Pediatric Fixed Knee Flexion Deformities Workup

  • Author: Peter M Stevens, MD; Chief Editor: Dennis P Grogan, MD   more...
 
Updated: Apr 4, 2011
 

Laboratory Studies

There are no particular lab studies that are relevant to the correction of fixed knee flexion deformity (FKFD). The only exception may be preoperative pulmonary function screening for patients in whom general anesthesia is associated with high risk.

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Imaging Studies

Patients with fixed knee flexion deformity (FKFD) may not be able to cooperate for meaningful, full-length, weight-bearing, anteroposterior radiographs of the lower extremities. It should be noted that if the x-ray beam is nonorthogonal to the distal femoral physis, physeal closure may incorrectly be suspected.

A close-up lateral radiograph of the knees will demonstrate whether or not the physes are open. It will demonstrate the presence or absence of posterior subluxation of the tibia relative to the femur. This view will also reflect the relative position of the patella and occasional disruption (tension failure) of the extensor mechanism in the form of patellar and/or tibial tuberosity avulsion.

The lateral radiograph best demonstrates the open The lateral radiograph best demonstrates the open physes and the stigmata of chronic fixed knee flexion deformity (FKFD). This patient has avulsion "fractures" of the superior pole of the patella and of the tibial tubercle.

If there is doubt about the time remaining for growth, a hand (Greulich and Pyle) or elbow (Demiglio) radiograph may be useful in estimating skeletal maturity.

Advanced imaging such as arthrography, computed tomography scanning, or magnetic resonance imaging is not likely to be of any benefit with respect to assessing FKFD.

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Other Tests

If available, gait analysis may help document the effect of fixed knee flexion deformity (FKFD) on the overall gait pattern.[17, 18, 21] Furthermore, concurrent and exacerbating sagittal plane deformities such as lumbar lordosis, pelvic tilt, hip flexion, and equinus or calcaneus may be identified. Many children need simultaneous or staged multilevel, and often bilateral, surgical intervention.[17, 22]

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Diagnostic Procedures

There may be an occasional need for consultation by a geneticist or neurologist, especially for those children with suspected syndromes. There may also be indications for electromyography, nerve conduction, or muscle biopsy. However, the majority of patients with fixed knee flexion deformity (FKFD) have well-established and chronic conditions, such as cerebral palsy, spina bifida, or arthrogryposis (amyoplasia).

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Histologic Findings

Generally, histologic studies are not relevant or necessary. The correction of fixed knee flexion deformity (FKFD) is the same, with or without this information. An exception would be a muscle biopsy for the workup of suspected myopathy.

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Staging

The degree of fixed knee flexion deformity (FKFD) is often best measured with a goniometer. One should differentiate between dynamic contracture and fixed deformity because their treatments differ. These are not mutually exclusive; a patient may have one or both.

For dynamic contractures, the generic options include hamstring stretching, physical therapy, orthoses, spasticity management (Botox/baclofen), and hamstring recession (proximal or distal).

Fixed deformities greater than 10º should be monitored, but surgical intervention is unlikely. However as the deformity surpasses 10º, progression is likely with growth, and surgical intervention should be considered.

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Contributor Information and Disclosures
Author

Peter M Stevens, MD  Professor, Director of Pediatric Orthopedic Fellowship Program, Department of Orthopedics, University of Utah School of Medicine

Peter M Stevens, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Orthopaedic Surgeons, American Orthopaedic Association, Limb Lengthening and Reconstruction Society ASAMI-North America, Pediatric Orthopaedic Society of North America, Utah Medical Association, and Western Orthopaedic Association

Disclosure: Orthofix Inc Royalty Independent contractor

Specialty Editor Board

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Paul E Di Cesare, MD, FACS  Chair and Professor, Department of Orthopedic Surgery, University of California Davis School of Medicine

Paul E Di Cesare, MD, FACS is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American College of Surgeons, and Sigma Xi

Disclosure: Stryker Consulting fee Consulting

Dinesh Patel, MD, FACS  Associate Clinical Professor of Orthopedic Surgery, Harvard Medical School; Chief of Arthroscopic Surgery, Department of Orthopedic Surgery, Massachusetts General Hospital

Dinesh Patel, MD, FACS is a member of the following medical societies: American Academy of Orthopaedic Surgeons

Disclosure: Nothing to disclose.

Chief Editor

Dennis P Grogan, MD  Clinical Professor, Department of Orthopedic Surgery, University of South Florida College of Medicine; Chief of Staff, Department of Orthopedic Surgery, Shriners Hospital for Children of Tampa

Dennis P Grogan, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Medical Association, American Orthopaedic Association, American Orthopaedic Foot and Ankle Society, Eastern Orthopaedic Association, Irish American Orthopaedic Society, Pediatric Orthopaedic Society of North America, and Scoliosis Research Society

Disclosure: Nothing to disclose.

References

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The lateral radiograph best demonstrates the open physes and the stigmata of chronic fixed knee flexion deformity (FKFD). This patient has avulsion "fractures" of the superior pole of the patella and of the tibial tubercle.
For flexion contracture, spasticity management (Botox/phenol/baclofen) or hamstring recession may offer some improvement, but these measures cannot overcome fixed knee flexion deformity (FKFD).
A posterior capsulotomy with or without PCL release can address fixed knee flexion deformity (FKFD), albeit with some risks, including neurovascular stretch injuries. Even with prolonged bracing following cast or frame removal, recurrent deformities are common.
Locking KAFO may support the patient for standing but cannot adequately address FKFD. When the deformity exceeds 20º, braces are poorly tolerated.
This child with arthrogryposis underwent unsuccessful posterior capsulotomies at age 3.
Starting at age 4, this patient subsequently underwent bilateral extension osteotomies 4 times, with recurrence each time as expected. Perhaps this sequence could have been abbreviated with guided growth, which, even if repeated, requires no casts or delay in weight bearing.
This ambulatory 15-year-old boy with arthrogryposis has never had an osteotomy; he was managed with stapling, followed by 8-plates, when he developed a recurrence. He has full extension on the right and 7º residual FKFD on the left. The 8-plates are still in situ (on the left) pending further growth.
The efficacy of floor reaction braces is compromised in the presence of FKFD. However, they may be continued following guided growth, pending correction, whereupon bracing may be unnecessary, provided the quadriceps are sufficiently strong.
Normal sagittal alignment permits the knee to lock in full extension, aided by powerful quadriceps and an intact extensor mechanism. The ground reaction force passes anterior to the "center of rotation" of the knee, while the PCL, posterior capsule, hamstrings, and gastrocnemius provide a tension band effect.
Fixed knee flexion deformity (FKFD). The knee is chronically bent, obligating the patient to walk with a crouch gait. The ground reaction force passes posterior to the center of rotation of the knee, where it overcomes the resistance of the weakened extensor mechanism. Secondary effects, including patella alta and fragmentation, are relatively common and painful.
(Images 11 through 15) This 5-year-old boy presented with a congenital knee flexion deformity. His only prior surgery was a Symes disarticulation for fibular absence and a rigid teratologic foot deformity. He was ambulatory in a prosthesis.
(Images 11 through 15) This patient underwent a supracondylar extension osteotomy of the femur.
(Images 11 through 15) Because of a relatively rapid recurrence of FKFD, this patient underwent anterior stapling of the femur; unfortunately, the staples migrated, but the physis is still open.
(Images 11 through 15) The staples in this patient were retrieved and replaced with a pair of 8-plates.
(Images 11 through 15) If we could turn back the clock, perhaps guided growth would have been sufficient to correct the problem in this patient, without an osteotomy or cast. The effective gain in limb length would occur gradually, without risk to the neurovascular structures.
This girl born with a teratologic knee flexion deformity and absent quadriceps had previous posterior capsulotomy, supracondylar osteotomy, and attempted stapling. Subsequently, she had a spatial frame applied to gradually extend the ankylosed knee; however, she fell and sustained a Salter I fracture of the proximal tibia.
Guided growth permits one to address the FKFD at or close to the level of the CORA (center of rotational axis of deformity). This is efficient and prevents the need for translocation, such as is required in an osteotomy. The gradual correction poses no risk to the neurovascular structures.
For FKFD, an 8-plate is placed on either side of the patellofemoral sulcus, through a small arthrotomy. Though intracapsular, the plates are nonarticular; synovitis has not been observed.
Depending on the etiology and the growth rate of the individual child, correction occurs fairly rapidly.
With the C-arm in the lateral, horizontal position, the physis is localized. A Keith needle is placed in the physis, and two 1.6-mm guide pins are inserted: one medial and one lateral to the sulcus. The cannulated 4.5-mm screws are then inserted. They need not be parallel, but they should not transgress the physis, joint, or posterior cortex.
(Images 21 and 22) This 4-year-old girl, born with congenital lateral dislocation of the patella compounding FKFD, underwent a posterior capsulotomy and patellar relocation with quadricepsplasty at age 2. By age 4, she had an oblique plane FKFD of 50º with 25º valgus. She had placement of a single anteromedial eight-plate. Eighteen months later, the valgus had corrected and the residual FKFD was 24º.
(Images 21 and 22) This patient underwent the addition of an anterolateral 8-plate to avoid varus and assist with correction of the residual FKFD.
This 12-year-old boy with spina bifida had previous stapling. It was felt that, with wide open physes, he would be better served by exchanging the loose staples for 8-plates rather than resort to an osteotomy.
(Images 24 and 25) A 12-year-old girl with evolving FKFD and patella alta, refractory to Botox, serial casts, therapy, and bracing.
(Images 24 and 25) This patient underwent bilateral supracondylar extension osteotomies with patellar tendon advancement. Because of limited space and compromised bone stock, fixation was lost on the left, and she presented with increased deformity. A revision osteotomy was required.
(Images 26 and 27) This patient has symptomatic and painful crouch gait due to FKFD.
(Images 26 and 27) This patient underwent guided growth with 8-plates and no "down time"; his FKFD corrected nicely during the ensuing 12 months, whereupon the plates were removed.
 
 
 
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