Patellar Instability

Paul M. Inclan, MD

Matthew J. Matava, MD

INTRODUCTION

In the ambulatory setting, up to one-fourth of all orthopedic office visits pertain to pathology involving the patellofemoral joint.¹ Though the differential diagnosis for such pathology is broad, the vast majority of patellofemoral complaints can be subclassified into three general conditions: patellofemoral pain syndrome, patellofemoral arthritis, and patellofemoral instability, although some overlap may occur. For example, patients with patellofemoral instability often have associated acute articular cartilage defects, which may progress to focal or diffuse osteoarthritis over time. All three conditions result from a complex interplay of pathologic processes related to patellar maltracking, increased patellofemoral joint loading, and altered somatosensory processes.²

Patellofemoral pain syndrome is one of the most common causes of knee pain in the United States with a prevalence cited between 15% and 45% in young adults.³,⁴ Often insidious in onset, and associated with overuse, this condition typically results in diffuse anterior knee pain most commonly in young, active individuals—especially females. This condition is not due to structural damage to the patellofemoral articulation but rather to functional muscle weakness of the core and lower extremity. Therefore, patellofemoral pain syndrome is usually amenable to nonoperative management including physical therapy with an emphasis on “closed-chain” quadriceps and core muscle strengthening,⁵,⁶ nonsteroidal anti-inflammatory drugs (NSAIDs),⁷ and activity modification with avoidance of prolonged bent-knee activities and “open-chain” knee extension.

At the other end of the spectrum is patellofemoral arthritis. This condition results in focal or diffuse degeneration of the patellar and/or trochlear articular surface(s), typically in middle-aged and older adults.⁸ This condition is manifested as peripatellar pain exacerbated by activities that increase loading of the patellofemoral joint such as climbing stairs, rising from a seated position, or kneeling. Though nonoperative management remains the mainstay of treatment for isolated patellofemoral arthritis, a variety of operative procedures to realign, reconstruct, or replace the articulating surfaces are available based on patient age and activity, severity of arthritis, and associated anatomical factors.

Both patellofemoral pain syndrome and patellofemoral arthritis exhibit pathomechanics and clinical features that overlap with the third, distinct clinical entity of patellofemoral instability. This condition is defined as either a single or recurrent episode(s) of patellar subluxation (partial pathological movement of the patella out of the trochlear groove with retention of some articular contact) or dislocation (complete movement of the patella out of the trochlear groove without retention of articular contact).⁹ The vast majority of cases involve lateral patellar instability, with medial instability most commonly due to iatrogenic causes following surgical procedures intended to address lateral instability such as an excessive lateral retinacular release, detachment of the vastus lateralis, and/or an overly tightened medial patellofemoral ligament (MPFL) repair/reconstruction.¹⁰ True medial patellar instability is extremely rare without a known incidence. Underlying hyperlaxity, trochlear dysplasia, and a deficient vastus lateralis musculature may play a role in patients medial instability with or without prior surgery.

With an annual incidence of 23.2 per 100,000 person-years,¹¹ a first-time patellar dislocation is a frequently encountered orthopedic complaint. Moreover, the adolescent population may experience an annual incidence nearly seven times that of the general population,¹¹ typically while engaging in athletic activites.¹² Unfortunately, affected individuals have an approximately 25% risk of recurrent instability up to 5 years following the initial event.¹³ This risk is higher in younger patients, females, and individuals with underlying anatomic predisposition such as patella alta, patellar and/or trochlear dysplasia, genu valgum, and lateral patellar maltracking¹³ (discussed below). In addition to the risk of recurrent instability, almost half of all affected individuals will eventually develop patellofemoral arthritis,¹⁴ likely secondary to either the initial traumatic insult or from repetitive patellar dislocation/relocation episodes. Therefore, patellar instability affects young, active individuals, many of whom will experience some form of continued patellofemoral symptoms during their lifetime, either because of recurrent instability or from articular cartilage damage.

ANATOMY AND BIOMECHANICS OF THE PATELLOFEMORAL JOINT

The patella represents the largest sesamoid bone in the body. Enveloped in the retinacular layer of the quadriceps tendon, it articulates with the trochlear groove of
the distal femur and possesses the thickest articular cartilage of any joint (up to 6 mm).¹⁵ The patella is typically described as containing two major facets—a long, shallow lateral facet and a short, steep medial facet—mirroring the anatomy of the trochlear groove. The anatomic symmetry between the patella and trochlea is evidence of the developmental codependence of these two structures, as abnormal articulation of the patella within the trochlea is theorized to yield a shallow trochlear groove with possible predisposition to patellar instability.¹⁶ In addition to the two major facets, a far medial, or “odd,” facet is often described, as are multiple subdivisions of the primary lateral and medial facets, based upon transverse ridges of the articular surface.¹⁷

Functionally, the patella serves as a vital link in the extensor mechanism by increasing the moment arm of the quadriceps tendon and providing a mechanical advantage to knee extension.¹⁸ Not surprisingly, loss of the patella from partial or complete patellectomy results in decreased quadriceps force and knee extension weakness.¹⁹ In addition to serving as a knee extensor, a portion of the quadriceps muscle—the vastus medialis obliquus (VMO)—is occasionally described as a “dynamic” stabilizer of the patella.²⁰ Originating from the intermuscular septum and adductor magnus approximately 3.3 cm proximal to the adductor tubercle,²¹ the oblique orientation of this muscle allows for a medially directed force during contraction, providing dynamic stabilization of the patella against lateral translation. However, biomechanical evidence indicates that the actual contribution of the VMO to patellar stability may be minimal,²² as isolated activation and strengthening of this structure for therapeutic purposes has proven difficult.²³

At early degrees of flexion, the MPFL represents the most important stabilizer of the patella, responsible for 50% to 60% of resistance to lateral patellar translation.²¹,²² Originating between the medial femoral epicondyle and adductor tubercle,²⁴ this trapezoidal-shaped “static” soft-tissue stabilizer receives decussating contributions from the proximal medial collateral ligament (MCL)²⁵ and is contained in layer II of the medial soft tissues, deep to the pes anserinus at the level of the superficial MCL.²⁵,²⁶ The MPFL inserts over a 2.5 cm expansion on both the proximal one-half of the patella and the distal portion of the quadriceps tendon.²⁷ This ligament is variable in diameter, and may contribute as little as 23% of the stabilizing force against lateral patellar translation in select individuals.²¹ The other soft-tissue stabilizers of the medial knee are of lesser importance during early flexion, with the medial patellomeniscal ligament (MPML) providing 22% and medial patellotibial ligament (MPTL) providing 5% of the resistance against lateral patellar translation in extension.²¹ Both aforementioned structures provide increasing contributions to patellar stability with increasing knee flexion but provide the majority of soft-tissue restraint only after the patella has engaged in the trochlear groove. In almost all cases of patellar dislocation, these medial soft-tissue stabilizers are at least partially disrupted in the form of an acute tear or attenuation from chronic instability resulting in a ligament that is intact but functionally incompetent.

Once the patella engages in the trochlear groove at approximately 30° of flexion, the bony configuration of the patellofemoral joint, rather than the soft-tissue stabilizers, becomes the primary restraint to lateral patellar translation. The lateral wall of the trochlea is more prominent anteriorly than its medial counterpart. The more posteriorly directed vector of the quadriceps tendon augments this bony stability during progressive knee flexion, which increases contact between the patella and lateral trochlear facet.²⁸,²⁹

Anatomic predispositions to instability primarily result in alteration of the normal biomechanics of the patellofemoral joint. Patella alta doubles the risk of recurrent patellar dislocation,³⁰ as higher degrees of flexion are required for the patella to engage the trochlear groove. As such, the medial soft-tissue restraints must resist the posterolateral pull of the quadriceps during knee flexion without the buttressing effect provided by the lateral femoral condyle placing these medial soft tissues at higher risk for failure. Similarly, in the case of a hypoplastic lateral femoral condyle, the buttressing effect of the trochlear groove is not available—even with progressive flexion— resulting in less resistance against lateral patellar translation³¹,³² and higher risk of dislocation. Complex torsional abnormalities throughout the lower extremity, resulting in increased femoral neck anteversion, internal femoral rotation, and external tibial torsion, increase the risk of instability through a clinical variant known as “miserable malalignment syndrome” (Fig. 19-1).

CLASSIFICATION OF PATELLAR INSTABILITY

Numerous classification systems⁹,³³,³⁴ have been proposed to aid in the understanding and treatment of patellar instability, as the condition represents a heterogenous collection of clinical entities (especially in the pediatric population). However, our approach to the classification of patellar instability is most similar to that described by Parikh and Lykissas⁹ and is based primarily on the chronicity of the condition and degree of trauma.

Acute patellar dislocation describes an index dislocation event in a patient with no prior episodes of patellar instability and warrants further subdivision based on mechanism: traumatic or atraumatic. In the traumatic setting, individuals with no discernible anatomic predisposition to instability and good quadriceps tone experience a blow to the medial patella resulting in a lateral dislocation. This dislocation event is often accompanied by a traumatic hemarthrosis and osteochondral fracture, with a presentation not dissimilar to an acute anterior cruciate ligament (ACL) rupture.³⁵
The risk of subsequent osteochondral injury is inversely related to the degree of generalized ligamentous laxity. The medial soft-tissue restraints from the patella are at least partially disrupted either in their mid-substance or from their patellar or femoral insertions.³⁶ However, an avulsion fracture of the MPFL’s patellar insertion may also occur.³⁷ Hiemstra and colleagues compare the STAID (Strong, Traumatic, Anatomy normal, Instability, and Dislocation) variant of acute traumatic patellar dislocation to the TUBS (Traumatic, Unilateral, Bankart lesion, and Surgery) variant of shoulder instability.³⁴ In contrast, an individual may also present with a first-time patellar dislocation without any identifiable trauma. These individuals report dislocation after turning, pivoting, or twisting. These atraumatic dislocations are less likely to be associated with a large hemarthrosis or osteochondral fracture and more likely to occur secondary to an underlying anatomic predisposition.³⁸ Hiemstra and colleagues summarize this as the WARPS (Weak, Atraumatic, Risky anatomy, Pain, and Subluxation) variant.³⁴ Importantly, these general descriptions provide merely a conceptual framework for patellar instability since actual clinical scenarios may not fit perfectly into one particular construct. For example, a patient suffering a traumatic dislocation may also possess an anatomic predisposition.

FIGURE 19-1 Clinical example of “miserable malalignment syndrome”. (From Parikh SN. Patellar Instability: Management Principles and Operative Techniques. Philadelphia: Wolters Kluwer; 2020.)

After presentation for acute patellar instability—either traumatic or atraumatic—subsequent subluxation and dislocation events are best classified as recurrent patellar instability.⁹ Numerous risk factors exist for the progression from a single acute instability event to recurrent patellar instability. Young (<14 years), skeletally immature patients with both patella alta and trochlear dysplasia demonstrate a significant (88%) chance of recurrent instability.³⁰ The distinction between acute and recurrent instability is significant, as the current standard of care for a first-time dislocation is nonoperative treatment in the absence of significant structural damage (discussed below); whereas, recurrent instability is an indication for operative management.³⁹

In less frequent cases, individuals may experience dislocation-relocation events with each flexion-extension cycle during ambulation. Such continuous dislocation-relocation is referred to as habitual patellar instability and is typically less painful than acute and recurrent episodes of instability.⁴⁰ Lateral patellar dislocation is required for knee flexion resulting from tight lateral soft tissues and a shortened extensor mechanism. This repetitive low-energy trauma results in severe chondral damage in young adulthood.⁴¹ In the pediatric population, congenital patellar dislocation occurs in utero and results in a flexion contracture of the knee at birth.⁴² Finally, patellar dislocation occurring during the early stages of ambulation is referred to as developmental patellar dislocation. These latter two subtypes are very uncommon and are rarely encountered in the routine clinical setting, particularly in adults.

HISTORY AND PHYSICAL EXAMINATION

History

As with all patient encounters, a thorough history is the initial step in patient evaluation. As discussed above, an understanding of the mechanism of injury and the activity at the time of dislocation is helpful in reaching a diagnosis. Further history should detail if a traumatic force was applied to the patella, whether the patella spontaneously reduced or required manual reduction, and if subsequent episodes occurred after the initial dislocation event. A history of giving-way, catching, clicking, or locking sensations occurring after the dislocation event is also informative, as osteochondral fractures commonly occur with patellar dislocation that results in loose bodies within the joint.⁴³ Moreover, instability of the tibiofemoral joint during twisting, pivoting, or landing may indicate ACL, meniscal, or collateral ligament injury, rather than isolated patellofemoral injury. Instability that occurs with only mild trauma suggests a greater degree of anatomic abnormalities, which increase the chance for recurrence. Additionally, since patellar instability affects young active patients, participation in sports and overall activity level
prior to the dislocation should be determined. Assessment of past surgical history may indicate prior attempts at stabilization. A family history of patellar instability may predict both recurrent ipsilateral and future contralateral instability.⁴⁴

Physical Examination

Our approach to the physical examination begins with general inspection of gait with an emphasis on dynamic lower limb alignment and the degree of foot pronation. The patient is examined in the standing position. With the feet pointing forward, the patellae should point straight ahead. A patella facing inward (“squinting patella”) or outward (“grasshopper patella”) may indicate significant underlying variation in torsional limb malalignment. Increased recurvatum in the sagittal plane should also be noted.

With the patient supine, general inspection of lower limb alignment will show generalized limb alignment, such as genu valgum (Fig. 19-2), and may reveal quadriceps atrophy in long-standing cases of instability. Although the patella tracks along an essentially straight line, the extensor mechanism forms an angle when viewed in the coronal plane. This is the quadriceps angle, commonly referred to as the Q-angle. This angle comprises a line connecting the anterior superior iliac spine to the center of the patella approximating the vector of the quadriceps musculature. The angle is completed by a line connecting the center of the patella to the tibial tuberosity. The existence of the Q-angle accounts for the tendency of the patella to displace laterally when the quadriceps muscles contract creating a “bowstring” effect, analogous to a lax rope straightening when rendered taut. The Q-angle is directly related to the patella’s tendency to displace laterally. Q-angle values greater than 20° are considered abnormal, though there may be variation in this angle based on whether the patient is sitting, standing, or supine. In general, the concept of the Q-angle must be questioned, given its variability and risk for false-negative measurements. For example, a patient with a patella that is “perched” on the lateral trochlea due to marked genu valgum or soft-tissue imbalance that is on the verge of dislocating will have a low Q-angle falsely suggesting a low risk of instability.

FIGURE 19-2 Patient demonstrating bilateral genu valgum.

Systematic palpation of the tibiofemoral and patellofemoral joints will likely reveal an effusion and diffuse tenderness indicative of nonspecific structural damage to the knee. However, the majority of patients with patellar instability have tenderness over the medial femoral condyle at the attachment of the MPFL and, less commonly, at the medial patellar border.⁴⁵ Tightness of the lateral retinaculum can be determined by palpation of the space between the lateral patellar border and trochlea. Normally, the lateral patellar facet can be elevated from the lateral trochlea parallel to the transepicondylar axis with the knee in full extension (Fig. 19-3). A tight lateral retinaculum prevents this passive rotation and may be a predisposing factor to lateral patellar instability. Patients with generalized laxity rarely have tightness of the lateral retinaculum.

FIGURE 19-3 Tightness of the lateral retinaculum can be determined by the ability to elevate the lateral patellar facet away from the lateral trochlea. Normally, the lateral facet should be elevated to at least parallel to the transepicondylar axis with the knee in full extension. (From Johnson D, Amendola NA, Barber F. Operative Arthroscopy. Philadelphia: Wolters Kluwer; 2015.)

FIGURE 19-4 Medial and lateral patellar translation tested with the knee at 20° of flexion and divided into longitudinal quadrants. Normal medial translation is one quadrant and lateral translation is two quadrants. A: Medial and B: Lateral.

Active and passive knee range of motion should be measured with evaluation of patellar tracking and the presence of retropatellar crepitus throughout the arc of motion. Crepitus is accentuated with active knee extension because of the elevated compressive force rendered by quadriceps contraction. The degree of flexion associated with the onset of crepitus can provide information regarding the location of any patellar cartilage defect since patellar contact with the trochlea progresses from distal to proximal as the knee moves from extension into flexion. Patellar tracking is usually symmetrical and within the trochlear groove; however, an abrupt lateral jump (“J-sign”) as the knee approaches full extension is indicative of lateral patellar subluxation.

Patellar translation in the coronal plane is quantified by dividing the patella into longitudinal quadrants, then placing a laterally and medially directed force on the patella at 20° of flexion to determine the amount of passive patellar translation (Fig. 19-4). It is important that this measurement be made in slight flexion in order to engage the patella in the trochlear groove and assess true ligamentous laxity. Normally, the patella cannot be translated more than two quadrants laterally and one quadrant medially. Increased passive lateral patellar translation is associated with patellar instability. A soft end point with lateral patellar translation may indicate either disruption or attenuation of the medial soft-tissue restraints. If the patient actively fires the quadriceps in an attempt to resist lateral patellar translation or endorses a sensation of anxiety due to impending subluxation, they are exhibiting a positive “apprehension sign.” Some authors advocate applying this lateral force on the patella throughout a full arc of flexion and extension (“moving patellar apprehension test”), which yields a high degree of sensitivity and specificity for patellar instability.⁴⁶

All patients with patellar instability should be assessed for generalized ligamentous laxity utilizing the Beighton criteria.⁴⁷ A score of 4 or more on this 9-point scale indicates generalized laxity, with females typically exhibiting higher scores than males.⁴⁸

Tests for meniscal pathology (i.e., McMurray test, Thessaly test, and pain with hyperflexion), ACL insufficiency (e.g., Lachman, anterior drawer, and pivot shift tests), injury to the MCL and lateral collateral ligament (valgus and varus stress testing at 0° and 30° of flexion, respectively), and posterolateral corner injury (i.e., dial, reverse pivot shift, and extension-recurvatum tests) should be performed in all patients following an acute injury.

The examination concludes with determination of passive hip range of motion in both the supine and prone positions. With the patient prone, increased anteversion may be a predisposing factor for patellar instability (Fig. 19-5).

RADIOGRAPHIC EVALUATION

Plain Radiographs

A thorough radiographic assessment of the entire lower extremity is imperative in the comprehensive evaluation of patients with patellar instability. We routinely obtain four views of the knee: anteroposterior, 45°
flexion weight-bearing (Rosenberg), axial (Merchant), and 30° lateral. Fracture fragments from the lateral femoral condyle or medial patellar facet may be appreciated (Fig. 19-6). However, small pieces of bone where the MPFL was avulsed off the medial patellar border are typically not loose within the joint and do not require removal (Fig. 19-7). Degenerative changes of the patellofemoral cartilage may also be seen with long-standing instability (Fig. 19-8). Patellar position, in reference to the trochlea on the Merchant view (with contralateral comparison), may show asymmetrical lateral patellar translation or tilt (Fig. 19-9). The depth of the trochlear groove can be quantified through measurement of the sulcus angle (normal: 137° ± 6°),⁴⁹ with a shallow trochlea associated with both instability and trochlear dysplasia.⁵⁰ Additionally, subluxation can be quantified with the congruence angle (normal: −8°± 6°),⁴⁹ with a more positive congruence angle representing increasing lateral patellar subluxation (Fig. 19-10). Finally, the degree of patellar tilt is determined through the lateral patellofemoral angle, with excessive patellar tilt (defined as >5°)⁵¹ potentially indicating a tight lateral retinaculum.

FIGURE 19-5 Prone patient demonstrating excessive femoral anteversion.

FIGURE 19-6 Lateral knee X-ray demonstrating a loose osteochondral body in the suprapatellar pouch.

FIGURE 19-7 Axial (Merchant) X-ray demonstrating an avulsed bony fragment attached to the medial patellofemoral ligament.

Patellar “height” is quantified with a 30° lateral radiograph. It is important that this measurement be made with the knee in a standardized degree of flexion. The anterior-most extent of the roof of the intercondylar fossa (Blumensaat line) should be at or just above the same level as the inferior pole of the patella. Numerous ratios (Insall-Salvati,⁵² Caton-Deschamps,⁵³ and Blackburne-Peel⁵⁴) have been developed for more objective quantification of patellar height (Fig. 19-11). The Insall-Salvati method divides the patellar tendon
length by the maximum patellar length from the superior to the inferior pole. This measurement requires an approximation of the tendon insertion into the tibial tubercle, which may introduce inconsistency into the measurement, especially in pediatric patients. Moreover, this ratio also remains unchanged during a tubercle osteotomy as neither patellar tendon nor patellar length change, potentially limiting its utility in the postoperative setting. The Caton-Deschamps and Blackburne-Peel methods utilize the length of the articular surface of the patella in relation to the patellar tendon length, with normal ratios being 0.8 to 1.2. As such, these two methods represent the most useful measurements for patella alta or baja, with the Blackburne-Peel ratio being the most consistently reproducible.⁵⁵ Patella alta can also be identified by the patella-plateau angle. This angle is formed by a line parallel to the tibial plateau and a line from the posterior tibial plateau to the most distal articulating surface of the patella. A normal angle is 25° with 90% of measurements between 20° and 30° (Fig. 19-12).⁵⁶

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