The Diagnosis and Initial Treatment of Patellofemoral Disorders

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The Diagnosis and Initial Treatment of Patellofemoral Disorders

Take-Home Points

  • Patellofemoral disorders should be classified and diagnosed according to specific diagnostic categories (eg, lateral patellar compression syndrome) based on etiology rather than nondescriptive terminology (eg, internal derangement, patellofemoral pain syndrome).
  • Patellofemoral dysplasia defines a spectrum of abnormalities ranging from the mild lateral patellar compression syndrome to the severe recurrent patellar dislocation.
  • There is an inverse relationship between patient activity level and underlying patellofemoral dysplasia. This relationship determines threshold levels for each patient becoming symptomatic.
  • Patients should be examined for 7 physical abnormalities, and if present, in what severity. These 7 are: vastus medialis obliquus deficiency, medial patellofemoral ligament laxity, lateral retinaculum tightness, increased quadriceps angle, hip abductor weakness, patella alta, and trochlear dysplasia.
  • Advanced imaging is rarely, if ever, needed to make a diagnosis or to formulate an initial treatment plan for these common patellofemoral disorders.

To diagnose any disease or disorder implies an understanding of the condition’s cause(s), which should then lead to a logical treatment plan. For all too long, however, the diagnosis and treatment of patellofemoral disorders have been hampered by diagnoses that lack specific definitions based on etiology. A few of these are: internal derangement, chondromalacia patellae, patellar maltracking, and patellofemoral pain syndrome.

To simplify the diagnosis of patellofemoral disorders, we use a clinical classification based on etiology. This system’s defined diagnostic categories are useful in identifying probable cause(s), which can be appropriately evaluated and treated (Table).1 In simple terms, the philosophy of this approach is to try to find out what’s wrong, and try to fix it!

This clinical classification provides a framework for common patellofemoral conditions that are more easily diagnosed, yet is intentionally incomplete omitting rare conditions (eg, tumors, metabolic bone disease, neurologic conditions).

Table.
This allows the focus to fall on the common and frequently misunderstood causes for patellofemoral pain and instability. In this article, we address patellofemoral dysplasia (section II of the Table) and its classification relating to initial evaluation and early treatment. This entity defines a spectrum of abnormalities, ranging from the mild lateral patellar compression syndrome (LPCS) to the moderate chronic subluxation of the patella (CSP) and severe recurrent dislocation of the patella (RDP). Each presumptive diagnosis is suggested by the patient’s history and confirmed by physical examination and radiography. Computed tomography (CT), magnetic resonance imaging (MRI), and other advanced imaging modalities are seldom needed to establish a working diagnosis and an initial treatment plan, though they can be important in operative planning for complex cases.

Patellofemoral Dysplasia

Patellofemoral dysplasia (or extensor mechanism malfunction) is a cluster of physical abnormalities relating to the patellofemoral joint that vary from mild to severe and affect the normal function of that joint. As such, patellofemoral dysplasia itself should be considered on a continuum of mild to severe. To simplify the diagnosis, the clinician should systematically identify these factors and their severity. Armed with this information, the clinician can make the diagnosis and formulate a logical treatment plan for each individual patient.

This article focuses on 7 physical abnormalities that are most likely developmental and that can be identified through physical and radiologic examination. When and how each patient with patellofemoral dysplasia becomes symptomatic are determined by 2 key factors: patellofemoral dysplasia severity and activity level (sedentary to strenuous), in an inverse relationship (Figure 1).2

Figure 1.
Their complex interplay determines when a patient exceeds the “envelope of function”3 and passes from asymptomatic to symptomatic.

Seven Key Patellofemoral Physical Abnormalities

Of the 7 commonly identified physical abnormalities that affect the normal functioning of the patellofemoral joint, 5 are discovered by physical examination and 2 by radiography; CT and MRI are seldom needed in the initial evaluation. The most accurate and objective method should be used to assess the presence and severity of each abnormality.

The 7 abnormalities are vastus medialis obliquus (VMO) deficiency, medial patellofemoral ligament (MPFL) laxity, lateral retinaculum (LR) tightness, increased quadriceps (Q) angle, hip abductor weakness, patella alta, and trochlear dysplasia. We list these not in order of importance but in the order in which they are usually encountered during initial evaluation. We advocate for examining both knees including axial patellofemoral radiographs because patellofemoral disorders are frequently bilateral. It is helpful to use an abnormality checklist so none are forgotten. Also useful is a simple shorthand for findings: 0 = normal (no abnormality), 1 = mild abnormality, 2 = moderate abnormality, 3 = severe abnormality, with the right knee always recorded first (R/L). For example, severe left MPFL laxity is recorded as 0/3. Numerical values (eg, Q angles) can be directly recorded in this manner: 14°/23°.

 

 

1. Vastus Medialis Obliquus Deficiency

VMO deficiency is best seen as the sitting patient actively maintains the unsupported foot and leg at 30° knee flexion. Normally, the VMO inserts into the upper half or third of the medial edge of the patella; a deficient VMO inserts higher into the medial edge of the quadriceps tendon, or it is absent and leaves a characteristic hollow at the medial edge of the patella (Figure 2).4

Figure 2.
Studies using ultrasonography and CT have found significant correlations between VMO abnormalities and anterior knee pain.5,6 Although there is no simple clinical method of measuring VMO deficiency, clinicians experienced in observing knees can assess VMO deficiency and grade each case mild, moderate, or severe. The VMO deficiency weakens the medial quadriceps vector, increasing the lateral vector, and thereby increases the “dynamic” Q angle, originally described by Brattström.7

2. Medial Patellofemoral Ligament Laxity

MPFL laxity is assessed with the lateral glide test. Again, the patient sits, but with quadriceps relaxed and foot and leg supported at 30° knee flexion. With the clinician mentally dividing the patella into vertical quadrants and pushing the patella laterally, the normal patella moves about 1 quadrant or 1 fingerbreadth. Severe MPFL laxity often elicits a positive apprehension response during the test. (Tip: Many patients are unable to relax the quadriceps while sitting; therefore, examine them supine and lift the knee into 30° flexion.) Such laxity usually means the MPFL was torn in a previous dislocation and remains elongated, leaving the patella vulnerable to repeated dislocations. The clinician should be alert to the possibility of hyperelastosis (Ehlers-Danlos syndrome) and a hyper-mobile patella. The opposite limb should be evaluated for asymmetric laxity.

3. Lateral Retinaculum Tightness

LR tightness is assessed with the medial glide test, again with the quadriceps relaxed and the knee supported at 30° flexion. With a normal LR, the patella can be pushed medially about 1 quadrant or 1 fingerbreadth. Some clinicians prefer the lateral tilt-up test, in which the lateral edge of the patella is lifted up, but this method is more difficult to quantify, is affected by the cross-sectional shape of the patella, and lacks consistency.

4. Increased Quadriceps Angle

The Q angle is one of the most important factors in the normal functioning of the patellofemoral joint. For more than a century,8 multiple operations have been used successfully to move the tibial tubercle (TT) and patellar ligament from a lateral position to a medial position thereby decreasing the Q angle. It is only logical to measure this angle at every knee examination to check for an abnormal increase, and the degree. The term quadriceps angle, or Q angle, was first used in 1964 by Brattström,7 who defined it as the “supplemental angle” to the valgus angle formed by the “quadriceps’ resultant” (line of force or vector) “+ patella + ligamentum patellae”. This might be called the dynamic Q angle. With there being no clinical method of measuring the “quadriceps line of force”, or quadriceps vector, clinicians used a line from the anterior superior iliac spine to the center of the patella, yet still called it the Q angle. By convention, this anatomical Q angle has been accepted as the Q angle.

Because the Q angle is the only clinical measurement of TT lateralization at initial evaluation, its measurement should be standardized, accurate, and simple to perform. Placing the patient supine with the lower limb in neutral rotation (patella anterior) and the knee in full extension standardizes the position. In full extension, the tibia reaches its maximum external rotation owing to the terminal “screw home” mechanism. The clinician should center the patella to the trochlear groove (TG) while measuring the Q angle, as it is the relationship of the TT to the trochlea, not to the patella, that is important. If LR tightness prevents the patella from centering, that fact should be recorded during the medial glide test for LR tightness.

Figure 3.
For accuracy, the goniometer should have one or more arms long enough to reach the anterior superior iliac spine. A long-armed goniometer is simple to make, and 2 extendable goniometers are commercially available (Figures 3A-3C).

Despite the importance of measuring the Q angle, there has been no standard technique. Multiple authors have attempted to define the “normal” Q angle. In 1999, Post9 reviewed 7 articles on the topic and found no agreement. Mean normal Q angles varied widely, from 5° to 23° (SD range, 0.08°-5°). Grelsamer and colleagues,10 using a long-armed goniometer and standard technique, found a mean Q angle of 15.7° for women and 13.3° for men; the small, 2.4° difference between them disappeared when the measurements were corrected for height. Men and women of similar height have similar Q angles. These findings disproved the common misattribution of the differences to the wider female pelvis.

Given this confusion and the lack of accuracy in measuring the Q angle, many, if not most, surgeons turned to special CT and MRI scanning techniques to measure the distance of lateralization from TT to TG (TT-TG distance). This technique, by necessity, enforced a standardization not found in the earlier Q angles studies. Patients were positioned supine with the knee fully extended, and patellar position was ignored in favor of the TG. However, recent articles11-14have called into question the accuracy and usefulness of TT-TG distance as an assessment of TT lateralization. As such, standardized measurement of the Q angle remains a simple, inexpensive, and clinically relevant method of assessing TT lateralization.

The possible causes of an increased Q angle are valgus limb alignment, internal femoral torsion, external tibial torsion, combined internal femoral and external tibial torsion with foot pronation (the “miserable malalignment” of James and colleagues15), and a TT-lateralizing proximal tibial malformation.

 

 

5. Hip Abductor Weakness

The step-down test is easily performed in the office by having the patient stand on a short stool or stair and then slowly step down with the opposite limb to just touch the heel and slowly arise again. A positive test is indicated by the Trendelenburg sign, with the pelvis dropping down and away from the symptomatic supporting limb, the flexing knee collapsing into valgus, and the patient tending to wobble and lack stability (Figure 4).16

Figure 4.
With mild hip abductor weakness, these changes can be subtle, but they may become more severe with increasing weakness. Khayambashi and colleagues17 found that hip abductor weakness can be a major cause of patellofemoral pain.

6. Patella Alta

Patella alta not only allows the patella to escape the confines of the trochlea earlier during active knee extension increasing the risk of patellar dislocation, but also decreases the contact footprint with the trochlea, increasing the patellofemoral joint reaction force and potentially causing patellofemoral pain and even secondary chondrosis. The simplest way to assess patellar height is with a lateral radiograph of the knee. The 3 popular methods (Insall-Salvati, Caton-Deschamps, Blackburn-Peel) all put the normal patellar height ratio at approximately 1:1, ± 20%. Berg and colleagues18 compared radiologic techniques for measuring patellar height ratio and found that Blackburn-Peel was the most accurate, reliable, and reproducible method.

7. Trochlear Dysplasia

Trochlear dysplasia, most simply a flattening of the TG, is perhaps the most important factor effecting normal patellofemoral function. However, it remains the most difficult to correctly address surgically. Senavongse and Amis19 conducted a cadaveric study demonstrating the prime importance of the TG. They found patellar stability was reduced 30% by releasing the VMO, 49% by cutting the MPFL in full knee extension, and 70% by flattening the trochlea. The most common, successful operations for correcting patellar instability depend on changing other factors that guide patellar excursion to compensate for this trochlear flattening.

The simplest way to assess trochlear dysplasia is to measure the sulcus angle on an accurate axial view radiograph of the knee at 45° flexion (Merchant view).20 Dejour and colleagues21 popularized a technique of assessing and classifying trochlear dysplasia from a true lateral radiograph of the knee, which has the advantage of showing the trochlear at its proximal extent. Davies and colleagues22 evaluated the Dejour technique, along with patellar tilt, patellar height, and sulcus angle, to identify a rapid and reproducible radiologic feature that would indicate the need for further analysis by other imaging studies (eg, CT, MRI). They found that, if the sulcus angle was normal, analysis of other radiologic features was unlikely to reveal additional useful information. They also showed a correlation of increasing sulcus angle and severity of those other dysplasia features. Merchant and colleagues20 found a mean normal sulcus angle of 138º (SD, 6º; range, 126º-150º), and Aglietti and colleagues23 confirmed those findings with nearly identical values (mean, 137º; SD, 6º; range, 116º-151º).

Diagnosis and Initial Treatment Plan

Patellofemoral disorders generally are divided into patellofemoral pain and instability, but these 2 diagnostic categories are too broad to be useful. Patellofemoral pain is a symptom. Patellofemoral pain syndrome should never be used as a diagnosis because there is no accepted definition for the cluster of findings that customarily defines a syndrome. At initial evaluation, after the easily diagnosed causes of anterior knee pain (eg, prepatellar bursitis, TT apophysitis, patellar and quadriceps tendinitis) have been ruled out, the clinician should consider types of patellofemoral dysplasia for a presumptive diagnosis, which will then lead to a logical treatment program for each identified disorder. With a presumptive diagnosis established, almost all patients suffering from chronic anterior knee pain without history of injury are treated initially with rest, ice, and nonsteroidal anti-inflammatory drugs to restore joint homeostasis.3

Lateral Patellar Compression Syndrome

In 1975, Ficat and colleagues24 described features of what they called syndrome d’hyperpression externe de la rotule. Two years later, Ficat and Hungerford25 defined the syndrome as one “in which the patella is well centered in the trochlear sulcus and stable, but in which there is a functional lateralization onto a physiologically and often anatomically predominant lateral facet.” Using the tools we have described here, the clinician usually finds the cause(s) of this “functional lateralization.” Four abnormalities—VMO deficiency, LR tightness, increased standardized Q angle, and hip abductor weakness—can cause functional lateralization either alone when severe or in combination when mild or moderate.

For a presumptive diagnosis of LPCS, initial treatment is nonoperative, and successful in about 90% of patients. It should be obvious that most patients with chronic anterior knee pain have quadriceps atrophy. Physical therapy should be specifically focused on quadriceps strengthening, with absolutely no stress placed on the patellofemoral joint in flexion initially, and on hip abductor strengthening. Progressive resistive isometric quadriceps exercises can be performed with a weight-bench technique (Figures 5A-5D).26

Figure 5.
These isometric progressive resistive quadriceps (DeHaven27) exercises can also be performed with a simple straight-leg weight-lifting program at home (Figure 6).28
Figure 6.
The advantage of isometric quadriceps strengthening is that the knee is in full extension, the patella lies above the trochlea, and there is no patellofemoral joint movement or compression. A patient of average stature can gradually increase quadriceps strength to resist or lift about 20 lb. Progressive hip abductor strengthening can be done in physical therapy or at home using side-lying abductor exercises with ankle weights. DeHaven27 exercises should be painless when done correctly, but contraindicated in patients with patellar tendinitis, quadriceps tendinitis, TT apophysitis (Osgood-Schlatter’s), and anterior fat pad (Hoffa’s) syndrome. When appropriate, certain adjunctive modalities for reducing functional lateralization should be tried. Use of McConnell taping and patellar bracing to resist this lateralization can be very helpful. If symptoms persist despite the 20-lb quadriceps goal being achieved and adequate hip abductor strength being demonstrated in a normal step-down test, conservative management has failed. Review and reassessment of the remaining abnormal physical factors (tight LR, increased Q angle) will lead to logical choices in surgical management.

 

 

Chronic Subluxation of Patella

With the use of axial patellofemoral radiographs (Merchant views),20 the clinician can determine if the “patella is well centered in the trochlear sulcus and stable” (an important part of the definition of LPCS). If the patient has no symptoms of recurrent instability or patellar dislocation, and these radiographs show a laterally subluxed patella (one not well centered in the trochlea), the diagnosis is most likely CSP, a moderate form of patellofemoral dysplasia (section II of the Table). In addition to the 4 abnormalities used in the diagnosis of LPCS (mentioned earlier), trochlear dysplasia also comes into play in the diagnosis of CSP. Just as the other abnormalities can vary from mild to severe, trochlear dysplasia can vary from mild (slightly shallow sulcus angle) to severe (flat or even convex sulcus angle). As the sulcus becomes shallower, the patella slides more laterally, increasing the likelihood of patellar dislocation.

As the patient with CSP gives no history of episodic patellar instability, treatment for CSP is almost identical to that for LPCS, with the primary focus on isometric quadriceps strengthening (DeHaven isometric exercises)27 and hip abductor muscle strengthening. In the presence of CSP radiographically, it is important to use McConnell taping and/or patellar bracing during muscular strengthening. A patient who achieves 20-lb isometric quadriceps strength, demonstrates a normal step-down test, and is assumed to be asymptomatic can be allowed to return to sports activities with use of a patellar brace. The patient should be counseled that there is an increased risk for patellar dislocation because of this chronic subluxation and the shallower sulcus.

As in LPCS, CSP symptoms that persist after dynamic strength is regained may require surgical intervention. The severity of identified abnormal factors (tight LR, increased Q angle, trochlear dysplasia) guides the surgeon in selecting appropriate corrective technique(s).

Recurrent Dislocation of Patella

Admittedly, given the number and subtlety of abnormal factors, the diagnosis of LPCS as a cause of patellofemoral pain can be challenging. However, RDP is at the opposite end of the spectrum. A history of prior patellar dislocation(s) almost always makes the diagnosis of RDP easier. The patient occasionally complains of a recurrent symptom, the knee “going out” or “giving way,” indicating that the diagnosis might be RDP. By carefully asking what the patient was doing and what happened when the knee “went out”, the clinician may be able to determine if the injury stemmed from sudden patellar pain causing reflex inhibition of the quadriceps or was a true dislocation. Both may be described as “going out” or “giving way”.

Assessment for the same 7 abnormalities helps establish the diagnosis, a logical treatment plan, and a guide for indicated surgery. The diagnostic focus is MPFL laxity and trochlear dysplasia. Prior lateral dislocation of the patella almost always requires rupture of the normal MPFL. The infrequent exception is a patient with hyper-elasticity of the skin and multiple joints (Ehlers-Danlos syndrome). Trochlear dysplasia is a significant risk factor for patellar dislocation. If the trochlea is normal and there is no MPFL laxity, the diagnosis of RDP should be questioned.

If surgery is indicated, the surgeon uses a list of the patient’s abnormalities and their severity as a guide in selecting reconstructive techniques. The more abnormalities found and the greater the severity of each, the more techniques are needed to achieve success. Preoperative exercises help speed postoperative recovery by addressing quadriceps and hip abductor weakness. In addition, an active exercise program gives the surgeon insight into the patient’s desire for and commitment to recovery. Other physical abnormalities to be considered in preoperative planning include MPFL laxity, LR tightness, increased Q angle, patella alta, and trochlear dysplasia.

Surgical tips: 1. When releasing the LR, never cut the vastus lateralis tendon, as this has a high likelihood of causing iatrogenic medial patellar subluxation.29 2. When medializing the TT, consider compensating for a shallow trochlea by “over-correcting” the Q angle to 5° to 10° measured with a surgical goniometer intraoperatively.

Summary

Basing clinical classification of disorders on etiology is a simple and effective way to diagnose common patellofemoral conditions. Identifying and rating the severity of patellofemoral dysplasia, using 7 commonly found physical abnormalities, guide the physician to a proper diagnosis and down logical treatment pathways. These principles should be incorporated into the routine evaluation of patellofemoral disorders to optimize diagnosis, formulate a treatment plan, and improve patient outcomes. After all, this is what our patients are asking us to do: Try to find what’s wrong, and then try to fix it!

Am J Orthop. 2017;46(2):68-75. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Merchant AC. Classification of patellofemoral disorders. Arthroscopy. 1988;4(4):235-240.

2. Merchant AC. Patellofemoral disorders: biomechanics, diagnosis, and nonoperative treatment. In: McGinty JB, Caspari RB, Jackson RW, Poehling GG, eds. Operative Arthroscopy. New York, NY: Raven Press; 1991:261-275.

3. Dye SF. The knee as a biologic transmission with an envelope of function: a theory. Clin Orthop Relat Res. 1996;(325):10-18.

4. Merchant AC. A philosophy of the patellofemoral joint: a logical clinical approach. In: Sanchis-Alfonso V, ed. Anterior Knee Pain and Patellar Instability. 2nd ed. London, England: Springer; 2011:519-530.

5. Jan MH, Lin DH, Lin JJ, Lin CH, Cheng CK, Lin YF. Differences in sonographic characteristics of the vastus medialis obliquus between patients with patellofemoral pain syndrome and healthy adults. Am J Sports Med. 2009;37(9):1743-1749.

6. Pattyn E, Verdonk P, Steyaert A, et al. Vastus medialis obliquus atrophy: does it exist in patellofemoral pain syndrome? Am J Sports Med. 2011;39(7):1450-1455.

7. Brattström H. Shape of the intercondylar groove normally and in recurrent dislocation of the patella. A clinical and x-ray anatomical investigation. Acta Orthop Scand Suppl. 1964;68:1-147.

8. Roux D. Luxation habituelle de la rotule: traitement operatoire. Rev Chir Orthop Reparatrice Appar Mot. 1888;8:682-689.

9. Post WR. Clinical evaluation of patients with patellofemoral disorders. Arthroscopy. 1999;15(8):841-851.

10. Grelsamer RP, Dubey A, Weinstein CH. Men and women have similar Q angles: a clinical and trigonometric evaluation. J Bone Joint Surg Br. 2005;87(11):1498-1501.

11. Skelley N, Friedman M, McGinnis M, Smith C, Hillen T, Matava M. Inter- and intraobserver reliability in the MRI measurement of the tibial tubercle-trochlear groove distance and trochlea dysplasia. Am J Sports Med. 2015;43(4):873-878.

12. Tensho K, Akaoka Y, Shimodaira H, et al. What components comprise the measurement of the tibial tuberosity-trochlear groove distance in a patellar dislocation population? J Bone Joint Surg Am. 2015;97(17):1441-1448.

13. Camp CL, Heidenreich MJ, Dahm DL, Stuart MJ, Levy BA, Krych AJ. Individualizing the tibial tubercle-trochlear groove distance: patellar instability ratios that predict recurrent instability. Am J Sports Med. 2016;44(2):393-399.

14. Ridley TJ, Hinckel BB, Kruckeberg BM, Agel J, Arendt EA. Anatomical patella instability risk factors on MRI show sensitivity without specificity in patients with patellofemoral instability: a systematic review. JISAKOS. 2016;1(3):141-152.

15. James SL, Bates BT, Osternig LR. Injuries to runners. Am J Sports Med. 1978;6(2):40-50.

16. Powers CM, Souza RB, Fulkerson JP. Patellofemoral joint. In: Magee DJ, Zachazewski JE, Quillen WS, eds. Pathology and Intervention in Musculoskeletal Rehabilitation. St. Louis, MO: Saunders Elsevier; 2008:601-636.

17. Khayambashi K, Mohammadkhani Z, Ghaznavi K, Lyle MA, Powers CM. The effects of isolated hip abductor and external rotator muscle strengthening on pain, health status, and strength in females with patellofemoral pain: a randomized controlled trial. J Orthop Sports Phys Ther. 2012;42(1):22-29.

18. Berg EE, Mason SL, Lucas MJ. Patellar height ratios. A comparison of four measurement methods. Am J Sports Med. 1996;24(2):218-221.

19. Senavongse W, Amis AA. The effects of articular, retinacular, or muscular deficiencies on patellofemoral joint stability: a biomechanical study in vitro. J Bone Joint Surg Br. 2005;87(4):577-582.

20. Merchant AC, Mercer RL, Jacobsen RH, Cool CR. Roentgenographic analysis of patellofemoral congruence. J Bone Joint Surg Am. 1974;56(7):1391-1396.

21. Dejour H, Neyret P, Walch G. Factors in patellar instability. In: Aichroth PM, Cannon WD Jr, Patel DV, eds. Knee Surgery: Current Practice. London, England: Martin Dunitz; 1992.

22. Davies AP, Costa ML, Shepstone L, Glasgow MM, Donell S. The sulcus angle and malalignment of the extensor mechanism of the knee. J Bone Joint Surg Br. 2000;82(8):1162-1166.

23. Aglietti P, Insall JN, Cerulli G. Patellar pain and incongruence. I: measurements of incongruence. Clin Orthop Relat Res. 1983;(176):217-224.

24. Ficat P, Ficat C, Bailieaux A. External hypertension syndrome of the patella. Its significance in the recognition of arthrosis [in French]. Rev Chir Orthop Reparatrice Appar Mot. 1975;61(1):39-59.

25. Ficat P, Hungerford DS. Disorders of the Patellofemoral Joint. Baltimore, MD: Williams & Wilkins; 1977.

26. Merchant AC. The lateral compression syndrome. In: Fox JM, Del Pizzo W, eds. The Patellofemoral Joint. New York, NY: McGraw-Hill; 1993:157-175.

27. DeHaven KE, Dolan WA, Mayer PJ. Chondromalacia patellae in athletes. Clinical presentation and conservative management. Am J Sports Med. 1979;7(1):5-11.

28. Merchant AC. Patellofemoral joint disorders. In: Chapman MW, ed. Operative Orthopedics. Vol 3. Philadelphia, PA: Lippincott; 1988:2321-2366.

29. Sanchis-Alfonso V, Merchant AC. Iatrogenic medial patellar instability: an avoidable injury. Arthroscopy. 2015;31(8):1628-1632.

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Take-Home Points

  • Patellofemoral disorders should be classified and diagnosed according to specific diagnostic categories (eg, lateral patellar compression syndrome) based on etiology rather than nondescriptive terminology (eg, internal derangement, patellofemoral pain syndrome).
  • Patellofemoral dysplasia defines a spectrum of abnormalities ranging from the mild lateral patellar compression syndrome to the severe recurrent patellar dislocation.
  • There is an inverse relationship between patient activity level and underlying patellofemoral dysplasia. This relationship determines threshold levels for each patient becoming symptomatic.
  • Patients should be examined for 7 physical abnormalities, and if present, in what severity. These 7 are: vastus medialis obliquus deficiency, medial patellofemoral ligament laxity, lateral retinaculum tightness, increased quadriceps angle, hip abductor weakness, patella alta, and trochlear dysplasia.
  • Advanced imaging is rarely, if ever, needed to make a diagnosis or to formulate an initial treatment plan for these common patellofemoral disorders.

To diagnose any disease or disorder implies an understanding of the condition’s cause(s), which should then lead to a logical treatment plan. For all too long, however, the diagnosis and treatment of patellofemoral disorders have been hampered by diagnoses that lack specific definitions based on etiology. A few of these are: internal derangement, chondromalacia patellae, patellar maltracking, and patellofemoral pain syndrome.

To simplify the diagnosis of patellofemoral disorders, we use a clinical classification based on etiology. This system’s defined diagnostic categories are useful in identifying probable cause(s), which can be appropriately evaluated and treated (Table).1 In simple terms, the philosophy of this approach is to try to find out what’s wrong, and try to fix it!

This clinical classification provides a framework for common patellofemoral conditions that are more easily diagnosed, yet is intentionally incomplete omitting rare conditions (eg, tumors, metabolic bone disease, neurologic conditions).

Table.
This allows the focus to fall on the common and frequently misunderstood causes for patellofemoral pain and instability. In this article, we address patellofemoral dysplasia (section II of the Table) and its classification relating to initial evaluation and early treatment. This entity defines a spectrum of abnormalities, ranging from the mild lateral patellar compression syndrome (LPCS) to the moderate chronic subluxation of the patella (CSP) and severe recurrent dislocation of the patella (RDP). Each presumptive diagnosis is suggested by the patient’s history and confirmed by physical examination and radiography. Computed tomography (CT), magnetic resonance imaging (MRI), and other advanced imaging modalities are seldom needed to establish a working diagnosis and an initial treatment plan, though they can be important in operative planning for complex cases.

Patellofemoral Dysplasia

Patellofemoral dysplasia (or extensor mechanism malfunction) is a cluster of physical abnormalities relating to the patellofemoral joint that vary from mild to severe and affect the normal function of that joint. As such, patellofemoral dysplasia itself should be considered on a continuum of mild to severe. To simplify the diagnosis, the clinician should systematically identify these factors and their severity. Armed with this information, the clinician can make the diagnosis and formulate a logical treatment plan for each individual patient.

This article focuses on 7 physical abnormalities that are most likely developmental and that can be identified through physical and radiologic examination. When and how each patient with patellofemoral dysplasia becomes symptomatic are determined by 2 key factors: patellofemoral dysplasia severity and activity level (sedentary to strenuous), in an inverse relationship (Figure 1).2

Figure 1.
Their complex interplay determines when a patient exceeds the “envelope of function”3 and passes from asymptomatic to symptomatic.

Seven Key Patellofemoral Physical Abnormalities

Of the 7 commonly identified physical abnormalities that affect the normal functioning of the patellofemoral joint, 5 are discovered by physical examination and 2 by radiography; CT and MRI are seldom needed in the initial evaluation. The most accurate and objective method should be used to assess the presence and severity of each abnormality.

The 7 abnormalities are vastus medialis obliquus (VMO) deficiency, medial patellofemoral ligament (MPFL) laxity, lateral retinaculum (LR) tightness, increased quadriceps (Q) angle, hip abductor weakness, patella alta, and trochlear dysplasia. We list these not in order of importance but in the order in which they are usually encountered during initial evaluation. We advocate for examining both knees including axial patellofemoral radiographs because patellofemoral disorders are frequently bilateral. It is helpful to use an abnormality checklist so none are forgotten. Also useful is a simple shorthand for findings: 0 = normal (no abnormality), 1 = mild abnormality, 2 = moderate abnormality, 3 = severe abnormality, with the right knee always recorded first (R/L). For example, severe left MPFL laxity is recorded as 0/3. Numerical values (eg, Q angles) can be directly recorded in this manner: 14°/23°.

 

 

1. Vastus Medialis Obliquus Deficiency

VMO deficiency is best seen as the sitting patient actively maintains the unsupported foot and leg at 30° knee flexion. Normally, the VMO inserts into the upper half or third of the medial edge of the patella; a deficient VMO inserts higher into the medial edge of the quadriceps tendon, or it is absent and leaves a characteristic hollow at the medial edge of the patella (Figure 2).4

Figure 2.
Studies using ultrasonography and CT have found significant correlations between VMO abnormalities and anterior knee pain.5,6 Although there is no simple clinical method of measuring VMO deficiency, clinicians experienced in observing knees can assess VMO deficiency and grade each case mild, moderate, or severe. The VMO deficiency weakens the medial quadriceps vector, increasing the lateral vector, and thereby increases the “dynamic” Q angle, originally described by Brattström.7

2. Medial Patellofemoral Ligament Laxity

MPFL laxity is assessed with the lateral glide test. Again, the patient sits, but with quadriceps relaxed and foot and leg supported at 30° knee flexion. With the clinician mentally dividing the patella into vertical quadrants and pushing the patella laterally, the normal patella moves about 1 quadrant or 1 fingerbreadth. Severe MPFL laxity often elicits a positive apprehension response during the test. (Tip: Many patients are unable to relax the quadriceps while sitting; therefore, examine them supine and lift the knee into 30° flexion.) Such laxity usually means the MPFL was torn in a previous dislocation and remains elongated, leaving the patella vulnerable to repeated dislocations. The clinician should be alert to the possibility of hyperelastosis (Ehlers-Danlos syndrome) and a hyper-mobile patella. The opposite limb should be evaluated for asymmetric laxity.

3. Lateral Retinaculum Tightness

LR tightness is assessed with the medial glide test, again with the quadriceps relaxed and the knee supported at 30° flexion. With a normal LR, the patella can be pushed medially about 1 quadrant or 1 fingerbreadth. Some clinicians prefer the lateral tilt-up test, in which the lateral edge of the patella is lifted up, but this method is more difficult to quantify, is affected by the cross-sectional shape of the patella, and lacks consistency.

4. Increased Quadriceps Angle

The Q angle is one of the most important factors in the normal functioning of the patellofemoral joint. For more than a century,8 multiple operations have been used successfully to move the tibial tubercle (TT) and patellar ligament from a lateral position to a medial position thereby decreasing the Q angle. It is only logical to measure this angle at every knee examination to check for an abnormal increase, and the degree. The term quadriceps angle, or Q angle, was first used in 1964 by Brattström,7 who defined it as the “supplemental angle” to the valgus angle formed by the “quadriceps’ resultant” (line of force or vector) “+ patella + ligamentum patellae”. This might be called the dynamic Q angle. With there being no clinical method of measuring the “quadriceps line of force”, or quadriceps vector, clinicians used a line from the anterior superior iliac spine to the center of the patella, yet still called it the Q angle. By convention, this anatomical Q angle has been accepted as the Q angle.

Because the Q angle is the only clinical measurement of TT lateralization at initial evaluation, its measurement should be standardized, accurate, and simple to perform. Placing the patient supine with the lower limb in neutral rotation (patella anterior) and the knee in full extension standardizes the position. In full extension, the tibia reaches its maximum external rotation owing to the terminal “screw home” mechanism. The clinician should center the patella to the trochlear groove (TG) while measuring the Q angle, as it is the relationship of the TT to the trochlea, not to the patella, that is important. If LR tightness prevents the patella from centering, that fact should be recorded during the medial glide test for LR tightness.

Figure 3.
For accuracy, the goniometer should have one or more arms long enough to reach the anterior superior iliac spine. A long-armed goniometer is simple to make, and 2 extendable goniometers are commercially available (Figures 3A-3C).

Despite the importance of measuring the Q angle, there has been no standard technique. Multiple authors have attempted to define the “normal” Q angle. In 1999, Post9 reviewed 7 articles on the topic and found no agreement. Mean normal Q angles varied widely, from 5° to 23° (SD range, 0.08°-5°). Grelsamer and colleagues,10 using a long-armed goniometer and standard technique, found a mean Q angle of 15.7° for women and 13.3° for men; the small, 2.4° difference between them disappeared when the measurements were corrected for height. Men and women of similar height have similar Q angles. These findings disproved the common misattribution of the differences to the wider female pelvis.

Given this confusion and the lack of accuracy in measuring the Q angle, many, if not most, surgeons turned to special CT and MRI scanning techniques to measure the distance of lateralization from TT to TG (TT-TG distance). This technique, by necessity, enforced a standardization not found in the earlier Q angles studies. Patients were positioned supine with the knee fully extended, and patellar position was ignored in favor of the TG. However, recent articles11-14have called into question the accuracy and usefulness of TT-TG distance as an assessment of TT lateralization. As such, standardized measurement of the Q angle remains a simple, inexpensive, and clinically relevant method of assessing TT lateralization.

The possible causes of an increased Q angle are valgus limb alignment, internal femoral torsion, external tibial torsion, combined internal femoral and external tibial torsion with foot pronation (the “miserable malalignment” of James and colleagues15), and a TT-lateralizing proximal tibial malformation.

 

 

5. Hip Abductor Weakness

The step-down test is easily performed in the office by having the patient stand on a short stool or stair and then slowly step down with the opposite limb to just touch the heel and slowly arise again. A positive test is indicated by the Trendelenburg sign, with the pelvis dropping down and away from the symptomatic supporting limb, the flexing knee collapsing into valgus, and the patient tending to wobble and lack stability (Figure 4).16

Figure 4.
With mild hip abductor weakness, these changes can be subtle, but they may become more severe with increasing weakness. Khayambashi and colleagues17 found that hip abductor weakness can be a major cause of patellofemoral pain.

6. Patella Alta

Patella alta not only allows the patella to escape the confines of the trochlea earlier during active knee extension increasing the risk of patellar dislocation, but also decreases the contact footprint with the trochlea, increasing the patellofemoral joint reaction force and potentially causing patellofemoral pain and even secondary chondrosis. The simplest way to assess patellar height is with a lateral radiograph of the knee. The 3 popular methods (Insall-Salvati, Caton-Deschamps, Blackburn-Peel) all put the normal patellar height ratio at approximately 1:1, ± 20%. Berg and colleagues18 compared radiologic techniques for measuring patellar height ratio and found that Blackburn-Peel was the most accurate, reliable, and reproducible method.

7. Trochlear Dysplasia

Trochlear dysplasia, most simply a flattening of the TG, is perhaps the most important factor effecting normal patellofemoral function. However, it remains the most difficult to correctly address surgically. Senavongse and Amis19 conducted a cadaveric study demonstrating the prime importance of the TG. They found patellar stability was reduced 30% by releasing the VMO, 49% by cutting the MPFL in full knee extension, and 70% by flattening the trochlea. The most common, successful operations for correcting patellar instability depend on changing other factors that guide patellar excursion to compensate for this trochlear flattening.

The simplest way to assess trochlear dysplasia is to measure the sulcus angle on an accurate axial view radiograph of the knee at 45° flexion (Merchant view).20 Dejour and colleagues21 popularized a technique of assessing and classifying trochlear dysplasia from a true lateral radiograph of the knee, which has the advantage of showing the trochlear at its proximal extent. Davies and colleagues22 evaluated the Dejour technique, along with patellar tilt, patellar height, and sulcus angle, to identify a rapid and reproducible radiologic feature that would indicate the need for further analysis by other imaging studies (eg, CT, MRI). They found that, if the sulcus angle was normal, analysis of other radiologic features was unlikely to reveal additional useful information. They also showed a correlation of increasing sulcus angle and severity of those other dysplasia features. Merchant and colleagues20 found a mean normal sulcus angle of 138º (SD, 6º; range, 126º-150º), and Aglietti and colleagues23 confirmed those findings with nearly identical values (mean, 137º; SD, 6º; range, 116º-151º).

Diagnosis and Initial Treatment Plan

Patellofemoral disorders generally are divided into patellofemoral pain and instability, but these 2 diagnostic categories are too broad to be useful. Patellofemoral pain is a symptom. Patellofemoral pain syndrome should never be used as a diagnosis because there is no accepted definition for the cluster of findings that customarily defines a syndrome. At initial evaluation, after the easily diagnosed causes of anterior knee pain (eg, prepatellar bursitis, TT apophysitis, patellar and quadriceps tendinitis) have been ruled out, the clinician should consider types of patellofemoral dysplasia for a presumptive diagnosis, which will then lead to a logical treatment program for each identified disorder. With a presumptive diagnosis established, almost all patients suffering from chronic anterior knee pain without history of injury are treated initially with rest, ice, and nonsteroidal anti-inflammatory drugs to restore joint homeostasis.3

Lateral Patellar Compression Syndrome

In 1975, Ficat and colleagues24 described features of what they called syndrome d’hyperpression externe de la rotule. Two years later, Ficat and Hungerford25 defined the syndrome as one “in which the patella is well centered in the trochlear sulcus and stable, but in which there is a functional lateralization onto a physiologically and often anatomically predominant lateral facet.” Using the tools we have described here, the clinician usually finds the cause(s) of this “functional lateralization.” Four abnormalities—VMO deficiency, LR tightness, increased standardized Q angle, and hip abductor weakness—can cause functional lateralization either alone when severe or in combination when mild or moderate.

For a presumptive diagnosis of LPCS, initial treatment is nonoperative, and successful in about 90% of patients. It should be obvious that most patients with chronic anterior knee pain have quadriceps atrophy. Physical therapy should be specifically focused on quadriceps strengthening, with absolutely no stress placed on the patellofemoral joint in flexion initially, and on hip abductor strengthening. Progressive resistive isometric quadriceps exercises can be performed with a weight-bench technique (Figures 5A-5D).26

Figure 5.
These isometric progressive resistive quadriceps (DeHaven27) exercises can also be performed with a simple straight-leg weight-lifting program at home (Figure 6).28
Figure 6.
The advantage of isometric quadriceps strengthening is that the knee is in full extension, the patella lies above the trochlea, and there is no patellofemoral joint movement or compression. A patient of average stature can gradually increase quadriceps strength to resist or lift about 20 lb. Progressive hip abductor strengthening can be done in physical therapy or at home using side-lying abductor exercises with ankle weights. DeHaven27 exercises should be painless when done correctly, but contraindicated in patients with patellar tendinitis, quadriceps tendinitis, TT apophysitis (Osgood-Schlatter’s), and anterior fat pad (Hoffa’s) syndrome. When appropriate, certain adjunctive modalities for reducing functional lateralization should be tried. Use of McConnell taping and patellar bracing to resist this lateralization can be very helpful. If symptoms persist despite the 20-lb quadriceps goal being achieved and adequate hip abductor strength being demonstrated in a normal step-down test, conservative management has failed. Review and reassessment of the remaining abnormal physical factors (tight LR, increased Q angle) will lead to logical choices in surgical management.

 

 

Chronic Subluxation of Patella

With the use of axial patellofemoral radiographs (Merchant views),20 the clinician can determine if the “patella is well centered in the trochlear sulcus and stable” (an important part of the definition of LPCS). If the patient has no symptoms of recurrent instability or patellar dislocation, and these radiographs show a laterally subluxed patella (one not well centered in the trochlea), the diagnosis is most likely CSP, a moderate form of patellofemoral dysplasia (section II of the Table). In addition to the 4 abnormalities used in the diagnosis of LPCS (mentioned earlier), trochlear dysplasia also comes into play in the diagnosis of CSP. Just as the other abnormalities can vary from mild to severe, trochlear dysplasia can vary from mild (slightly shallow sulcus angle) to severe (flat or even convex sulcus angle). As the sulcus becomes shallower, the patella slides more laterally, increasing the likelihood of patellar dislocation.

As the patient with CSP gives no history of episodic patellar instability, treatment for CSP is almost identical to that for LPCS, with the primary focus on isometric quadriceps strengthening (DeHaven isometric exercises)27 and hip abductor muscle strengthening. In the presence of CSP radiographically, it is important to use McConnell taping and/or patellar bracing during muscular strengthening. A patient who achieves 20-lb isometric quadriceps strength, demonstrates a normal step-down test, and is assumed to be asymptomatic can be allowed to return to sports activities with use of a patellar brace. The patient should be counseled that there is an increased risk for patellar dislocation because of this chronic subluxation and the shallower sulcus.

As in LPCS, CSP symptoms that persist after dynamic strength is regained may require surgical intervention. The severity of identified abnormal factors (tight LR, increased Q angle, trochlear dysplasia) guides the surgeon in selecting appropriate corrective technique(s).

Recurrent Dislocation of Patella

Admittedly, given the number and subtlety of abnormal factors, the diagnosis of LPCS as a cause of patellofemoral pain can be challenging. However, RDP is at the opposite end of the spectrum. A history of prior patellar dislocation(s) almost always makes the diagnosis of RDP easier. The patient occasionally complains of a recurrent symptom, the knee “going out” or “giving way,” indicating that the diagnosis might be RDP. By carefully asking what the patient was doing and what happened when the knee “went out”, the clinician may be able to determine if the injury stemmed from sudden patellar pain causing reflex inhibition of the quadriceps or was a true dislocation. Both may be described as “going out” or “giving way”.

Assessment for the same 7 abnormalities helps establish the diagnosis, a logical treatment plan, and a guide for indicated surgery. The diagnostic focus is MPFL laxity and trochlear dysplasia. Prior lateral dislocation of the patella almost always requires rupture of the normal MPFL. The infrequent exception is a patient with hyper-elasticity of the skin and multiple joints (Ehlers-Danlos syndrome). Trochlear dysplasia is a significant risk factor for patellar dislocation. If the trochlea is normal and there is no MPFL laxity, the diagnosis of RDP should be questioned.

If surgery is indicated, the surgeon uses a list of the patient’s abnormalities and their severity as a guide in selecting reconstructive techniques. The more abnormalities found and the greater the severity of each, the more techniques are needed to achieve success. Preoperative exercises help speed postoperative recovery by addressing quadriceps and hip abductor weakness. In addition, an active exercise program gives the surgeon insight into the patient’s desire for and commitment to recovery. Other physical abnormalities to be considered in preoperative planning include MPFL laxity, LR tightness, increased Q angle, patella alta, and trochlear dysplasia.

Surgical tips: 1. When releasing the LR, never cut the vastus lateralis tendon, as this has a high likelihood of causing iatrogenic medial patellar subluxation.29 2. When medializing the TT, consider compensating for a shallow trochlea by “over-correcting” the Q angle to 5° to 10° measured with a surgical goniometer intraoperatively.

Summary

Basing clinical classification of disorders on etiology is a simple and effective way to diagnose common patellofemoral conditions. Identifying and rating the severity of patellofemoral dysplasia, using 7 commonly found physical abnormalities, guide the physician to a proper diagnosis and down logical treatment pathways. These principles should be incorporated into the routine evaluation of patellofemoral disorders to optimize diagnosis, formulate a treatment plan, and improve patient outcomes. After all, this is what our patients are asking us to do: Try to find what’s wrong, and then try to fix it!

Am J Orthop. 2017;46(2):68-75. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

  • Patellofemoral disorders should be classified and diagnosed according to specific diagnostic categories (eg, lateral patellar compression syndrome) based on etiology rather than nondescriptive terminology (eg, internal derangement, patellofemoral pain syndrome).
  • Patellofemoral dysplasia defines a spectrum of abnormalities ranging from the mild lateral patellar compression syndrome to the severe recurrent patellar dislocation.
  • There is an inverse relationship between patient activity level and underlying patellofemoral dysplasia. This relationship determines threshold levels for each patient becoming symptomatic.
  • Patients should be examined for 7 physical abnormalities, and if present, in what severity. These 7 are: vastus medialis obliquus deficiency, medial patellofemoral ligament laxity, lateral retinaculum tightness, increased quadriceps angle, hip abductor weakness, patella alta, and trochlear dysplasia.
  • Advanced imaging is rarely, if ever, needed to make a diagnosis or to formulate an initial treatment plan for these common patellofemoral disorders.

To diagnose any disease or disorder implies an understanding of the condition’s cause(s), which should then lead to a logical treatment plan. For all too long, however, the diagnosis and treatment of patellofemoral disorders have been hampered by diagnoses that lack specific definitions based on etiology. A few of these are: internal derangement, chondromalacia patellae, patellar maltracking, and patellofemoral pain syndrome.

To simplify the diagnosis of patellofemoral disorders, we use a clinical classification based on etiology. This system’s defined diagnostic categories are useful in identifying probable cause(s), which can be appropriately evaluated and treated (Table).1 In simple terms, the philosophy of this approach is to try to find out what’s wrong, and try to fix it!

This clinical classification provides a framework for common patellofemoral conditions that are more easily diagnosed, yet is intentionally incomplete omitting rare conditions (eg, tumors, metabolic bone disease, neurologic conditions).

Table.
This allows the focus to fall on the common and frequently misunderstood causes for patellofemoral pain and instability. In this article, we address patellofemoral dysplasia (section II of the Table) and its classification relating to initial evaluation and early treatment. This entity defines a spectrum of abnormalities, ranging from the mild lateral patellar compression syndrome (LPCS) to the moderate chronic subluxation of the patella (CSP) and severe recurrent dislocation of the patella (RDP). Each presumptive diagnosis is suggested by the patient’s history and confirmed by physical examination and radiography. Computed tomography (CT), magnetic resonance imaging (MRI), and other advanced imaging modalities are seldom needed to establish a working diagnosis and an initial treatment plan, though they can be important in operative planning for complex cases.

Patellofemoral Dysplasia

Patellofemoral dysplasia (or extensor mechanism malfunction) is a cluster of physical abnormalities relating to the patellofemoral joint that vary from mild to severe and affect the normal function of that joint. As such, patellofemoral dysplasia itself should be considered on a continuum of mild to severe. To simplify the diagnosis, the clinician should systematically identify these factors and their severity. Armed with this information, the clinician can make the diagnosis and formulate a logical treatment plan for each individual patient.

This article focuses on 7 physical abnormalities that are most likely developmental and that can be identified through physical and radiologic examination. When and how each patient with patellofemoral dysplasia becomes symptomatic are determined by 2 key factors: patellofemoral dysplasia severity and activity level (sedentary to strenuous), in an inverse relationship (Figure 1).2

Figure 1.
Their complex interplay determines when a patient exceeds the “envelope of function”3 and passes from asymptomatic to symptomatic.

Seven Key Patellofemoral Physical Abnormalities

Of the 7 commonly identified physical abnormalities that affect the normal functioning of the patellofemoral joint, 5 are discovered by physical examination and 2 by radiography; CT and MRI are seldom needed in the initial evaluation. The most accurate and objective method should be used to assess the presence and severity of each abnormality.

The 7 abnormalities are vastus medialis obliquus (VMO) deficiency, medial patellofemoral ligament (MPFL) laxity, lateral retinaculum (LR) tightness, increased quadriceps (Q) angle, hip abductor weakness, patella alta, and trochlear dysplasia. We list these not in order of importance but in the order in which they are usually encountered during initial evaluation. We advocate for examining both knees including axial patellofemoral radiographs because patellofemoral disorders are frequently bilateral. It is helpful to use an abnormality checklist so none are forgotten. Also useful is a simple shorthand for findings: 0 = normal (no abnormality), 1 = mild abnormality, 2 = moderate abnormality, 3 = severe abnormality, with the right knee always recorded first (R/L). For example, severe left MPFL laxity is recorded as 0/3. Numerical values (eg, Q angles) can be directly recorded in this manner: 14°/23°.

 

 

1. Vastus Medialis Obliquus Deficiency

VMO deficiency is best seen as the sitting patient actively maintains the unsupported foot and leg at 30° knee flexion. Normally, the VMO inserts into the upper half or third of the medial edge of the patella; a deficient VMO inserts higher into the medial edge of the quadriceps tendon, or it is absent and leaves a characteristic hollow at the medial edge of the patella (Figure 2).4

Figure 2.
Studies using ultrasonography and CT have found significant correlations between VMO abnormalities and anterior knee pain.5,6 Although there is no simple clinical method of measuring VMO deficiency, clinicians experienced in observing knees can assess VMO deficiency and grade each case mild, moderate, or severe. The VMO deficiency weakens the medial quadriceps vector, increasing the lateral vector, and thereby increases the “dynamic” Q angle, originally described by Brattström.7

2. Medial Patellofemoral Ligament Laxity

MPFL laxity is assessed with the lateral glide test. Again, the patient sits, but with quadriceps relaxed and foot and leg supported at 30° knee flexion. With the clinician mentally dividing the patella into vertical quadrants and pushing the patella laterally, the normal patella moves about 1 quadrant or 1 fingerbreadth. Severe MPFL laxity often elicits a positive apprehension response during the test. (Tip: Many patients are unable to relax the quadriceps while sitting; therefore, examine them supine and lift the knee into 30° flexion.) Such laxity usually means the MPFL was torn in a previous dislocation and remains elongated, leaving the patella vulnerable to repeated dislocations. The clinician should be alert to the possibility of hyperelastosis (Ehlers-Danlos syndrome) and a hyper-mobile patella. The opposite limb should be evaluated for asymmetric laxity.

3. Lateral Retinaculum Tightness

LR tightness is assessed with the medial glide test, again with the quadriceps relaxed and the knee supported at 30° flexion. With a normal LR, the patella can be pushed medially about 1 quadrant or 1 fingerbreadth. Some clinicians prefer the lateral tilt-up test, in which the lateral edge of the patella is lifted up, but this method is more difficult to quantify, is affected by the cross-sectional shape of the patella, and lacks consistency.

4. Increased Quadriceps Angle

The Q angle is one of the most important factors in the normal functioning of the patellofemoral joint. For more than a century,8 multiple operations have been used successfully to move the tibial tubercle (TT) and patellar ligament from a lateral position to a medial position thereby decreasing the Q angle. It is only logical to measure this angle at every knee examination to check for an abnormal increase, and the degree. The term quadriceps angle, or Q angle, was first used in 1964 by Brattström,7 who defined it as the “supplemental angle” to the valgus angle formed by the “quadriceps’ resultant” (line of force or vector) “+ patella + ligamentum patellae”. This might be called the dynamic Q angle. With there being no clinical method of measuring the “quadriceps line of force”, or quadriceps vector, clinicians used a line from the anterior superior iliac spine to the center of the patella, yet still called it the Q angle. By convention, this anatomical Q angle has been accepted as the Q angle.

Because the Q angle is the only clinical measurement of TT lateralization at initial evaluation, its measurement should be standardized, accurate, and simple to perform. Placing the patient supine with the lower limb in neutral rotation (patella anterior) and the knee in full extension standardizes the position. In full extension, the tibia reaches its maximum external rotation owing to the terminal “screw home” mechanism. The clinician should center the patella to the trochlear groove (TG) while measuring the Q angle, as it is the relationship of the TT to the trochlea, not to the patella, that is important. If LR tightness prevents the patella from centering, that fact should be recorded during the medial glide test for LR tightness.

Figure 3.
For accuracy, the goniometer should have one or more arms long enough to reach the anterior superior iliac spine. A long-armed goniometer is simple to make, and 2 extendable goniometers are commercially available (Figures 3A-3C).

Despite the importance of measuring the Q angle, there has been no standard technique. Multiple authors have attempted to define the “normal” Q angle. In 1999, Post9 reviewed 7 articles on the topic and found no agreement. Mean normal Q angles varied widely, from 5° to 23° (SD range, 0.08°-5°). Grelsamer and colleagues,10 using a long-armed goniometer and standard technique, found a mean Q angle of 15.7° for women and 13.3° for men; the small, 2.4° difference between them disappeared when the measurements were corrected for height. Men and women of similar height have similar Q angles. These findings disproved the common misattribution of the differences to the wider female pelvis.

Given this confusion and the lack of accuracy in measuring the Q angle, many, if not most, surgeons turned to special CT and MRI scanning techniques to measure the distance of lateralization from TT to TG (TT-TG distance). This technique, by necessity, enforced a standardization not found in the earlier Q angles studies. Patients were positioned supine with the knee fully extended, and patellar position was ignored in favor of the TG. However, recent articles11-14have called into question the accuracy and usefulness of TT-TG distance as an assessment of TT lateralization. As such, standardized measurement of the Q angle remains a simple, inexpensive, and clinically relevant method of assessing TT lateralization.

The possible causes of an increased Q angle are valgus limb alignment, internal femoral torsion, external tibial torsion, combined internal femoral and external tibial torsion with foot pronation (the “miserable malalignment” of James and colleagues15), and a TT-lateralizing proximal tibial malformation.

 

 

5. Hip Abductor Weakness

The step-down test is easily performed in the office by having the patient stand on a short stool or stair and then slowly step down with the opposite limb to just touch the heel and slowly arise again. A positive test is indicated by the Trendelenburg sign, with the pelvis dropping down and away from the symptomatic supporting limb, the flexing knee collapsing into valgus, and the patient tending to wobble and lack stability (Figure 4).16

Figure 4.
With mild hip abductor weakness, these changes can be subtle, but they may become more severe with increasing weakness. Khayambashi and colleagues17 found that hip abductor weakness can be a major cause of patellofemoral pain.

6. Patella Alta

Patella alta not only allows the patella to escape the confines of the trochlea earlier during active knee extension increasing the risk of patellar dislocation, but also decreases the contact footprint with the trochlea, increasing the patellofemoral joint reaction force and potentially causing patellofemoral pain and even secondary chondrosis. The simplest way to assess patellar height is with a lateral radiograph of the knee. The 3 popular methods (Insall-Salvati, Caton-Deschamps, Blackburn-Peel) all put the normal patellar height ratio at approximately 1:1, ± 20%. Berg and colleagues18 compared radiologic techniques for measuring patellar height ratio and found that Blackburn-Peel was the most accurate, reliable, and reproducible method.

7. Trochlear Dysplasia

Trochlear dysplasia, most simply a flattening of the TG, is perhaps the most important factor effecting normal patellofemoral function. However, it remains the most difficult to correctly address surgically. Senavongse and Amis19 conducted a cadaveric study demonstrating the prime importance of the TG. They found patellar stability was reduced 30% by releasing the VMO, 49% by cutting the MPFL in full knee extension, and 70% by flattening the trochlea. The most common, successful operations for correcting patellar instability depend on changing other factors that guide patellar excursion to compensate for this trochlear flattening.

The simplest way to assess trochlear dysplasia is to measure the sulcus angle on an accurate axial view radiograph of the knee at 45° flexion (Merchant view).20 Dejour and colleagues21 popularized a technique of assessing and classifying trochlear dysplasia from a true lateral radiograph of the knee, which has the advantage of showing the trochlear at its proximal extent. Davies and colleagues22 evaluated the Dejour technique, along with patellar tilt, patellar height, and sulcus angle, to identify a rapid and reproducible radiologic feature that would indicate the need for further analysis by other imaging studies (eg, CT, MRI). They found that, if the sulcus angle was normal, analysis of other radiologic features was unlikely to reveal additional useful information. They also showed a correlation of increasing sulcus angle and severity of those other dysplasia features. Merchant and colleagues20 found a mean normal sulcus angle of 138º (SD, 6º; range, 126º-150º), and Aglietti and colleagues23 confirmed those findings with nearly identical values (mean, 137º; SD, 6º; range, 116º-151º).

Diagnosis and Initial Treatment Plan

Patellofemoral disorders generally are divided into patellofemoral pain and instability, but these 2 diagnostic categories are too broad to be useful. Patellofemoral pain is a symptom. Patellofemoral pain syndrome should never be used as a diagnosis because there is no accepted definition for the cluster of findings that customarily defines a syndrome. At initial evaluation, after the easily diagnosed causes of anterior knee pain (eg, prepatellar bursitis, TT apophysitis, patellar and quadriceps tendinitis) have been ruled out, the clinician should consider types of patellofemoral dysplasia for a presumptive diagnosis, which will then lead to a logical treatment program for each identified disorder. With a presumptive diagnosis established, almost all patients suffering from chronic anterior knee pain without history of injury are treated initially with rest, ice, and nonsteroidal anti-inflammatory drugs to restore joint homeostasis.3

Lateral Patellar Compression Syndrome

In 1975, Ficat and colleagues24 described features of what they called syndrome d’hyperpression externe de la rotule. Two years later, Ficat and Hungerford25 defined the syndrome as one “in which the patella is well centered in the trochlear sulcus and stable, but in which there is a functional lateralization onto a physiologically and often anatomically predominant lateral facet.” Using the tools we have described here, the clinician usually finds the cause(s) of this “functional lateralization.” Four abnormalities—VMO deficiency, LR tightness, increased standardized Q angle, and hip abductor weakness—can cause functional lateralization either alone when severe or in combination when mild or moderate.

For a presumptive diagnosis of LPCS, initial treatment is nonoperative, and successful in about 90% of patients. It should be obvious that most patients with chronic anterior knee pain have quadriceps atrophy. Physical therapy should be specifically focused on quadriceps strengthening, with absolutely no stress placed on the patellofemoral joint in flexion initially, and on hip abductor strengthening. Progressive resistive isometric quadriceps exercises can be performed with a weight-bench technique (Figures 5A-5D).26

Figure 5.
These isometric progressive resistive quadriceps (DeHaven27) exercises can also be performed with a simple straight-leg weight-lifting program at home (Figure 6).28
Figure 6.
The advantage of isometric quadriceps strengthening is that the knee is in full extension, the patella lies above the trochlea, and there is no patellofemoral joint movement or compression. A patient of average stature can gradually increase quadriceps strength to resist or lift about 20 lb. Progressive hip abductor strengthening can be done in physical therapy or at home using side-lying abductor exercises with ankle weights. DeHaven27 exercises should be painless when done correctly, but contraindicated in patients with patellar tendinitis, quadriceps tendinitis, TT apophysitis (Osgood-Schlatter’s), and anterior fat pad (Hoffa’s) syndrome. When appropriate, certain adjunctive modalities for reducing functional lateralization should be tried. Use of McConnell taping and patellar bracing to resist this lateralization can be very helpful. If symptoms persist despite the 20-lb quadriceps goal being achieved and adequate hip abductor strength being demonstrated in a normal step-down test, conservative management has failed. Review and reassessment of the remaining abnormal physical factors (tight LR, increased Q angle) will lead to logical choices in surgical management.

 

 

Chronic Subluxation of Patella

With the use of axial patellofemoral radiographs (Merchant views),20 the clinician can determine if the “patella is well centered in the trochlear sulcus and stable” (an important part of the definition of LPCS). If the patient has no symptoms of recurrent instability or patellar dislocation, and these radiographs show a laterally subluxed patella (one not well centered in the trochlea), the diagnosis is most likely CSP, a moderate form of patellofemoral dysplasia (section II of the Table). In addition to the 4 abnormalities used in the diagnosis of LPCS (mentioned earlier), trochlear dysplasia also comes into play in the diagnosis of CSP. Just as the other abnormalities can vary from mild to severe, trochlear dysplasia can vary from mild (slightly shallow sulcus angle) to severe (flat or even convex sulcus angle). As the sulcus becomes shallower, the patella slides more laterally, increasing the likelihood of patellar dislocation.

As the patient with CSP gives no history of episodic patellar instability, treatment for CSP is almost identical to that for LPCS, with the primary focus on isometric quadriceps strengthening (DeHaven isometric exercises)27 and hip abductor muscle strengthening. In the presence of CSP radiographically, it is important to use McConnell taping and/or patellar bracing during muscular strengthening. A patient who achieves 20-lb isometric quadriceps strength, demonstrates a normal step-down test, and is assumed to be asymptomatic can be allowed to return to sports activities with use of a patellar brace. The patient should be counseled that there is an increased risk for patellar dislocation because of this chronic subluxation and the shallower sulcus.

As in LPCS, CSP symptoms that persist after dynamic strength is regained may require surgical intervention. The severity of identified abnormal factors (tight LR, increased Q angle, trochlear dysplasia) guides the surgeon in selecting appropriate corrective technique(s).

Recurrent Dislocation of Patella

Admittedly, given the number and subtlety of abnormal factors, the diagnosis of LPCS as a cause of patellofemoral pain can be challenging. However, RDP is at the opposite end of the spectrum. A history of prior patellar dislocation(s) almost always makes the diagnosis of RDP easier. The patient occasionally complains of a recurrent symptom, the knee “going out” or “giving way,” indicating that the diagnosis might be RDP. By carefully asking what the patient was doing and what happened when the knee “went out”, the clinician may be able to determine if the injury stemmed from sudden patellar pain causing reflex inhibition of the quadriceps or was a true dislocation. Both may be described as “going out” or “giving way”.

Assessment for the same 7 abnormalities helps establish the diagnosis, a logical treatment plan, and a guide for indicated surgery. The diagnostic focus is MPFL laxity and trochlear dysplasia. Prior lateral dislocation of the patella almost always requires rupture of the normal MPFL. The infrequent exception is a patient with hyper-elasticity of the skin and multiple joints (Ehlers-Danlos syndrome). Trochlear dysplasia is a significant risk factor for patellar dislocation. If the trochlea is normal and there is no MPFL laxity, the diagnosis of RDP should be questioned.

If surgery is indicated, the surgeon uses a list of the patient’s abnormalities and their severity as a guide in selecting reconstructive techniques. The more abnormalities found and the greater the severity of each, the more techniques are needed to achieve success. Preoperative exercises help speed postoperative recovery by addressing quadriceps and hip abductor weakness. In addition, an active exercise program gives the surgeon insight into the patient’s desire for and commitment to recovery. Other physical abnormalities to be considered in preoperative planning include MPFL laxity, LR tightness, increased Q angle, patella alta, and trochlear dysplasia.

Surgical tips: 1. When releasing the LR, never cut the vastus lateralis tendon, as this has a high likelihood of causing iatrogenic medial patellar subluxation.29 2. When medializing the TT, consider compensating for a shallow trochlea by “over-correcting” the Q angle to 5° to 10° measured with a surgical goniometer intraoperatively.

Summary

Basing clinical classification of disorders on etiology is a simple and effective way to diagnose common patellofemoral conditions. Identifying and rating the severity of patellofemoral dysplasia, using 7 commonly found physical abnormalities, guide the physician to a proper diagnosis and down logical treatment pathways. These principles should be incorporated into the routine evaluation of patellofemoral disorders to optimize diagnosis, formulate a treatment plan, and improve patient outcomes. After all, this is what our patients are asking us to do: Try to find what’s wrong, and then try to fix it!

Am J Orthop. 2017;46(2):68-75. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Merchant AC. Classification of patellofemoral disorders. Arthroscopy. 1988;4(4):235-240.

2. Merchant AC. Patellofemoral disorders: biomechanics, diagnosis, and nonoperative treatment. In: McGinty JB, Caspari RB, Jackson RW, Poehling GG, eds. Operative Arthroscopy. New York, NY: Raven Press; 1991:261-275.

3. Dye SF. The knee as a biologic transmission with an envelope of function: a theory. Clin Orthop Relat Res. 1996;(325):10-18.

4. Merchant AC. A philosophy of the patellofemoral joint: a logical clinical approach. In: Sanchis-Alfonso V, ed. Anterior Knee Pain and Patellar Instability. 2nd ed. London, England: Springer; 2011:519-530.

5. Jan MH, Lin DH, Lin JJ, Lin CH, Cheng CK, Lin YF. Differences in sonographic characteristics of the vastus medialis obliquus between patients with patellofemoral pain syndrome and healthy adults. Am J Sports Med. 2009;37(9):1743-1749.

6. Pattyn E, Verdonk P, Steyaert A, et al. Vastus medialis obliquus atrophy: does it exist in patellofemoral pain syndrome? Am J Sports Med. 2011;39(7):1450-1455.

7. Brattström H. Shape of the intercondylar groove normally and in recurrent dislocation of the patella. A clinical and x-ray anatomical investigation. Acta Orthop Scand Suppl. 1964;68:1-147.

8. Roux D. Luxation habituelle de la rotule: traitement operatoire. Rev Chir Orthop Reparatrice Appar Mot. 1888;8:682-689.

9. Post WR. Clinical evaluation of patients with patellofemoral disorders. Arthroscopy. 1999;15(8):841-851.

10. Grelsamer RP, Dubey A, Weinstein CH. Men and women have similar Q angles: a clinical and trigonometric evaluation. J Bone Joint Surg Br. 2005;87(11):1498-1501.

11. Skelley N, Friedman M, McGinnis M, Smith C, Hillen T, Matava M. Inter- and intraobserver reliability in the MRI measurement of the tibial tubercle-trochlear groove distance and trochlea dysplasia. Am J Sports Med. 2015;43(4):873-878.

12. Tensho K, Akaoka Y, Shimodaira H, et al. What components comprise the measurement of the tibial tuberosity-trochlear groove distance in a patellar dislocation population? J Bone Joint Surg Am. 2015;97(17):1441-1448.

13. Camp CL, Heidenreich MJ, Dahm DL, Stuart MJ, Levy BA, Krych AJ. Individualizing the tibial tubercle-trochlear groove distance: patellar instability ratios that predict recurrent instability. Am J Sports Med. 2016;44(2):393-399.

14. Ridley TJ, Hinckel BB, Kruckeberg BM, Agel J, Arendt EA. Anatomical patella instability risk factors on MRI show sensitivity without specificity in patients with patellofemoral instability: a systematic review. JISAKOS. 2016;1(3):141-152.

15. James SL, Bates BT, Osternig LR. Injuries to runners. Am J Sports Med. 1978;6(2):40-50.

16. Powers CM, Souza RB, Fulkerson JP. Patellofemoral joint. In: Magee DJ, Zachazewski JE, Quillen WS, eds. Pathology and Intervention in Musculoskeletal Rehabilitation. St. Louis, MO: Saunders Elsevier; 2008:601-636.

17. Khayambashi K, Mohammadkhani Z, Ghaznavi K, Lyle MA, Powers CM. The effects of isolated hip abductor and external rotator muscle strengthening on pain, health status, and strength in females with patellofemoral pain: a randomized controlled trial. J Orthop Sports Phys Ther. 2012;42(1):22-29.

18. Berg EE, Mason SL, Lucas MJ. Patellar height ratios. A comparison of four measurement methods. Am J Sports Med. 1996;24(2):218-221.

19. Senavongse W, Amis AA. The effects of articular, retinacular, or muscular deficiencies on patellofemoral joint stability: a biomechanical study in vitro. J Bone Joint Surg Br. 2005;87(4):577-582.

20. Merchant AC, Mercer RL, Jacobsen RH, Cool CR. Roentgenographic analysis of patellofemoral congruence. J Bone Joint Surg Am. 1974;56(7):1391-1396.

21. Dejour H, Neyret P, Walch G. Factors in patellar instability. In: Aichroth PM, Cannon WD Jr, Patel DV, eds. Knee Surgery: Current Practice. London, England: Martin Dunitz; 1992.

22. Davies AP, Costa ML, Shepstone L, Glasgow MM, Donell S. The sulcus angle and malalignment of the extensor mechanism of the knee. J Bone Joint Surg Br. 2000;82(8):1162-1166.

23. Aglietti P, Insall JN, Cerulli G. Patellar pain and incongruence. I: measurements of incongruence. Clin Orthop Relat Res. 1983;(176):217-224.

24. Ficat P, Ficat C, Bailieaux A. External hypertension syndrome of the patella. Its significance in the recognition of arthrosis [in French]. Rev Chir Orthop Reparatrice Appar Mot. 1975;61(1):39-59.

25. Ficat P, Hungerford DS. Disorders of the Patellofemoral Joint. Baltimore, MD: Williams & Wilkins; 1977.

26. Merchant AC. The lateral compression syndrome. In: Fox JM, Del Pizzo W, eds. The Patellofemoral Joint. New York, NY: McGraw-Hill; 1993:157-175.

27. DeHaven KE, Dolan WA, Mayer PJ. Chondromalacia patellae in athletes. Clinical presentation and conservative management. Am J Sports Med. 1979;7(1):5-11.

28. Merchant AC. Patellofemoral joint disorders. In: Chapman MW, ed. Operative Orthopedics. Vol 3. Philadelphia, PA: Lippincott; 1988:2321-2366.

29. Sanchis-Alfonso V, Merchant AC. Iatrogenic medial patellar instability: an avoidable injury. Arthroscopy. 2015;31(8):1628-1632.

References

1. Merchant AC. Classification of patellofemoral disorders. Arthroscopy. 1988;4(4):235-240.

2. Merchant AC. Patellofemoral disorders: biomechanics, diagnosis, and nonoperative treatment. In: McGinty JB, Caspari RB, Jackson RW, Poehling GG, eds. Operative Arthroscopy. New York, NY: Raven Press; 1991:261-275.

3. Dye SF. The knee as a biologic transmission with an envelope of function: a theory. Clin Orthop Relat Res. 1996;(325):10-18.

4. Merchant AC. A philosophy of the patellofemoral joint: a logical clinical approach. In: Sanchis-Alfonso V, ed. Anterior Knee Pain and Patellar Instability. 2nd ed. London, England: Springer; 2011:519-530.

5. Jan MH, Lin DH, Lin JJ, Lin CH, Cheng CK, Lin YF. Differences in sonographic characteristics of the vastus medialis obliquus between patients with patellofemoral pain syndrome and healthy adults. Am J Sports Med. 2009;37(9):1743-1749.

6. Pattyn E, Verdonk P, Steyaert A, et al. Vastus medialis obliquus atrophy: does it exist in patellofemoral pain syndrome? Am J Sports Med. 2011;39(7):1450-1455.

7. Brattström H. Shape of the intercondylar groove normally and in recurrent dislocation of the patella. A clinical and x-ray anatomical investigation. Acta Orthop Scand Suppl. 1964;68:1-147.

8. Roux D. Luxation habituelle de la rotule: traitement operatoire. Rev Chir Orthop Reparatrice Appar Mot. 1888;8:682-689.

9. Post WR. Clinical evaluation of patients with patellofemoral disorders. Arthroscopy. 1999;15(8):841-851.

10. Grelsamer RP, Dubey A, Weinstein CH. Men and women have similar Q angles: a clinical and trigonometric evaluation. J Bone Joint Surg Br. 2005;87(11):1498-1501.

11. Skelley N, Friedman M, McGinnis M, Smith C, Hillen T, Matava M. Inter- and intraobserver reliability in the MRI measurement of the tibial tubercle-trochlear groove distance and trochlea dysplasia. Am J Sports Med. 2015;43(4):873-878.

12. Tensho K, Akaoka Y, Shimodaira H, et al. What components comprise the measurement of the tibial tuberosity-trochlear groove distance in a patellar dislocation population? J Bone Joint Surg Am. 2015;97(17):1441-1448.

13. Camp CL, Heidenreich MJ, Dahm DL, Stuart MJ, Levy BA, Krych AJ. Individualizing the tibial tubercle-trochlear groove distance: patellar instability ratios that predict recurrent instability. Am J Sports Med. 2016;44(2):393-399.

14. Ridley TJ, Hinckel BB, Kruckeberg BM, Agel J, Arendt EA. Anatomical patella instability risk factors on MRI show sensitivity without specificity in patients with patellofemoral instability: a systematic review. JISAKOS. 2016;1(3):141-152.

15. James SL, Bates BT, Osternig LR. Injuries to runners. Am J Sports Med. 1978;6(2):40-50.

16. Powers CM, Souza RB, Fulkerson JP. Patellofemoral joint. In: Magee DJ, Zachazewski JE, Quillen WS, eds. Pathology and Intervention in Musculoskeletal Rehabilitation. St. Louis, MO: Saunders Elsevier; 2008:601-636.

17. Khayambashi K, Mohammadkhani Z, Ghaznavi K, Lyle MA, Powers CM. The effects of isolated hip abductor and external rotator muscle strengthening on pain, health status, and strength in females with patellofemoral pain: a randomized controlled trial. J Orthop Sports Phys Ther. 2012;42(1):22-29.

18. Berg EE, Mason SL, Lucas MJ. Patellar height ratios. A comparison of four measurement methods. Am J Sports Med. 1996;24(2):218-221.

19. Senavongse W, Amis AA. The effects of articular, retinacular, or muscular deficiencies on patellofemoral joint stability: a biomechanical study in vitro. J Bone Joint Surg Br. 2005;87(4):577-582.

20. Merchant AC, Mercer RL, Jacobsen RH, Cool CR. Roentgenographic analysis of patellofemoral congruence. J Bone Joint Surg Am. 1974;56(7):1391-1396.

21. Dejour H, Neyret P, Walch G. Factors in patellar instability. In: Aichroth PM, Cannon WD Jr, Patel DV, eds. Knee Surgery: Current Practice. London, England: Martin Dunitz; 1992.

22. Davies AP, Costa ML, Shepstone L, Glasgow MM, Donell S. The sulcus angle and malalignment of the extensor mechanism of the knee. J Bone Joint Surg Br. 2000;82(8):1162-1166.

23. Aglietti P, Insall JN, Cerulli G. Patellar pain and incongruence. I: measurements of incongruence. Clin Orthop Relat Res. 1983;(176):217-224.

24. Ficat P, Ficat C, Bailieaux A. External hypertension syndrome of the patella. Its significance in the recognition of arthrosis [in French]. Rev Chir Orthop Reparatrice Appar Mot. 1975;61(1):39-59.

25. Ficat P, Hungerford DS. Disorders of the Patellofemoral Joint. Baltimore, MD: Williams & Wilkins; 1977.

26. Merchant AC. The lateral compression syndrome. In: Fox JM, Del Pizzo W, eds. The Patellofemoral Joint. New York, NY: McGraw-Hill; 1993:157-175.

27. DeHaven KE, Dolan WA, Mayer PJ. Chondromalacia patellae in athletes. Clinical presentation and conservative management. Am J Sports Med. 1979;7(1):5-11.

28. Merchant AC. Patellofemoral joint disorders. In: Chapman MW, ed. Operative Orthopedics. Vol 3. Philadelphia, PA: Lippincott; 1988:2321-2366.

29. Sanchis-Alfonso V, Merchant AC. Iatrogenic medial patellar instability: an avoidable injury. Arthroscopy. 2015;31(8):1628-1632.

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A Practical Guide to Understanding and Treating Patellofemoral Pain

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A Practical Guide to Understanding and Treating Patellofemoral Pain

Take-Home Points

  • Anterior knee pain is common, particularly in young females.
  • For most patients, activity modification and rest will control the pain; continuing to engage in painful activity only prolongs symptoms.
  • In physical therapy, core stability, weight loss, and hip strengthening are essential.
  • Surgery is required only in a very small subset of patients with anterior knee pain.
  • Traumatic and overload- related chondral defects that have resisted a reasonable amount of conservative (nonoperative) treatment may be arthroscopically assessed and treated when documented to cause persistent pain.

Anterior knee pain is common (AKP), particularly in young females. Understanding the biomechanics of a rapidly growing young female knee, whose pelvis is relatively wider than her male counterpart, helps greatly in understanding origins of AKP.1

Compared with males of similar weight and size, females often walk and run with increased valgus at the knee and internal rotation of the hip on heel strike. The patella contacts the lateral edge of the trochlea with more focal load on the distal lateral patella for a longer time in a female than in a male of similar stature because of the increased lateral force vector. Add the rigors of athletics, excessive body weight, use of high heels, or a predisposing structural anomaly, and painful focal overload can develop—resulting in pain on stairs, inability to run, and a visit to your office. Some male patients also develop AKP, often related to patellofemoral dysplasia or activity-related overload leading to a similar pattern and need for care. Fortunately, most young patients improve when they reduce physical activity, attain stable musculoskeletal maturity, or both.

In addition to focal articular overload occurring, retinacular structures about the anterior knee can be stressed by the structural imbalance resulting from the excessive and sudden internal rotation of the hip that occurs even during normal gait and often is related to female lower extremity function. Small nerve damage in the stressed retinaculum is an important cause of peripatellar pain2 and is best identified by clinical examination. Additionally, the infrapatellar fat pad may become pinched, causing synovial inflammation.

With these patients, reassurance can go a long way, and resting, taping, bracing, and anti-inflammatory medications are helpful. Dye3 has emphasized nonoperative treatmentand allowing patients to re-establish homeostatic balance of the patellofemoral joint. Establishing normal body weight plays a key role in the process, and focusing on lower extremity core stability, starting with increased strength in the hip external rotators, is important.4 In the majority of patients, these measures are all that is needed.

Traumatic Anterior Knee Pain

Direct trauma to the anterior knee causes an entirely different sort of pain. Knee pain may be retinacular, neuronal, synovial, bony, or articular. Nothing replaces careful, detailed clinical history taking and physical examination in determining the source of this pain. Much AKP, particularly in its early stages, is very focal. A specific injection of an anesthetic into a suspected retinacular pain location may solve the diagnostic dilemma. With many patients, paying attention to the specific degree of knee flexion in which the injury occurred helps in localizing the lesion. A flexed-knee impact injury (dashboard or fall directly onto anterior knee) is a common cause of articular damage on the mid or proximal patella and distal medial femoral condyle. Identifying this cause is particularly important in worker’s compensation cases, as the pattern is diagnostic of a direct blow to the knee and may confirm the patient’s history.

Treating painful patellofemoral lesions related to direct trauma can be difficult. Once they are identified and correlated with the physical examination and magnetic resonance imaging (MRI) findings, a treatment plan can be developed.

Examination, Testing, Imaging

Knowing how AKP started is important. Asking a patient to point to the origin of pain is essential. A pain diagram (having the patient draw a picture of the pain location) is also very helpful.5 Spontaneous onset suggests an underlying structural and/or functional problem rather than a traumatic event. Examination should include palpation of all structures and the retinaculum about the knee; careful appraisal of patella tracking, location of pain, and crepitus (angle of knee flexion), and evidence of possible pain referred from the back or hip; gait analysis for functional aberrations; assessment of patellar mobility; and standard radiographs, including a perfect lateral radiograph and a knee-flexion axial radiograph of no more than 30° to 45°. Computed tomography, radionuclide scintigraphy,3 and MRI can be very useful in select patients, but such imaging generally is not necessary in the management of routine AKP. However, these studies can be extremely helpful in patients with resistant pain.

 

 

Resistant Anterior Knee Pain

When nonoperative measures (rest, bracing, taping, physical therapy, activity modification) fail to relieve pain, more aggressive treatment may be warranted. The clinician must take extra time to listen to the patient, look for the precise source of the pain, and address it directly. Treatment depends on the specific source of pain. A chronically painful retinacular lesion or neuroma usually responds to release of the painful segment. After a retinacular source of pain has been identified and temporarily eliminated with injection of a local anesthetic, the pain source can be accurately resected and the patient quickly cured. When the chronically painful locus is an injured fat pad, resection provides complete relief.

For most orthopedic surgeons, the greatest dilemma is how to address a young person’s persistent pain in the setting of minimal objective evidence. In my experience with hundreds of arthroscopies, distinct distal lateral patella articular softening is common. In some cases, the degree of articular softening can be extreme, extending toward the central ridge or even across the center of the patella and involving 40% to 50% of the patella articular surface. This spongy, soft cartilage does not resist load normally, and in many cases pain is disabling. Most important is to acknowledge the problem, as many of these patients have been living with articular lesion pain for a year or more. As quality of life can be severely diminished by chronic patellofemoral pain, it behooves us to find answers and provide appropriate treatment. Although patients with this degree of articular softening and breakdown represent a small percentage of all patients with patellofemoral pain, identifying these cases is essential.

However benign-appearing, a resistant, painful patella articular lesion can be disabling. The key to treating a young person with a patella articular lesion objectively proved with imaging or arthroscopy is to inform the patient and family of the resistant nature of some lesions. In a referral patellofemoral practice, I see many patients who are disabled and depressed about the results of articular breakdown related to focal overload. Once the problem is identified, there is hope.

Prolonged rest and activity withdrawal usually help, but in some cases pain with stairs and daily activities continues. Running is usually impossible, which can be devastating for many young people.

My approach is to exhaust the nonoperative measures, which include focusing intensely on core stability training. The physical therapist must understand the importance of this treatment component; the patient must understand the importance of strengthening the hip external rotators and the vastus medialis oblique, modifying gait, avoiding pain-inducing activities, controlling weight, using proper footwear, and being patient. Applying heavy resistance to the quadriceps during rehabilitation will likely perpetuate or exacerbate the problem. The goals are to limit loading of the articular lesion and improve lower extremity function emphasizing reduction and balanced distribution of load.

Other Causes of Anterior Knee Pain

The possibility of an unusual source of pain should always be considered. Some causes (osteochondral lesion, bipartite patella, patella baja, radiographic evidence of focal overload) are apparent only on imaging. MRI may provide evidence of hypertrophic synovium, thickened fat pad, or patellar tendonitis. The physical examination is important in determining unusual sources of pain, such as those related to trauma or retinacular neuronal injury from direct impact. Pain referred from the hip or back can also cause AKP. As kinesiophobia may also play a role, it should be considered whenever an objective cause of the pain cannot be identified.

Surgery for Anterior Knee Pain

Surgery should be considered only after prolonged rest and healing have failed to resolve the pain caused by sustained direct trauma to the anterior knee. Physical therapy typically is not useful in direct trauma. If a painful traumatic articular lesion persists, then direct treatment—removing loose articular fragments and resurfacing or unloading a damaged articular surface—may be appropriate. In most cases, 6 to 12 months should be allowed before considering surgery. Meanwhile, rest, bracing, anti-inflammatory measures, reassurance, and work modification are the cornerstones of treatment.

After all conservative measures have failed in a patient with spontaneous-onset AKP related to repetitive focal overload, and disability caused by an objectively proven articular lesion related to mechanical dysfunction or dysplasia, diagnostic arthroscopy may be appropriate. Quantitation and characterization of the lesion with images and measurements are imperative in forming an optimal surgical plan. Remember that not all problems can be cured with surgery, and there is no patellofemoral problem that cannot potentially be made worse with improper surgery.

Am J Orthop. 2017;46(2):101-103. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Sanchis-Alfonso V, Dye SF. How to deal with anterior knee pain in the active young patient. Sports Health. 2016 Dec 5. [Epub ahead of print]

2. Fulkerson JP, Tennant R, Jaivin JS, Grunnet M. Histologic evidence of retinacular nerve injury associated with patellofemoral malalignment. Clin Orthop Relat Res. 1985;(197):196-205.

3. Dye SF. The pathophysiology of patellofemoral pain: a tissue homeostasis perspective. Clin Orthop Relat Res. 2005;(436):100-110.

4. Souza RB, Powers CM. Differences in hip kinematics, muscle strength, and muscle activation between subjects with and without patellofemoral pain. J Orthop Sports Phys Ther. 2009;39(1):12-19.

5. Post WR, Fulkerson J. Knee pain diagrams: correlation with physical examination findings in patients with anterior knee pain. Arthroscopy. 1994;10(6):618-623.

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Take-Home Points

  • Anterior knee pain is common, particularly in young females.
  • For most patients, activity modification and rest will control the pain; continuing to engage in painful activity only prolongs symptoms.
  • In physical therapy, core stability, weight loss, and hip strengthening are essential.
  • Surgery is required only in a very small subset of patients with anterior knee pain.
  • Traumatic and overload- related chondral defects that have resisted a reasonable amount of conservative (nonoperative) treatment may be arthroscopically assessed and treated when documented to cause persistent pain.

Anterior knee pain is common (AKP), particularly in young females. Understanding the biomechanics of a rapidly growing young female knee, whose pelvis is relatively wider than her male counterpart, helps greatly in understanding origins of AKP.1

Compared with males of similar weight and size, females often walk and run with increased valgus at the knee and internal rotation of the hip on heel strike. The patella contacts the lateral edge of the trochlea with more focal load on the distal lateral patella for a longer time in a female than in a male of similar stature because of the increased lateral force vector. Add the rigors of athletics, excessive body weight, use of high heels, or a predisposing structural anomaly, and painful focal overload can develop—resulting in pain on stairs, inability to run, and a visit to your office. Some male patients also develop AKP, often related to patellofemoral dysplasia or activity-related overload leading to a similar pattern and need for care. Fortunately, most young patients improve when they reduce physical activity, attain stable musculoskeletal maturity, or both.

In addition to focal articular overload occurring, retinacular structures about the anterior knee can be stressed by the structural imbalance resulting from the excessive and sudden internal rotation of the hip that occurs even during normal gait and often is related to female lower extremity function. Small nerve damage in the stressed retinaculum is an important cause of peripatellar pain2 and is best identified by clinical examination. Additionally, the infrapatellar fat pad may become pinched, causing synovial inflammation.

With these patients, reassurance can go a long way, and resting, taping, bracing, and anti-inflammatory medications are helpful. Dye3 has emphasized nonoperative treatmentand allowing patients to re-establish homeostatic balance of the patellofemoral joint. Establishing normal body weight plays a key role in the process, and focusing on lower extremity core stability, starting with increased strength in the hip external rotators, is important.4 In the majority of patients, these measures are all that is needed.

Traumatic Anterior Knee Pain

Direct trauma to the anterior knee causes an entirely different sort of pain. Knee pain may be retinacular, neuronal, synovial, bony, or articular. Nothing replaces careful, detailed clinical history taking and physical examination in determining the source of this pain. Much AKP, particularly in its early stages, is very focal. A specific injection of an anesthetic into a suspected retinacular pain location may solve the diagnostic dilemma. With many patients, paying attention to the specific degree of knee flexion in which the injury occurred helps in localizing the lesion. A flexed-knee impact injury (dashboard or fall directly onto anterior knee) is a common cause of articular damage on the mid or proximal patella and distal medial femoral condyle. Identifying this cause is particularly important in worker’s compensation cases, as the pattern is diagnostic of a direct blow to the knee and may confirm the patient’s history.

Treating painful patellofemoral lesions related to direct trauma can be difficult. Once they are identified and correlated with the physical examination and magnetic resonance imaging (MRI) findings, a treatment plan can be developed.

Examination, Testing, Imaging

Knowing how AKP started is important. Asking a patient to point to the origin of pain is essential. A pain diagram (having the patient draw a picture of the pain location) is also very helpful.5 Spontaneous onset suggests an underlying structural and/or functional problem rather than a traumatic event. Examination should include palpation of all structures and the retinaculum about the knee; careful appraisal of patella tracking, location of pain, and crepitus (angle of knee flexion), and evidence of possible pain referred from the back or hip; gait analysis for functional aberrations; assessment of patellar mobility; and standard radiographs, including a perfect lateral radiograph and a knee-flexion axial radiograph of no more than 30° to 45°. Computed tomography, radionuclide scintigraphy,3 and MRI can be very useful in select patients, but such imaging generally is not necessary in the management of routine AKP. However, these studies can be extremely helpful in patients with resistant pain.

 

 

Resistant Anterior Knee Pain

When nonoperative measures (rest, bracing, taping, physical therapy, activity modification) fail to relieve pain, more aggressive treatment may be warranted. The clinician must take extra time to listen to the patient, look for the precise source of the pain, and address it directly. Treatment depends on the specific source of pain. A chronically painful retinacular lesion or neuroma usually responds to release of the painful segment. After a retinacular source of pain has been identified and temporarily eliminated with injection of a local anesthetic, the pain source can be accurately resected and the patient quickly cured. When the chronically painful locus is an injured fat pad, resection provides complete relief.

For most orthopedic surgeons, the greatest dilemma is how to address a young person’s persistent pain in the setting of minimal objective evidence. In my experience with hundreds of arthroscopies, distinct distal lateral patella articular softening is common. In some cases, the degree of articular softening can be extreme, extending toward the central ridge or even across the center of the patella and involving 40% to 50% of the patella articular surface. This spongy, soft cartilage does not resist load normally, and in many cases pain is disabling. Most important is to acknowledge the problem, as many of these patients have been living with articular lesion pain for a year or more. As quality of life can be severely diminished by chronic patellofemoral pain, it behooves us to find answers and provide appropriate treatment. Although patients with this degree of articular softening and breakdown represent a small percentage of all patients with patellofemoral pain, identifying these cases is essential.

However benign-appearing, a resistant, painful patella articular lesion can be disabling. The key to treating a young person with a patella articular lesion objectively proved with imaging or arthroscopy is to inform the patient and family of the resistant nature of some lesions. In a referral patellofemoral practice, I see many patients who are disabled and depressed about the results of articular breakdown related to focal overload. Once the problem is identified, there is hope.

Prolonged rest and activity withdrawal usually help, but in some cases pain with stairs and daily activities continues. Running is usually impossible, which can be devastating for many young people.

My approach is to exhaust the nonoperative measures, which include focusing intensely on core stability training. The physical therapist must understand the importance of this treatment component; the patient must understand the importance of strengthening the hip external rotators and the vastus medialis oblique, modifying gait, avoiding pain-inducing activities, controlling weight, using proper footwear, and being patient. Applying heavy resistance to the quadriceps during rehabilitation will likely perpetuate or exacerbate the problem. The goals are to limit loading of the articular lesion and improve lower extremity function emphasizing reduction and balanced distribution of load.

Other Causes of Anterior Knee Pain

The possibility of an unusual source of pain should always be considered. Some causes (osteochondral lesion, bipartite patella, patella baja, radiographic evidence of focal overload) are apparent only on imaging. MRI may provide evidence of hypertrophic synovium, thickened fat pad, or patellar tendonitis. The physical examination is important in determining unusual sources of pain, such as those related to trauma or retinacular neuronal injury from direct impact. Pain referred from the hip or back can also cause AKP. As kinesiophobia may also play a role, it should be considered whenever an objective cause of the pain cannot be identified.

Surgery for Anterior Knee Pain

Surgery should be considered only after prolonged rest and healing have failed to resolve the pain caused by sustained direct trauma to the anterior knee. Physical therapy typically is not useful in direct trauma. If a painful traumatic articular lesion persists, then direct treatment—removing loose articular fragments and resurfacing or unloading a damaged articular surface—may be appropriate. In most cases, 6 to 12 months should be allowed before considering surgery. Meanwhile, rest, bracing, anti-inflammatory measures, reassurance, and work modification are the cornerstones of treatment.

After all conservative measures have failed in a patient with spontaneous-onset AKP related to repetitive focal overload, and disability caused by an objectively proven articular lesion related to mechanical dysfunction or dysplasia, diagnostic arthroscopy may be appropriate. Quantitation and characterization of the lesion with images and measurements are imperative in forming an optimal surgical plan. Remember that not all problems can be cured with surgery, and there is no patellofemoral problem that cannot potentially be made worse with improper surgery.

Am J Orthop. 2017;46(2):101-103. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

  • Anterior knee pain is common, particularly in young females.
  • For most patients, activity modification and rest will control the pain; continuing to engage in painful activity only prolongs symptoms.
  • In physical therapy, core stability, weight loss, and hip strengthening are essential.
  • Surgery is required only in a very small subset of patients with anterior knee pain.
  • Traumatic and overload- related chondral defects that have resisted a reasonable amount of conservative (nonoperative) treatment may be arthroscopically assessed and treated when documented to cause persistent pain.

Anterior knee pain is common (AKP), particularly in young females. Understanding the biomechanics of a rapidly growing young female knee, whose pelvis is relatively wider than her male counterpart, helps greatly in understanding origins of AKP.1

Compared with males of similar weight and size, females often walk and run with increased valgus at the knee and internal rotation of the hip on heel strike. The patella contacts the lateral edge of the trochlea with more focal load on the distal lateral patella for a longer time in a female than in a male of similar stature because of the increased lateral force vector. Add the rigors of athletics, excessive body weight, use of high heels, or a predisposing structural anomaly, and painful focal overload can develop—resulting in pain on stairs, inability to run, and a visit to your office. Some male patients also develop AKP, often related to patellofemoral dysplasia or activity-related overload leading to a similar pattern and need for care. Fortunately, most young patients improve when they reduce physical activity, attain stable musculoskeletal maturity, or both.

In addition to focal articular overload occurring, retinacular structures about the anterior knee can be stressed by the structural imbalance resulting from the excessive and sudden internal rotation of the hip that occurs even during normal gait and often is related to female lower extremity function. Small nerve damage in the stressed retinaculum is an important cause of peripatellar pain2 and is best identified by clinical examination. Additionally, the infrapatellar fat pad may become pinched, causing synovial inflammation.

With these patients, reassurance can go a long way, and resting, taping, bracing, and anti-inflammatory medications are helpful. Dye3 has emphasized nonoperative treatmentand allowing patients to re-establish homeostatic balance of the patellofemoral joint. Establishing normal body weight plays a key role in the process, and focusing on lower extremity core stability, starting with increased strength in the hip external rotators, is important.4 In the majority of patients, these measures are all that is needed.

Traumatic Anterior Knee Pain

Direct trauma to the anterior knee causes an entirely different sort of pain. Knee pain may be retinacular, neuronal, synovial, bony, or articular. Nothing replaces careful, detailed clinical history taking and physical examination in determining the source of this pain. Much AKP, particularly in its early stages, is very focal. A specific injection of an anesthetic into a suspected retinacular pain location may solve the diagnostic dilemma. With many patients, paying attention to the specific degree of knee flexion in which the injury occurred helps in localizing the lesion. A flexed-knee impact injury (dashboard or fall directly onto anterior knee) is a common cause of articular damage on the mid or proximal patella and distal medial femoral condyle. Identifying this cause is particularly important in worker’s compensation cases, as the pattern is diagnostic of a direct blow to the knee and may confirm the patient’s history.

Treating painful patellofemoral lesions related to direct trauma can be difficult. Once they are identified and correlated with the physical examination and magnetic resonance imaging (MRI) findings, a treatment plan can be developed.

Examination, Testing, Imaging

Knowing how AKP started is important. Asking a patient to point to the origin of pain is essential. A pain diagram (having the patient draw a picture of the pain location) is also very helpful.5 Spontaneous onset suggests an underlying structural and/or functional problem rather than a traumatic event. Examination should include palpation of all structures and the retinaculum about the knee; careful appraisal of patella tracking, location of pain, and crepitus (angle of knee flexion), and evidence of possible pain referred from the back or hip; gait analysis for functional aberrations; assessment of patellar mobility; and standard radiographs, including a perfect lateral radiograph and a knee-flexion axial radiograph of no more than 30° to 45°. Computed tomography, radionuclide scintigraphy,3 and MRI can be very useful in select patients, but such imaging generally is not necessary in the management of routine AKP. However, these studies can be extremely helpful in patients with resistant pain.

 

 

Resistant Anterior Knee Pain

When nonoperative measures (rest, bracing, taping, physical therapy, activity modification) fail to relieve pain, more aggressive treatment may be warranted. The clinician must take extra time to listen to the patient, look for the precise source of the pain, and address it directly. Treatment depends on the specific source of pain. A chronically painful retinacular lesion or neuroma usually responds to release of the painful segment. After a retinacular source of pain has been identified and temporarily eliminated with injection of a local anesthetic, the pain source can be accurately resected and the patient quickly cured. When the chronically painful locus is an injured fat pad, resection provides complete relief.

For most orthopedic surgeons, the greatest dilemma is how to address a young person’s persistent pain in the setting of minimal objective evidence. In my experience with hundreds of arthroscopies, distinct distal lateral patella articular softening is common. In some cases, the degree of articular softening can be extreme, extending toward the central ridge or even across the center of the patella and involving 40% to 50% of the patella articular surface. This spongy, soft cartilage does not resist load normally, and in many cases pain is disabling. Most important is to acknowledge the problem, as many of these patients have been living with articular lesion pain for a year or more. As quality of life can be severely diminished by chronic patellofemoral pain, it behooves us to find answers and provide appropriate treatment. Although patients with this degree of articular softening and breakdown represent a small percentage of all patients with patellofemoral pain, identifying these cases is essential.

However benign-appearing, a resistant, painful patella articular lesion can be disabling. The key to treating a young person with a patella articular lesion objectively proved with imaging or arthroscopy is to inform the patient and family of the resistant nature of some lesions. In a referral patellofemoral practice, I see many patients who are disabled and depressed about the results of articular breakdown related to focal overload. Once the problem is identified, there is hope.

Prolonged rest and activity withdrawal usually help, but in some cases pain with stairs and daily activities continues. Running is usually impossible, which can be devastating for many young people.

My approach is to exhaust the nonoperative measures, which include focusing intensely on core stability training. The physical therapist must understand the importance of this treatment component; the patient must understand the importance of strengthening the hip external rotators and the vastus medialis oblique, modifying gait, avoiding pain-inducing activities, controlling weight, using proper footwear, and being patient. Applying heavy resistance to the quadriceps during rehabilitation will likely perpetuate or exacerbate the problem. The goals are to limit loading of the articular lesion and improve lower extremity function emphasizing reduction and balanced distribution of load.

Other Causes of Anterior Knee Pain

The possibility of an unusual source of pain should always be considered. Some causes (osteochondral lesion, bipartite patella, patella baja, radiographic evidence of focal overload) are apparent only on imaging. MRI may provide evidence of hypertrophic synovium, thickened fat pad, or patellar tendonitis. The physical examination is important in determining unusual sources of pain, such as those related to trauma or retinacular neuronal injury from direct impact. Pain referred from the hip or back can also cause AKP. As kinesiophobia may also play a role, it should be considered whenever an objective cause of the pain cannot be identified.

Surgery for Anterior Knee Pain

Surgery should be considered only after prolonged rest and healing have failed to resolve the pain caused by sustained direct trauma to the anterior knee. Physical therapy typically is not useful in direct trauma. If a painful traumatic articular lesion persists, then direct treatment—removing loose articular fragments and resurfacing or unloading a damaged articular surface—may be appropriate. In most cases, 6 to 12 months should be allowed before considering surgery. Meanwhile, rest, bracing, anti-inflammatory measures, reassurance, and work modification are the cornerstones of treatment.

After all conservative measures have failed in a patient with spontaneous-onset AKP related to repetitive focal overload, and disability caused by an objectively proven articular lesion related to mechanical dysfunction or dysplasia, diagnostic arthroscopy may be appropriate. Quantitation and characterization of the lesion with images and measurements are imperative in forming an optimal surgical plan. Remember that not all problems can be cured with surgery, and there is no patellofemoral problem that cannot potentially be made worse with improper surgery.

Am J Orthop. 2017;46(2):101-103. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Sanchis-Alfonso V, Dye SF. How to deal with anterior knee pain in the active young patient. Sports Health. 2016 Dec 5. [Epub ahead of print]

2. Fulkerson JP, Tennant R, Jaivin JS, Grunnet M. Histologic evidence of retinacular nerve injury associated with patellofemoral malalignment. Clin Orthop Relat Res. 1985;(197):196-205.

3. Dye SF. The pathophysiology of patellofemoral pain: a tissue homeostasis perspective. Clin Orthop Relat Res. 2005;(436):100-110.

4. Souza RB, Powers CM. Differences in hip kinematics, muscle strength, and muscle activation between subjects with and without patellofemoral pain. J Orthop Sports Phys Ther. 2009;39(1):12-19.

5. Post WR, Fulkerson J. Knee pain diagrams: correlation with physical examination findings in patients with anterior knee pain. Arthroscopy. 1994;10(6):618-623.

References

1. Sanchis-Alfonso V, Dye SF. How to deal with anterior knee pain in the active young patient. Sports Health. 2016 Dec 5. [Epub ahead of print]

2. Fulkerson JP, Tennant R, Jaivin JS, Grunnet M. Histologic evidence of retinacular nerve injury associated with patellofemoral malalignment. Clin Orthop Relat Res. 1985;(197):196-205.

3. Dye SF. The pathophysiology of patellofemoral pain: a tissue homeostasis perspective. Clin Orthop Relat Res. 2005;(436):100-110.

4. Souza RB, Powers CM. Differences in hip kinematics, muscle strength, and muscle activation between subjects with and without patellofemoral pain. J Orthop Sports Phys Ther. 2009;39(1):12-19.

5. Post WR, Fulkerson J. Knee pain diagrams: correlation with physical examination findings in patients with anterior knee pain. Arthroscopy. 1994;10(6):618-623.

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The American Journal of Orthopedics - 46(2)
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The American Journal of Orthopedics - 46(2)
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A Practical Guide to Understanding and Treating Patellofemoral Pain
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