a spectrum that ranges from initial overuse inflammatory
changes to chronic degenerative breakdown.2 Clinically, this spectrum can be divided into four
stages based on symptoms:
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Stage 1: Pain occurs only after activity;
Stage 2: Pain starts at the beginning of activity, dissipates after warm-up, and recurs
with fatigue;
Stage 3: Pain occurs at rest and with activity and affects performance; and
Stage 4: The patellar ligament completely ruptures.1,2
Acute patellar ligament ruptures occur more often in men than in women and usually affect
athletes who are younger than 40.2,5,6 The mechanism of injury involves an eccentric
contraction of the quadriceps, usually during landing after a jump.1,2 Surgical repair is
successful with good functional outcome when performed within 2 weeks of injury.2,4-7 Poor
outcomes have been observed in patients with postoperative patellofemoral incongruity, patella
alta, or chondromalacia.2,4,6,7 This case report, involving stage 4 tendinopathy, helps illustrate
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The Physician and Sportsmedicine: Patellar Tendinosis
predisposing factors, optimal diagnosis and treatment, and preventive interventions.
Case Report
While participating in a three-on-three basketball tournament, a 34-year-old recreational
athlete "landed hard" after a lay-up. He heard an immediate "pop" and felt a cramp in his left
knee. The patient was not able to bear weight or actively extend his knee.
After a courtside evaluation, he was taken to the emergency department. He reported no
history of traumatic knee injuries or systemic disorders; however, during physical examination,
he remembered he had been previously told by an orthopedic specialist that he had patellar
"tendinitis." The condition had resolved with rest and traditional anti-inflammatory agents. The
patient disclosed that he experienced intermittent anterior knee pain with squatting and
ascending stairs in the month prior to his injury.
Exam. On inspection, the patella was located proximal to the tibiofemoral joint with a large
effusion. The inferior patellar pole was tender, and a palpable gap in the patellar tendon was
noted. The athlete could not actively extend his knee against gravity, nor could he maintain
extension when his leg was passively placed in this position.
Tests and diagnosis. Plain radiographs revealed patella alta with avulsed bone fragments in
the proximal portion of the patellar tendon. The distal patellar pole was elongated, possibly
indicative of chronic distal patellar traction stresses, and soft-tissue shadows were consistent
with induration and effusion (figure 2). The Insall-Salvati ratio (ratio of patellar tendon length
to patellar height) was measured at 2.1. A normal knee is 1.0, and a variation of more than
20% indicates abnormal position of the patella. The Caton ratio (ratio between patellar articular
length and the distance between inferior pole and tibial tubercle) was measured as 1.9; normal
is 0.8.
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Treatment. On day 6 after the injury, the patient underwent surgical repair with wire
reinforcement. Both medial and lateral extensor retinacular tears were also repaired.
Postoperative radiographs revealed an Insall-Salvati ratio of 1.5 and a Caton ratio of 1.2
(figure 3). Initial postoperative rehabilitation included weight bearing as tolerated, isometric
knee extension, and active knee flexion to 60° at 2 weeks. At 6 weeks, the patient
incorporated active knee extension into his regimen. By 3 months after surgery, he had
progressed to closed-chain activities (eg, leg presses, calf raises) that addressed hip, thigh,
and ankle muscle strength and flexibility. At 9 months after repair, the athlete reported mild
swelling with light athletic activity, but no recurrent anterior knee pain. He returned to shooting
baskets, but we do not know if he ever returned to his preinjury level of play.
The Patellar Tendinopathy Spectrum
Prior damage to the knee from overuse or trauma, biomechanic factors, and the forces
inherent in landing from a jump probably contribute to tendon fatigue and patellar tendon
rupture.
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Tissue damage. Patellar tendinopathy has commonly been labeled "patellar tendinitis" without
histologic evidence supporting this diagnosis. Histologic studies of patellar tendon specimens
obtained during surgical repair have demonstrated intratendinous mucoid degeneration without
the presence of inflammatory cells.2,3,5,8 However, in the acute stages, inflammatory cells may
be present in the paratenon.2,8
At the advanced stage, when surgical treatment is pursued, clinically painful tendons are
characterized at the cellular level by collagen fragmentation, increased ground substance, and
neovascularization.2,8 This abnormal tissue may develop from the ineffectual healing response
to repetitive microtears within the tendon. The natural healing process may not be capable of
healing the lesion once this abnormal tissue develops.2,5,6 Therefore, it is more appropriate to
diagnose "jumper's knee" as patellar tendinopathy rather than as patellar tendinitis.2,8
Treatment efforts should focus on functional restoration rather than on curtailing an
inflammatory reaction.
A study by McMaster9 documented that healthy tendons do not rupture, and this construct has
been widely accepted.2,6,7 Minimal differences in tensile and viscoelastic properties of the
patellar tendon exist between younger and older age-groups.10 Hence, a threshold level of
tendon degeneration is probably requisite to tendon rupture.7
In the athlete older than 35, less intense repetitive microtrauma can induce age-related
pathologic changes,6 perhaps because of less efficient vascular and reparative properties.7
Although conclusive evidence is lacking, otherwise healthy patellar tendons probably rupture as
a consequence of repetitive-microtrauma–induced degeneration. More important, it has not
been proven whether structural changes of tendinopathy or a decreased resistance to fatigue is
integral to injury. Regardless, this moment of tendon failure represents end-stage (stage 4)
jumper's knee.
The athlete in this case report did not undergo histologic examination. Within the 6 months
before his injury, an orthopedic specialist had diagnosed him with patellar "tendinitis," and he
was symptomatic with activities of daily living (stage 2).
Biomechanic factors. Several static and dynamic biomechanic factors that increase tensile
load on the patellar tendon have been related to patellar tendinopathy.2 However, few studies
have identified the causal relationships between these factors and the incidence of patellar
tendinopathy.
Anatomic characteristics that may be associated with patellar tendinopathy include patella alta,
poor patellofemoral tracking, patellar instability, malalignment, and leg-length discrepancy.2,11
Distal and proximal abnormalities, such as pes planus, decreased ankle dorsiflexion, coxa vara,
and femoral anteversion, contribute as well.2,8
Forces generated in landing are substantially greater than those generated during jumping.
Approximately 60% of the landing force is absorbed distal to the knee.8 A wide range of hip or
knee flexion combined with forefoot landing can further reduce landing forces by another 25%.
Inflexibility or weakness of the gluteal, quadriceps, hamstrings, tensor fascia lata, or calf
musculature can restrict range of motion and increase loads experienced by the anterior
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knee.8,12 Rapid midfoot pronation on dynamic testing allowed more force transmission to the
knee.8
When surgical intervention occurs within 2 weeks after a complete rupture, good functional
outcome typified by less knee pain, minimal lower limb muscle atrophy with less than 20% loss
of strength, and return to baseline activity have been achieved.2,5,13 The presence of pre- and
postoperative patella alta or baja, chondromalacia, or patellofemoral incongruity can
predispose the patient to recurrent anterior knee pain and adversely affect functional
outcome.6,13 A high-riding patella (confirmed by an increased Insall-Salvati or Caton ratio) will
decrease the moment arm of the knee extensor mechanism, increasing tensile loads placed on
the patellar ligament.6 Furthermore, patella alta may initiate chondromalacia, leading to
patellofemoral pain.6 Biomechanic abnormalities that increase tensile load on the patellar
tendon have been related to patellar tendinopathy, but the causal contribution of these findings
is still uncertain.
Studies, such as the one by Witvrouw et al,14 have documented the positive correlation
between clinical overloading of the patellar tendon and the development of jumper's knee.
However, strong prospective evidence is lacking regarding the relationship of intrinsic factors
and patellar tendinopathy.
Flexibility. Retrospective and cohort studies support the concept of a relative lack of flexibility
leading to tendon strain and subsequent tendon overload injury.11,14 Witvrouw et al14
prospectively studied the incidence of patellar tendinopathy in student-athletes 17 to 21 years
old and found that decreased flexibility of the quadriceps and hamstring muscles predisposed
the subjects to patellar tendinitis. The authors suggested that routine evaluation for inflexibility
and properly restoring flexibility when identified is crucial to preventing patellar tendinitis.
Our literature search failed to discover a randomized, prospective study assessing the effect of
such stretching efforts on the incidence of patellar tendinitis. A 1984 epidemiologic study15 of
the occurrence of jumper's knee in volleyball players did not find a significant difference in the
incidence of patellar tendinopathy between players who used plyometric training (ie, jumping
after landing from jumps of various heights) and those who did not. The authors concluded
that plyometric training, three times per week, was less harmful to tendons than once believed.
Recommendations
A conditioning program incorporating routine trunk and lower-limb stretching, as well as
plyometric training, may help diminish excessive stress on the patient's anterior knee. Further
research is warranted to delineate the relationship between conditioning and anterior knee
stress and the specific training parameters necessary to minimize strain on the tendon.
However, it is intuitive that repetitive landing with one or more predisposing biomechanic
factors brings the tendon to the fatigue threshold more quickly. Thus, the entire kinetic chain
must be addressed when physicians approach functional restoration of jumping athletes.
References
1. Blazina ME, Kerlan RK, Jobe FW, et al: Jumper's knee. Orthop Clin North Am 1973;4
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The Physician and Sportsmedicine: Patellar Tendinosis
(3):665-678
2. Rodeo SA, Izawa K: Diagnosis and treatment of knee tendon injury, in Garrett WE Jr,
Speer KP, Kirkendall DT (eds): Principles and Practice of Orthopaedic Sports Medicine.
Philadelphia, Lippincott Williams & Wilkins, 2000, pp 687-708
3. Panni AS, Tartarone M, Maffulli N: Patellar tendinopathy in athletes: outcome of
nonoperative and operative management. Am J Sports Med 2000;28(3):392-397
4. Ferretti A, Ippolito E, Mariani P, et al: Jumper's knee. Am J Sports Med 1983;11(2):5862
5. Khan KM, Bonar F, Desmond PM, et al: Patellar tendinosis (jumper's knee): findings at
histopathologic examination, US, and MR imaging. Victorian Institute of Sport Tendon
Study Group. Radiology 1996;200(3):821-827
6. Siwek CW, Rao JP: Ruptures of the extensor mechanism of the knee joint. J Bone Joint
Surg Am 1981;63(6):932-937
7. Kelly DW, Carter VS, Jobe FW, et al: Patellar and quadriceps tendon ruptures: jumper's
knee. Am J Sports Med 1984;12(5):375-380
8. Larsen E, Lund PM: Ruptures of the extensor mechanism of the knee joint: clinical
results and patellofemoral articulation. Clin Orthop 1986;213(Dec):150-153
9. McMaster PE: Tendon and muscle ruptures: clinical and experimental studies on the
causes and location of subcutaneous ruptures. J Bone Joint Surg 1933;15(July):705-722
10. Johnson GA, Tramaglini DM, Levine RE, et al: Tensile and viscoelastic properties of
human patellar tendon. J Orthop Res 1994;12(6):796-803
11. Gleim GW, McHugh MP: Flexibility and its effect on sports injury and performance.
Sports Med 1997;24(5):289-299
12. Cook JL, Khan KM, Maffulli N, et al: Overuse tendinosis, not tendinitis, part 2: applying
the new approach to patellar tendinopathy. Phys Sportsmed 2000;28(6):31-46
13. Marder RA, Timmerman LA: Primary repair of patellar tendon rupture without
augmentation. Am J Sports Med 1999;27(3):304-307
14. Witvrouw E, Bellemans J, Lysens R, et al: Intrinsic risk factors for the development of
patellar tendinitis in an athletic population: a two-year prospective study. Am J Sports
Med 2001;29(2):190-195
15. Ferretti A, Puddu G, Mariani PP, et al: Jumper's knee: an epidemiological study of
volleyball players. Phys Sportsmed 1984;12(10):97-106
Dr DePalma is chief resident and Dr Perkins is a clinical assistant professor in the department
of physical medicine and rehabilitation at The Ohio State University in Columbus, Ohio.
Address correspondence to Michael J. DePalma, MD, Dodd Hall, The Ohio State University,
480 West Ninth Ave, Columbus, OH 43210; e-mail to [email protected].
Disclosure information: Drs DePalma and Perkins disclose no significant relationship with
any manufacturer of any commercial product mentioned in this article. No drug is mentioned in
this article for an unlabeled use.
RETURN TO MAY 2004 TABLE OF CONTENTS
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The Physician and Sportsmedicine: Patellar Tendinosis
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