Orthopedics - Oleksa A.P. 2006

Congenital and Acquired Deformities of the Lower Extremity
Congenital Deformities of the Knee Joint
Congenital Dislocation of the Patella

Congenital dislocation of the Patella (luxatio patellae congenitum) is a rare clinical entity, accounting for 0.45% of all dislocations according to V. N. Tikhonov.

Although patellar dislocations have been known since the time of Hippocrates, the literature on the subject remains relatively sparse. Published studies (Fridland M. O., 1954; Boychev B., 1959; Heywood A.W., 1961; Volkov M.V., 1962; Simenach B.I., 1990, and others) are based on the observation of small patient cohorts.

The patella is a sesamoid bone embedded within the tendon of the quadriceps femoris Muscle. Its cartilaginous surface articulates congruently with the cartilaginous surfaces of the femoral condyles, acting as a pulley mechanism that ensures smooth knee movement, enhances the efficiency of the quadriceps muscle, and prevents tendon friction.

Normally, the lateral femoral condyle projects slightly further anteriorly than the medial condyle, ensuring congruence with lateral excursion of up to 6° and stable patellar gliding along the cartilaginous surface of the trochlear groove (Fig. 165). During knee flexion, the quadriceps muscle contracts, seating the patella deeper into the trochlear groove closer to the lateral condyle. At this point, the patella is stabilized laterally by the aponeurotic expansions of the vastus Muscles of the thigh.

Several theories exist regarding the Etiology of congenital patellar dislocations. The most widely accepted are: 1) impaired femoral torsion during Embryogenesis, resulting in lateral Displacement of the patella and the rectus femoris muscle; 2) hypoplasia of the lateral femoral condyle, leading to lateral displacement of the patella; and 3) laxity of the knee joint ligamentous apparatus (De Palma A. F., 1954; Carter C., Sweetnam J., 1958, and others).

Class="center">

Fig. 165. Diagram illustrating the normal anatomical relationship between the femoral condyles and the patella, including its permissible lateral deviation.

M. V. Volkov (1968) points out that impaired femoral rotation during embryogenesis may be caused by a developmental anomaly affecting all Tissues of the lower half of the thigh—specifically, a lack of clear Separation and differentiation between the rectus femoris and the lateral portion of the quadriceps muscle, potentially accompanied by their shortening and hypoplasia of the lateral femoral condyle. Excessive tension and tightness of the lateral thigh muscles lead to Genu Valgum (knock-knee deformity).

In cases of incomplete femoral torsion, the lateral condyle is positioned more posteriorly relative to the medial condyle, predisposing the patella to lateral subluxation or dislocation, particularly when combined with genu valgum. Valgus deformity of any etiology creates conditions favorable for lateral patellar displacement during knee flexion, as the tibial tuberosity and patellar tendon are displaced laterally.

When the lower limb is extended and the quadriceps muscle is relaxed, the patella typically returns to its normal position or remains slightly lateralized. This continuous lateral displacement during movement leads to overstretching of the medial fibrous retinaculum, resulting in recurrent subluxation and, subsequently, dislocation of the patella.

Furthermore, overstretching of the ligamentous structures can lead to patellar dislocation following minor trauma. V. N. Parin previously noted that nearly half of all lateral patellar dislocations are congenital, while Heywood (1961) indicated that only 5% of dislocations result from acute trauma, with the remainder stemming from congenital anomalies.

Thus, the mechanogenesis of lateral patellar dislocation is driven by specific anatomical alterations within the knee joint region.

Recurrent congenital patellar dislocations are more frequently observed in boys and are typically diagnosed during childhood or adolescence.

Clinical examination may reveal a valgus deformity of the leg, while Palpation demonstrates excessive lateral mobility of the patella and hypotrophy of the quadriceps muscle in the extended lower limb. During knee flexion, the patella displaces not only vertically but also laterally.

According to M. V. Volkov (1968), patients can be classified into three groups based on the severity of the deformity.

In mild cases, knee flexion causes the patella to shift toward the lateral femoral condyle, while extension reveals excessive lateral mobility. Patients in this group typically have no significant Complaints.

In moderate cases, alongside the aforementioned signs, the patella exhibits rotational instability in the sagittal plane. Such patients experience joint instability during ambulation, and children frequently suffer from knee abrasions due to frequent falls.

In severe cases, knee flexion results in complete dislocation of the patella, causing it to rest lateral to the lateral femoral condyle, or even posterior to it when the knee is fully flexed. Following knee extension, the patella remains displaced but can be easily manually reduced into its proper position.

The Diagnosis of recurrent patellar dislocation is confirmed radiographically using an anteroposterior view of the knee joint with the leg maximally flexed (Fig. 166). Lateral radiographs reveal hypoplasia of the lateral femoral condyle in 12–14% of children.

As a result of frequent dislocations and chronic overstrain of the lateral portion of the quadriceps muscle, valgus knee deformity in children may progressive, accompanied by potential growth retardation of the lateral femoral condyle.

Long-standing recurrent patellar dislocation inevitably leads to The Development of gonarthrosis. B. I. Simenach et al. (1990) note that patellar maltracking follows a staged clinical course and thus distinguish three main stages: 1) the preclinical stage, lacking classic patient complaints or any reactive joint changes; 2) the clinical stage, characterized by lateralization of the patella and reactive joint changes—manifested as inflammatory and dystrophic arthrotic processes arising as a systemic response to Cartilage destruction; and 3) the post-clinical stage, featuring an indolent, chronic reactive process within the joint and slowly progressive destruction.

All three stages can be observed only in the absence of timely pathogenetic Treatment.

Based on the interpretation of dysplastic gonarthrosis as a consequence of a reactive process accompanied by diffuse dystrophic Changes in the joint (Simenach B. I. et al., 1990, and others), the primary objective for orthopedic surgeons should be early diagnosis and surgical management of patients with dysplastic knee joint anomalies—specifically in the pre-arthrotic stage—to prevent the development of deforming osteoarthritis.

Additionally, cases of hereditary recurrent patellar dislocation have been documented. This condition has an insidious progression, and timely medical consultation helps prevent the detrimental consequences of recurrent patellar instability. Patients generally seek medical attention due to recurrent patellofemoral dislocation and knee instability, which cause chronic apprehension, despite the fact that the dislocation is easily self-reducible.

Treatment for recurrent patellar dislocation is exclusively surgical, as conservative measures such as elastic bracing, knee bandaging, and massage therapies prove ineffective.

The Nature of the surgical intervention depends, first, on the Specific features of carefully verified (goniometrically and radiometrically) dysplastic changes in the knee joint, the condition of the extensor and auxiliary extensor apparatus, as well as the patellar gliding mechanism, the degree of subluxation, and the frequency of patellar dislocation; second, on the patient's age and the severity of secondary degenerative changes in the joint. Thus, The Scope of surgical intervention is determined individually for each patient.

There are several soft-tissue surgical Procedures used for recurrent patellar dislocation.

1. Division of the lateral patellar retinaculum.

Using a Skin and subcutaneous incision up to 5 cm long in the anterolateral region of the patellar edge, the ligamentous apparatus is exposed. The lateral horizontal retinacula are divided near the patella; if necessary—when the patella does not shift medially enough—the tendinous expansion of the vastus lateralis muscle is partially incised at its insertion site. The integrity of the Joint Capsule must be preserved. By flexing the lower leg to an acute angle, the surgeon checks whether the division of the ligaments and the displacement of the patella are sufficient, extending the incision if necessary. Sutures are applied to the skin and subcutaneous tissue, followed by an aseptic dressing and a long posterior plaster splint applied to the knee in a semi-flexed position for 7–10 days.

Fig. 166. Recurrent patellar dislocation (a), tangential radiograph of the knee with a flexed lower leg (b).

Subsequently, muscle massage is performed and joint mobility is rehabilitated, with full squatting permitted in 2–3 months.

2. Reconstruction of the extensor and auxiliary extensor apparatus of the knee joint According to the Kharkiv Research Institute of Orthopedics method (Simenach B.I.).

Using an arcuate lateral parapatellar incision that ends slightly below and medial to the tibial tuberosity, the lateral ligamentous apparatus is exposed and divided. The exposed tibial tuberosity is osteotomized in a horizontal plane using an osteotome so that its medial edge remains somewhat elevated (4–5 mm thick). If necessary, a cancellous bone graft is inserted into this gap (Cox J.S., Cooper P.S., 1994) (Fig. 167). Depending on the degree of patellar lateralization and the lateral deviation of the patellar tendon, a bone bed is formed medial to the previous attachment site, and the detached tuberosity is placed subperiosteally and temporarily secured with a thin awl.

By flexing the lower leg to a right angle, the correct positioning of the created bed is verified, and if the desired result is achieved, the tuberosity is fixed with a screw.

A plaster cast is applied for the time required for bony union of the transferred tuberosity.

3. Reconstruction of the extensor apparatus with patellar distalization.

Using the same surgical approach and technique as in the previous operation, the patella and tibial tuberosity are medialized, but the bone bed for the tuberosity is created slightly medial and distal to its previous attachment level. This method additionally lowers a high-riding patella (Fig. 168).

Fig. 167. Patellar osteotomy with medialization and elevation of its upper part using a bone graft (Cox J.S., Cooper P.S., 1964).

The operation is performed in cases of lateralization of the tibial tuberosity accompanied by patella alta, and lateral Hypertension during lower leg flexion, which contributes to patellar dislocation.

4. Reconstruction of the extensor apparatus with patellar distalization and shortening of the patellar tendon.

Shortening of the patellar tendon is performed when There is a need to lower the tibial tuberosity by two or more centimeters, which fails to meet physiological biomechanical requirements.

Fig. 168. Medialization of the tibial tuberosity with patellar distalization according to Elmslie-Trillat (a), Vreden (b).

In such cases, the patellar tendon can be shortened using a purse-string/pleating Dacron suture or via a Z-shaped or oblique incision in the frontal plane to form a duplication.

At the Kharkiv Institute of Orthopedics, the tendon is shortened by lowering the tibial tuberosity into a new bed, while the displaced tuberosity and the lower part of the tendon are covered with a special contoured metal plate. This presses the tendon down to the level of the osteotomized tuberosity to achieve fusion of the free portion of the patellar tendon at that site (Fig. 169). This approach achieves tendon shortening while establishing a functionally advantageous attachment site.

The surgery is performed in the same manner as the previous ones: the lateral ligamentous apparatus is transected, the tibial tuberosity is osteotomized, lowered, and temporarily fixed with an awl in the new bed. After verifying the achieved result by flexing the lower leg, the tuberosity is secured with a screw, and the lower part of the tendon is covered with a metal plate extending to its normal attachment site on the Tibia. The wound is closed, and a plaster cast is applied for 12–16 days.

In cases of a dysplastic flattened femoral trochlea, to prevent lateral displacement of the patella during movement, the same operation is supplemented by fixing the distal part of the quadriceps tendon to the medial femoral epicondyle using a Dacron strip acting as a bridle.

5. Varus osteotomy of the tibia.

Varus osteotomy is performed for valgus deformity of the lower leg when the angle exceeds 7°. To achieve a successful outcome, the osteotomy must be supplemented by the sectioning of the collateral ligaments that support the patella.

The surgery is performed in stages. First, an osteotomy of the Fibula is carried out at the junction of its upper and middle thirds to avoid damaging the common peroneal nerve. Next, through a separate approach, the patellar collateral ligaments are incised, and using a gouge chisel, the tibia is osteotomized to create a semi-circular protrusion in the peripheral fragment.

Fig. 169. Medialization and distal advancement of the tibial tuberosity with shortening of its ligament using a staple.

For better exposure to perform the tibial osteotomy directly above the attachment site of the patellar ligament, B.I. Simenach et al. (1990) recommend chiseling off and reflecting the tuberosity upward, and following the osteotomy and limb axis correction, fixing it back in place with a screw or, if necessary, medializing or lowering it.

Additionally, if required, this Procedure can be supplemented by fixing the quadriceps tendon with a Dacron (lavsan) tape to the medial epicondyle of the Femur.

Regarding the fixation of osteotomized bone fragments, various opinions exist. One may resort solely to a plaster cast with temporary fixation using several percutaneously inserted Kirschner wires, which are removed after three weeks, or perform more stable fixation using metal rods or a compression-distraction apparatus. The Use of Kirschner wires and apparatuses leaves the option open to adjust the limb axis in the postoperative period if necessary.

Bone surgeries—such as Fowler's (patellectomy) modified by Lorenc (defect closure using a rectus femoris muscle flap), Chaput's (patellectomy with femoral osteotomy for valgus deformity), Lucas-Championnière's (deepening of the intercondylar notch), Trendelenburg–Albee (arthrorisis via the lateral process), as well as supracondylar osteotomies including McEwen's transverse osteotomy and Schanz's Rotation of the distal femur—are now rarely used.