Knee




(1)
Groningen, The Netherlands

 




Knee Misalignment



Bowleg






  • A312070_1_En_10_Figa_HTML.gif Complaint: unilateral or bilateral bowleg(s).


  • A312070_1_En_10_Figb_HTML.gif Assessment: the lower leg is in adduction with respect to the upper leg. Many researchers use the distance between the medial femoral condyles as a measure for genua vara. There has been no longitudinal research on this measurement. It is better to measure the angle between the upper and the lower leg.


  • A312070_1_En_10_Figc_HTML.gif Differential diagnosis:



    • physiological genua vara


    • idiopathic excessive genua vara


    • Blount disease (tibia vara, osteochondrosis deformans tibiae)



      • infantile type


      • adolescent type


    • rickets (infantile osteomalacia)


    • skeletal dysplasia


    • focal fibrocartilaginous dysplasia


    • dysplasia epiphysealis hemimelica (Trevor disease)


    • infected or fractured growth plate


  • A312070_1_En_10_Figd_HTML.gif Explanatory note: physiological genua vara. There is a varus position in the knees up to 15° physiologically from birth until the age of 1 year. This physiological development is bilateral and appears to increase when the child stands and walks (Fig. 10.1). The varus position is localized in the distal part of the femur as well as in the proximal part of the tibia. There is often a lateral bowing of the tibiae. In many cases the bowlegs are optically accentuated by an enhanced external rotation in the hip joints and an internal torsion of the lower legs. In most cases bowlegs undergo spontaneous, slow correction and the legs straighten up when the child is 1½–2 years old, (Fig. 10.2). In isolated cases the spontaneous correction is completed only after ages 3–4. The best method to see whether the bowlegs will correct spontaneously is by placing the child lying in a supine position on the examination table so that the medial malleoli are approximated. It is almost certain that the bowleg posture will correct spontaneously if the knees straighten when you apply pressure on the outer sides.

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    Fig. 10.1
    (a) A physiological genua vara may occur up to 15° from the birth until the age of 1 year. (b) Once the child reaches the age of 1½–2 years, the genua vara has generally corrected slowly. The legs are now straight. (c) During the second and third years of life knock knees develop. (d) The valgus deviation corrects itself gradually, so that by the age of 7 a normal femorotibial valgus angle has developed in 95 % of cases


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    Fig. 10.2
    (a) One-year-old boy. Physiological genua vara. (b) The same boy as in Fig. 10.2a, now 2 years old. The bowlegs have spontaneously corrected. There is even a slight light valgus deviation of both knees


Idiopathic excessive genua vara

This deformity is bilateral and most common in Asians and may be familial. Operative treatment is seldom required. It is not clear from the literature whether and to what degree there is an increased chance of degenerative arthritis of the medial compartment.


Blount disease

Blount disease is a rare anomaly. It is a metaphyseal developmental disorder on the medial side in the proximal part of the tibia. The disease can cause unilateral or bilateral bowlegs at the age of 1½–3 years (infantile type), as well as starting at 8 years of age (adolescent type) (Table 10.1). A juvenile type is also recognized that occurs between the ages of 4 and 8, but it is probably an infantile type that has been diagnosed too late. That type is always bilateral. The disease affects girls as much as boys, and is most common among children of African origin.


Table 10.1
Differences between infantile and adolescent type of Blount disease























 
Infantile type

Adolescent type

Varus > 20°

Nearly always

Never

Internal torsion of the tibia

Frequent

Seldom

Recurrence chance after treatment

Frequent

Seldom


Infantile type

Radiological assessment is indicated when both legs are not straight at the age of 1½–2 years, or when bowlegs develop after that age. The infantile type is bilateral in 60 % of cases (Fig. 10.3). A unilateral bowleg is always abnormal. The infantile type often presents with internal torsion of the tibia. Six stages can be distinguished radiologically (Figs. 10.4 and 10.5).

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Fig. 10.3
Bilateral bowlegs as a result of an infantile type of Blount disease in 3-year-old identical twins


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Fig. 10.4
Langenskiöld and Riska classification for infantile Blount disease (Redrawn from: Langenskiöld A, Riska EB. Tibia vara (osteochondrosis deformans tibiae): a survey of seventy-one cases. J Bone Joint Surg Am. 1964;46:1405–20). I beak-shaped or irregular ossification of the medial side of the proximal tibial metaphysis. II and III progressive sagging of the medial side of the proximal tibial metaphysis. IV also sagging of the medial part of the proximal tibial epiphysis. V sagging of the medial part of the proximal tibial metaphysis and proximal tibial epiphysis is halted, and the medial and lateral parts of the proximal tibial epiphysis are now separated. VI a bony connection has appeared between the medial side of the proximal tibial metaphysis and epiphysis


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Fig. 10.5
(a) Blount disease (infantile type) stage III. (b) Blount disease (infantile type) stage VI


Adolescent type

The adolescent type is generally less pronounced than the infantile type. The varus position in adolescence never exceeds 20°. In 20 % of cases this type is bilateral (Fig. 10.6). In the unilateral adolescent type a difference in leg length of 1–3 cm may be seen (Fig. 10.7).

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Fig. 10.6
(a) Bilateral Blount disease (adolescent type). This 15-year-old girl developed genua vara within a half year due to a bilateral Blount disease. (b) Anteroposterior X-ray of the knees of the same girl as in 10.6a. On the medial side a bony connection has appeared between the proximal tibial metaphysis and epiphysis (arrow). The lateral part of the proximal tibial growth plate is intact and keeps growing causing a bowleg


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Fig. 10.7
An unilateral genu varum is always pathological. This 14-year-old girl developed a leftsided bowleg within half a year due to Blount disease (adolescent type)


Rickets

Bowlegs can also be caused by a lack of vitamin D. This is known as rickets, infantile osteomalacia or the English disease. Children don’t generally have a vitamin D deficiency in developed countries and the disease is rare. It tends to be caused by an hereditary enzymatic defect (pseudovitamin D-deficiency I), a congenital resistance (pseudovitamin D-deficiency II) or a renal phosphate loss in familial phosphate diabetes (X-chromosome dominant hereditary renal tubular disorder).

In addition to bowlegs, physical assessment shows skull thinning (craniotabes) as well as broad wrists, knees and ankles. As a result of the broadening of the junction between the ribs and the rib cartilage, a “rosary” forms on the anterior side of the ribs at the level of the sternum. There may also be a pigeon breast and antecurvatum deformity of the lower legs. X-rays show widened growth plates and the metaphyses appear frayed (Fig. 10.8).

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Fig. 10.8
(a) Bowlegs as a result of rickets (pseudovitamin D-deficiency). In this patient the distal femoral and distal tibial growth plates appear frayed. (b) One year after treatment of the pseudovitamin D-deficiency the appearance of the growth plates is normal and the varus deviation has spontaneously corrected


Skeletal dysplasia

Bowlegs can be part of generalized skeletal anomalies such as achondroplasia and multiple epiphyseal dysplasia1. A shorter body height (Fig. 10.9) is seen in skeletal dysplasia.

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Fig. 10.9
(a) Bowlegs in achondroplasia. The arms and legs are relatively short with respect to the rest of the body. Normally, the hands reach about halfway down the upper legs. (b) Patients with achondroplasia (see appendix) have a lumbar hyperlordosis


Focal fibrocartilaginous dysplasia

In focal fibrocartilaginous dysplasia there is a unilateral genu varum resulting from a local abnormality on the medial side in the proximal part of the tibia (Fig. 10.10). MRI assessment shows an elliptical cortical bone defect. Microscopical assessment shows fibrous tissue with small areas of cartilage. This abnormal tissue stunts growth on the medial side of the tibia, but on the other side it keeps growing and a bowleg develops.

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Fig. 10.10
Right-sided bowleg caused by focal fibrocartilaginous dysplasia (arrow)


Dysplasia epiphysealis hemimelica

This is an osteochondral overgrowth of an epiphysis or articular cartilage. It is a rare, non-painful condition with an incidence of 1 in 1,000,000. The condition manifests itself mostly between the ages of 2 and 14 years. It is three times more common in boys than in girls. There is a hereditary factor. The anomaly is intra-articular and remains limited to half of the extremity. The medial side is affected twice as often as the lateral part, and in two-thirds of the patients the condition is present in several epiphyses simultaneously. The most common localizations are the distal part of the femur, the distal part of the tibia and talus. A varus deformity will develop if the anomaly is localized on the lateral side. A valgus deformity will develop if the anomaly is localized on the medial side (Fig. 10.22). There is also movement limitation and a swelling of the knee, in case of a bowleg on the lateral side. Radiological assessment shows a lobe-shaped swelling on the lateral side of the distal femoral epiphysis, accompanied by multiple calcifications. Histologically speaking, the anomaly cannot be distinguished from an extra-articular osteochondroma. Malignant degeneration has never been described.


Infected or fractured growth plate

A bowleg can also be caused by an infection or a fracture, in which the growth plate is damaged on the medial side just above or just below the knee. Part of the cartilage of the growth plate is replaced by bony tissue, creating a bony connection between the epiphysis and metaphysis. If the bony connection is centrally located, then only leg shortening occurs. If the bony bridge is medially located, then the medial side of the corresponding growth plate stops length growth and the lateral side keeps growing so a bowleg develops (Fig. 10.11).

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Fig. 10.11
(a) Unilateral right-sided bowleg resulting from a bone fracture in the right proximal tibial growth plate. (b) Anteroposterior tomogram of the right knee, same patient as in Fig. 10.11a. Bony connection (arrow) between the epiphysis and metaphysis (bone bridge). In this case the medial side of this growth plate stops growing. The lateral side of the growth plate provides continuous growth causing a bowleg





  • A312070_1_En_10_Fige_HTML.gif Supplementary assessment: standing anteroposterior and lateral X-rays of the legs are requested in the case of unilateral or bilateral bowlegs that have not straightened out or become worse by the age of 2 years, as well as when one or two bowlegs develop in adolescence. In the infantile type the metadiaphsyeal angle in the proximal part of the tibia should be measured when in doubt as to whether one is dealing with physiological bowlegs or Blount disease (stage 1) (Fig. 10.12). The chances of developing Blount disease are less than 2 % (Fig. 10.13) if this angle is 11° or less. There is a strongly increased risk if the angle is between 11° and 16°. Blount disease is confirmed if the angle is greater than 16° (Fig. 10.14). At the level of the growth plate in the proximal part of the tibia there is a bony connection between the medial side of the epiphysis and the metaphysis in an adolescent type of Blount disease. The lateral part of the growth plate is intact. There is a loss of height on the medial side of the proximal tibial epiphysis (Fig. 10.6). A MRI is also requested for focal fibrocartilaginous dysplasia and dysplasia epiphysealis hemimelica.

    It is recommended to carry out blood tests for calcium, phosphate, parathyroidhormone, 25 hydroxy vitamin D and 1,25 dihydroxy vitamin D if rickets is suspected. A supplementary CT-scan is requested for growth plate damage caused by an infection or a fracture.


  • A312070_1_En_10_Figf_HTML.gif Primary care treatment: the parents should be reassured in cases of physiological genua vara.


  • A312070_1_En_10_Figg_HTML.gif When to refer: if genua vara persists or develops after the age of 18 months. A unilateral bowleg is always abnormal and should always be referred. The child should first be referred to a pediatrician in a case with rickets.


  • A312070_1_En_10_Figh_HTML.gif Secondary care treatment: idiopathic excessive genua vara. One should consider a hemi-epiphysiodesis on the lateral side.


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Fig. 10.12
Metadiaphyseal angle. This is the angle between the longitudinal axis of the tibia and the line that connects the most prominent part of the lateral and medial sides of the proximal tibial metaphysis


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Fig. 10.13
Anteroposterior X-rays of both legs with a varus position on both sides, both in the distal part of the femur and the proximal part of the tibia. The metadiaphyseal angle is less than 11°, so in this case we probably are dealing with physiological bowlegs. These bowlegs correct spontaneously


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Fig. 10.14
Anteroposterior X-rays of both legs. In this case the metadiaphyseal angle is 20°, indicating Blount disease


Blount disease (infantile type)

There are chances of spontaneous recovery in stages I and II of Blount disease The chances of recovery are greater (90 %) if stages I and II are treated with antivarus splints (Fig. 10.15). It seems to make no difference whether splint treatment is applied for the entire day or only at night. We advise prescribing antivarus splints only for night use for children younger than 3. A proximal tibial valgus osteotomy (just distal to the tibial tuberosity) with a distal fibulotomy is indicated if there has been no recovery within 1 year or if the child is older than 3. The same applies in a child with Blount disease stage III. A similar intervention should be carried out before the age of 4 in stages I, II and III. The chances of recurrence are higher if the operation is postponed until after that age, A valgus position of 5°–10° should be aimed for. For stages I, II and III a lateral hemi-epiphysiodesis of the growth plate of the proximal part of the tibia could be an alternative. This prevents progression of the anomaly, but correction will not be achieved. What’s more, it will stagnate the growth from this growth plate. In stages IV and V children are at least 6 years of age. A growth plate distraction of the medial part of the proximal tibial growth plate and also a proximal tibial valgus osteotomy just distal of the tibial tuberosity with a fibulotomy, may be considered, in which the proximal tibial growth plate on the medial side has not yet closed.

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Fig. 10.15
Antivarus knees splints

In stage VI the child is older than 9 and there is a bony connection between the epiphysis and the metaphysis on the medial side of the proximal tibial growth plate. The position of the proximal part of the tibia is corrected by a corrective osteotomy of the medial tibial plateau and a proximal tibial valgus osteotomy with a distal fibulotomy (Fig. 10.16). The lateral part of the proximal tibial growth plate of the affected tibia is destroyed to prevent recurrence. An epiphysiodesis of the proximal tibial growth plate on the non-affected side may be performed in addition to prevent a difference in leg length.

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Fig. 10.16
(a) Stage VI of infantile type of Blount disease. (b) The proximal medial part of the tibia is corrected by a straightening osteotomy of the medial tibial plateau and a proximal tibial valgus osteotomy together with a distal fibulotomy. The lateral part of the proximal tibial growth plate is destroyed. (c) Bowlegs in a Blount disease stage VI. (d) The same patient as in Fig. 10.16c after operative correction


Blount disease (adolescent type)

The adolescent type of this anomaly is not as pronounced as in the infantile type (Table 10.1). A definitive hemi-epiphysiodesis in which the lateral part of the proximal tibial growth plate is destroyed is usually sufficient. A proximal tibial valgus osteotomy can be performed in combination with a distal fibulotomy for a severe type. If necessary, an epiphysiodesis of the contralateral proximal tibial growth plate should also be carried out in order to prevent progression in the leg length difference depending on the growth expectations.


Rickets

Rickets should first be treated by a pediatrician. Spontaneous improvement of the deformity may occur after treatment of the underlying cause (Fig. 10.8), as healthy growth plates redirect themselves perpendicular to the weightbearing lines (Hueter-Volkmann law, 1862). A temporary hemi-epiphysiodesis of the lateral side of the growth plates in the distal part of the femur and/or the proximal part of the tibia will be performed using clamps, eight-plates or screws depending on the localization in severe cases where no improvement occurs. The fixation materials are removed as soon as the legs are straight.


Skeletal dysplasia

Operative intervention is indicated in 50 % of achondrodysplasia2 cases with such a misalignment. A temporary epiphysiodesis of the lateral side of the growth plates in the distal part of the femur and the proximal part of the tibia can be performed using clamps or eight-plates if the child is still growing. A correction osteotomy is an option if the child is no longer growing,


Focal fibrocartilaginous dysplasia

At first the bowleg will increase, but between the ages of 4 and 8 the defect will be spontaneously filled up with bony tissue; the bowleg position will tend to correct spontaneously if there is a varus deformity of less than 30°. A proximal valgus osteotomy of the tibia in combination with a distal fibulotomy may be performed if there is no spontaneous correction between the ages of 4 and 8.


Dysplasia epiphysealis hemimelica

Wedge excision at the level of the deformity, thus correcting the abnormal position. The chances of recurrence are great.


Infected or fractured growth plate

This bony bridge can be removed operatively if the bony connection between the epiphysis and metaphysis resulting from growth plate damage due to infection or fracture amounts to less than one-third of the total area of the growth plate. The growth plate usually recovers full function after this, and in a large number of cases the misalignment will correct spontaneously because the growth plate tries to direct itself perpendicular to the load line (Hueter-Volkmann law, 1862). In some cases, however, it is not possible to remove the bony bridge, or because the bone bridge consists of more than one-third of the total area of the total growth plate. In such cases it is best to destroy the lateral part of the growth plate and perform a correction osteotomy. The difference in leg length should be subsequently corrected at the appropriate time.


Knock Knee






  • A312070_1_En_10_Figa_HTML.gif Complaint: unilateral or bilateral knock knee(s).


  • A312070_1_En_10_Figb_HTML.gif Assessment: the lower leg is in abduction with respect to the upper leg.


  • A312070_1_En_10_Figc_HTML.gif Differential diagnosis:



    • physiological genua valga


    • idiopathic excessive genua valga


    • rickets (infantile osteomalacia)


    • skeletal dysplasia


    • multiple osteochondromata (exostoses)


    • dysplasia epiphysealis hemimelica (Trevor disease)


    • infected or fractured growth plate


    • fractured proximal tibial metaphysis


  • A312070_1_En_10_Figd_HTML.gif Explanatory note: the distance between the medial malleoli is usually used to determine the degree of knock knee. There are no publications with a longitudinal assessment of this deformity. The distance is also influenced by the leg length. The longer the legs, the larger the intermalleolar distance will be without an increase in the knock knee.


  • This measurement is even more unreliable in the case of a unilateral knock knee. In a physical assessment it is much better to measure the angle between the thigh and lower leg with a goniometer and to use the femoral tibial angle as a measurement.


Physiological genua valga

During the second and third years of life knock knees develop slowly with an average annual rate of 12° between the upper and lower leg after the legs with a physiological genua vara have straightened by the age of 18 months, This physiological development is bilateral. A knock knee is often optically enhanced by a simultaneous development of external rotation in the lower legs and in some cases an enhanced internal rotation in the hip joints. This can also be accentuated in cases with thick thighs and flatfeet. The valgus position corrects itself gradually, so that by the age of 7 years a normal valgus angle of 8° in girls and 7° in boys has developed in more than 95 % of cases (Fig. 10.17).

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Fig. 10.17
(a) Four-year-old boy with physiological genua valga, accentuated by thick thighs and flatfeet. (b) The same boy as in Fig. 10.17a placed on the examination table in such a way that the patellae point forward. The effect of any existing flatfeet is neutralized in this situation, so that the genua valga are already less noticeable. You say to the parents: “that’s the way they are now”. (c) Next, you grab both ankles and press the medial malleoli against each other, then say to the parents: “that’s the way they will be in the future”. (d) The same boy as in Fig. 10.17a, now 8 years old. The knock knees have spontaneously corrected

Parents ask for advice more often with knock knees than with bowlegs. This is because in physiological bowlegs children have been on their feet and walking only for a short time, if at all. In older children, the legs are longer and the “anomaly” is more noticeable.

A good method to show parents that the knock knees will correct spontaneously is to place the child supine on the examination table so that the medial femoral condyles are approximated. Next, encompass both ankles and try to press the medial malleoli against each other. The chances of spontaneous correction are great if you can do that, (Fig. 10.17). The chances are great that the knock knees will not correct spontaneously if this is not possible.


Idiopathic excessive genua valga

If there is still a genua valga in excess of 10° the chances of spontaneous recovery are minimal after the physiological period, after 7 years of age, (Fig. 10.18)

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Fig. 10.18
A 9-year-old girl with idiopathic excessive genua valga


Rickets

Rickets can give rise to bowlegs as well as knock knees (see pp. 172).


Skeletal dysplasia

Knock knees can also develop in addition to bowlegs (Fig. 10.19) in generalized bony anomalies such as achondroplasia3 and multiple epiphyseal dysplasia,3 (see pp. 172).

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Fig. 10.19
Knock knees in achondroplasia


Multiple osteochondromata

This is a developmental disorder in the periphery of the epiphyseal plates. The benign bony growth develops mostly with a cartilaginous cap. The anomaly increases in size until the patient stops growing. This problem may be solitary but can also appear in multiple areas. Multiple osteochondromata are involved in a hereditary disease in more than 60 % of cases. Hereditary multiple exostoses (or osteochondromata), are abbreviated as HME or HMO. There is often a knock knee position in multiple osteochondromata (Fig. 10.20). This is caused by a large osteochondroma in the proximal part of the fibula. There is reduced growth in length of the fibula, as a result of which the bone works as a brake, causing a valgus deformity in the proximal part of the lower leg (Fig. 10.21).

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Fig. 10.20
Genua valga as a result of multiple osteochondromata (exostoses) around the knees


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Fig. 10.21
Osteochondromata in the proximal part of the fibula cause disturbed growth of the fibula; the fibula works as a brake and causes a valgus position of the knee


Dysplasia epiphysealis hemimelica

This is an osteochondral overgrowth of the epiphysis on the medial side of the femur (Fig. 10.22). Besides the valgus 0 there is a limitation in movement and a swelling on the medial side of the knee (for explanatory note, see pp. 173).

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Fig. 10.22
Hemimelic epiphyseal dysplasia. This is an intra-articular osteochondroma around the medial femoral condyle (arrow) that causes a knock knee


Infected or fractured growth plate

A unilateral knock knee is always abnormal. Part of the cartilage of the growth plate will be replaced by bone tissue if there is damage to the growth plate caused by an infection or fracture. A knock knee develops if this bony connection appears on the lateral side of the distal femoral or proximal tibial growth plate in the distal part of the femur or the proximal part of the tibia.


Fractured proximal tibial metaphysis

A genu valgum may also be the result of a fracture on the medial side in the proximal tibial metaphysis (Fig. 10.23). A valgus deformity develops in a large number of cases after cast immobilization. This is probably caused by interposition of the periosteum at the level of the fracture, which will not allow closed (noninvasive) anatomical reduction.

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Fig. 10.23
(a) Lateral and anteroposterior X-rays of the left lower leg in a 5-year-old boy with a fracture of the left proximal tibial metaphysis. (b) Same patient as in Fig. 10.23a. After healing of the fracture a tibia valgum developed. (c) The same patient as in Fig. 10.23a, b. The tibia is now S-shaped. This can only be seen on the X-rays. The leg looks straight on physical assessment. (d and e) In this case no spontaneous correction has occurred. (f) In those cases where no spontaneous correction occurs a temporary hemi-epiphysiodesis on the medial side in the proximal tibial growth plate can be performed





  • A312070_1_En_10_Fige_HTML.gif Supplementary assessment: anteroposterior standing and lateral X-rays of the legs, and for hemimelic epiphyseal dysplasia a MRI. If rickets is suspected it is recommended to do blood tests to access calcium, phosphate, parathormone, 25 hydroxy vitamin D and 1,25 dihydroxy vitamin D. A supplementary CT-scan is requested in the case of growth plate damage caused by an infection or a fracture.


  • A312070_1_En_10_Figf_HTML.gif Primary care treatment: in the case of physiological knock knee you should reassure the parents and tell them that their child should come back if the deformity is still present at the age of 10.


  • A312070_1_En_10_Figg_HTML.gif When to refer: if there is a genua valgum with a femorotibial angle of 10° or more after the age of 10. The child should be referred to a pediatrician in the case of rickets.


  • A312070_1_En_10_Figh_HTML.gif Secondary care treatment: idiopathic excessive genua valga. One may consider a temporary hemi-epiphysiodesis using clamps, an eight-plate or screws on the medial side of the growth plates in the distal part of the femora for 11-year-old girls and 12-year-old boys if there are excessive knock knees with an angle of 10° or more between the upper and lower leg, (Fig. 10.24). The lateral part of the growth plates keep on growing, so that the leg straightens. The osteosynthetic materials are removed as soon as the knees are straight (usually 3–9 months after the initial operation). This operation is often carried out for cosmetic reasons. It is not clear in the literature which valgus position one should accept as an increased risk for degenerative arthritis in the lateral joint compartment. Once the child is fully grown, pathological knock knees can no longer be corrected by a temporary hemi-epiphysiodesis – instead, a distal femoral varus osteotomy should be considered.


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Fig. 10.24
(a) Temporary hemi-epiphysiodesis on the medial side of the distal femoral growth plate of the left knee using clamps, or (b) using an eight-plate (left knee)


Rickets

Rickets should be initially treated by a pediatrician. Spontaneous improvement of the deformity occurs after treatment of the underlying cause. In this situation the growth plates are directed perpendicularly to the weight-bearing lines (Hueter-Volkmann law, 1862). A temporary hemi-epiphysiodesis on the medial side of the affected epiphysis or a correction osteotomy may be necessary in severe cases where no improvement occurs.


Skeletal dysplasia

Temporary hemi-epiphysiodesis of the medial side of the growth plate in the distal part of the femur and proximal part of the tibia. A correction osteotomy may be considered if correction is insufficient once the child is fully grown.


Multiple osteochondromata

In order to correct or stop the valgus misalignment a temporary hemi-epiphysiodesis on the medial side of the growth plates in the proximal part of both tibiae and a partial resection of the fibula shaft including the periosteum should be performed. The clamps or eight-plate should never be allowed to remain in place for more than 2 years, or a bony bridge will develop in the growth plate. At some point it often becomes necessary to remove the osteochondromata as much as possible and carry out a proximal tibial varus osteotomy at the end of the growth period. In young children there is very high risk of recurrence.


Dysplasia epiphysealis hemimelica

Wedge excision at the level of the anomaly, thus correcting the misalignment. However, the chances of recurrence are great even after a wedge excision.


Infected or fractured growth plate

Operative removal may be considered if the bony bridge covers less than one-third of the total surface of the growth plate. Once the bony bridge is removed, the abnormal position of the knee will be spontaneously corrected during growth, because the growth plates try to direct themselves towards the weight-bearing lines of the leg (Hueter-Volkmann law, 1862). Sometimes it isn’t possible to remove the bony bridge, or because the bone bridge comprises more than one-third of the total growth plate. In such cases it is advisable to destroy the rest of the growth plate and perform a correction osteotomy. A difference in leg length should be subsequently corrected at an appropriate time.


Fractured proximal tibial metaphysis

A wait-and-see policy is adopted for an entire year in the case of a genu valgum caused by a fracture on the medial side in the proximal part of the tibia just distal to the growth plate. A valgus position in the proximal part of the tibia can spontaneous be corrected by the distal tibial growth plate, because it starts directing itself perpendicular to the weight-bearing line (Hueter-Volkmann law, 1862). An S-shaped tibia develops which can only be observed on X-rays (Fig. 10.23). The leg is straight on physical assessment. If this spontaneous correction does not occur, a temporary hemi-epiphysiodesis can be performed by placing an eightplate, clamps or a screw on the medial side of the proximal tibial growth plate in older children Sometimes a decision may be made to do a correction osteotomy, preferably at the end of the growth period. One should realize that in young children there is high risk of recurrence.


Overstretched Knee Deformity






  • A312070_1_En_10_Figa_HTML.gif Complaint: the knee or knees are overstretched.


  • A312070_1_En_10_Figb_HTML.gif Assessment: one or both lower legs are in hyperextension with respect to the upper leg(s).


  • A312070_1_En_10_Figc_HTML.gif Differential diagnosis:



    • nonstructural knee hyperextension



      • postural knee hyperextension


      • hypermobility


    • structural knee hyperextension



      • congenital knee hyperextension


      • congenital knee subluxation


      • congenital knee dislocation


    • tibial tuberosity abnormality



      • acquired recurvatum deformity of the proximal part of the tibia


  • A312070_1_En_10_Figd_HTML.gif Explanatory note: nonstructural hyperextension. The knee can be fully flexed passively in nonstructural hyperextension


Postural knee hyperextension

The knees of normal babies have a flexion deformity of 10°–20° up to the age of 2–3 months. The knees may display a hyperextension of 20° after a breech birth (Fig. 10.25). They can be fully flexed on passive assessment. The postural anomaly corrects spontaneously within 3 months. After a breech birth one should also check for developmental dysplasia of the hips. A312070_1_En_10_Figi_HTML.gif

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Fig. 10.25
After a breech presentation the knees may show a hyperextension of 20° (also watch out for developmental dysplasia of one or both hips)


Hypermobility

There may also be knees that can hyperextend 10° or more if there is general hypermobility of the joints resulting from joint laxity (Figs. 10.26 and 10.27). The knees can in this case be fully flexed. One can see the hyper-extension of the knee when these children stand and walk. Pronounced hypermobile joints are a feature of Ehlers-Danlos syndrome4.

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Fig. 10.26
(a) In practice, frequent use is made of the Beighton criteria for hypermobility: 1 passive opposition of the thumb against the anterior side of the forearm. 2 passive hyperextension in the metacarpophalangeal joint of more than 90°. 3 hyperextension in the elbows of more than 10°. 4 hyperextension in the knees of more than 10°. 5 the ability to place one’s hand flat on the ground when bending the trunk with extended knees. While testing, the examiner looks at both sides of the body, and one point is allocated per test item, with a maximum of nine attainable points. Hypermobility is present with a score of four points or more. (b) Passive position of the thumb against the anterior side of the forearm


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Fig. 10.27
A 12-year-old girl. The knees can be usually hyperextended if there is hypermobility as a result of congenital ligamental laxity


Structural hyperextension

In structural hyperextension the knees cannot be completely flexed actively or passively. It can be classified as congenital hyperextension, subluxation or dislocation if the anomaly is present from birth (Fig. 10.28).

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Fig. 10.28
(a) Two-month-old baby with Larsen syndrome, with bilateral knee dislocations and clubfeet. (b, c) Adult with Larsen syndrome, with untreated bilateral knee and elbow dislocations


Congenital knee hyperextension

Hyperextension of 15°–20°. The knee can be brought passively into 45°–90° of flexion.


Congenital knee subluxation

Hyperextension of 25–45°. The knee can be brought passively into a neutral (0°) position.


Congenital knee dislocation

Hyperextension position of 25–45°. Passive flexion is impossible. A congenital knee dislocation is seen in 1 in 100,000 births. There is a bilateral dislocation in one-third of cases. It is three times more common in girls than in boys. There is also a developmental dysplasia of one or both hips in 70 % of children and in 50 % of these children they additionally have congenital foot deformities. In a congenital subluxation/dislocation of the knee the proximal part of the tibia is dislocated anteriorly. The term dislocation specifies that the tibial joint surface is not in contact with the femur at all. The term subluxation is used when the proximal tibial joint surface is in partial contact with the distal femur joint surface. There can also be a lateral translation of the tibia with respect to the femur, as well as a valgus position, as a result of a contracture of the iliotibial tract. Semitendinosus and semimembranosus muscles on the medial side of the collateral ligaments may be displaced anteriorly. The quadriceps muscle is shortened, and the suprapatellar recess is fixed onto the femur. The cruciate ligaments may be absent. A congenital knee subluxation/dislocation may be part of the Larsen syndrome5 (Fig. 10.28) and arthrogryposis multiplex congenita5. In Larsen syndrome there may be multiple dislocations of hips, knees and elbows. These children have characteristic facial features, such as a prominent forehead, widely spaced eyes (hypertelorism), and a depressed nasal bridge.


Tibial tuberosity abnormality

The knee can be fully flexed and the anomaly is not in the joint but just distal to it.


Acquired recurvatum deformity of the proximal part of the tibia

A premature closure of the anterior side of the proximal tibial growth plate may occur in rare cases, after infection or a fracture of the tibial tuberosity. A recurvation deformity develops due to damage to the anterior side of this growth plate because the apophysis is in continuity with the proximal tibial growth plate, (Fig. 10.29). In extremely rare cases this can also be caused by Osgood-Schlatter disease, which is an apophysitis of the tibial tuberosity (see pp. 231–234).

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Fig. 10.29
Recurvatum deformity of the proximal part of the tibia resulting from premature closure of the apophysis of the tibial tuberosity





  • A312070_1_En_10_Fige_HTML.gif Supplementary assessment: It is recommended to take lateral X-rays of the knee in newborns if there is hyperextension of 10° or more and if the ipsilateral knee flexion is less than 90°. The X-rays will show an anteriorly displacement of the tibia with respect to the femur if there is a subluxation or dislocation, (Figs. 10.30 and 10.31). X-rays of the knees and CT-scans should be also taken in older children with no previous genu recurvatum but who have developed it in the course of time after a trauma, infection or Osgood-Schlatter disease.


  • A312070_1_En_10_Figf_HTML.gif Primary care treatment: children with congenital ligamental laxity and hyperextended knees sometimes complain of pain in the posterior side of the knees. The symptoms usually disappear after introducing a heel elevation under the shoes. As the child grows older it becomes stiffer and the ligamental laxity as well as the hyperextension will tend to disappear.


  • A312070_1_En_10_Figg_HTML.gif When to refer: in cases of congenital hyperextension and congenital subluxation/dislocation of the knee in newborns, and when a genu recurvatum deformity occurs at an older age.


  • A312070_1_En_10_Figh_HTML.gif Secondary care treatment: congenital knee hyperextension, congenital knee subluxation and mild congenital knee dislocation. The practitioner holds the upper leg with one hand and the lower leg with the other. The knee is brought into flexion under traction. Simultaneously, the distal part of the femur is pushed anteriorly. Next, an upper leg cast is applied with the knee in the reduced position. This is repeated until a flexion position of 60° is obtained, after which the knee is treated with a Pavlik harness for 2–3 months (Fig. 9.​20).


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Fig. 10.30
(a) Congenital hyperextension of the knee. (b) Congenital subluxation of the knee. (c) Congenital dislocation of the knee. In a subluxation/dislocation the proximal part of the tibia is shifted anteriorly (Redrawn from: Curtis BH, Fisher RL. Congenital hyperextension with anterior subluxation of the knee. Surgical treatment and long-term observations. J Bone Joint Surg Am. 1969;51-A:255–69)


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Fig. 10.31
(a) Lateral X-ray of one of the knees of the child from Fig. 10.28a. The tibia is shifted anteriorly with respect to the femur. (b) Lateral X-ray of one of the knees of the adult in Fig. 10.28b, c


Severe congenital knee dislocation

In this case the quadriceps tendon is lengthened in a v-shape, the capsule is divided on the anterior side, and the tensor fascia lata is divided transversely to correct the valgus position (Fig. 10.32). The knee is reduced and immobilized in 30° of flexion for 4–6 weeks in a plaster of Paris cast. After which, a long leg orthosis is worn for an entire year in order to prevent hyperextension.

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Fig. 10.32
Operative treatment of a congenital knee dislocation. The quadriceps tendon is lengthened in a V-shape, the capsule is transversely divided on the anterior side and the tensor fascia lata is released to correct the valgus position (Redrawn from: Curtis BH, Fisher RL. Congenital hyperextension with anterior subluxation of the knee. Surgical treatment and longterm observations. J Bone Joint Surg Am. 1969;51-A:255–69)


Acquired recurvatum deformity of the proximal part of the tibia

A proximal tibial osteotomy is recommended at the end of growth in cases with a recurvation deformity of the proximal part of the tibia. Note that the tibia is usually angled at about 9° posteriorally.


Bent Knee Deformity






  • A312070_1_En_10_Figa_HTML.gif Complaint: the baby keeps the knee flexed, and it cannot be extended passively.


  • A312070_1_En_10_Figb_HTML.gif Assessment: the knee is flexed and is in valgus, the lower leg is in external rotation, or the knee is only flexed.


  • A312070_1_En_10_Figc_HTML.gif Differential diagnosis:



    • congenital patellar dislocation


    • congenital absent patella


  • A312070_1_En_10_Figd_HTML.gif Explanatory note: congenital patellar dislocation. A congenital dislocation of the patellofemoral joint is rare. The dislocation is present at birth but is often diagnosed only at an older age. The patella is laterally dislocated and cannot be reduced manually. The patella is underdeveloped and there is no femoral groove. This anomaly can be unilateral or bilateral, as well as familial. The knee is flexed and is in valgus and the lower leg is in external torsion.


  • The flexed knee is not neatly rounded but flat, and the femoral condyles are prominent (Fig. 10.33). The patella is not at the front on palpation. The flexion contracture and the valgus position of the knee increase as the child grows. The patella does not ossify before the age of 3, which is why the dislocation isn’t visible on X-rays before that time.

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    Fig. 10.33
    (a) Congenital dislocation of the right patella. (b) Axial X-ray of both patellofemoral joints. The right patella is laterally dislocated. An absent femoral groove on the right side is noticeable


Congenital absent patella

This is a rare condition, one of 10,000 live birth’s, that tends to be bilateral and often occurs in combination with other congenital anomalies such as developmental dysplasia of the hip, clubfoot and nail-patella syndrome (onycho-osteodysplasia)6. The extension mechanism of the knee remains intact and the knee can be extended actively if the quadriceps femoris muscle is normal. An active extension deficit in the knee will be present if there is reduced quadriceps muscle strength in addition to an absent patella.





  • A312070_1_En_10_Fige_HTML.gif Supplementary assessment: X-rays of the knee before the age of 3 are not necessary because the patella is not yet ossified. Anteroposterior as well as lateral X-rays of the knee as well as an additional X-ray of the patellofemoral joint can be requested after the age of 3. The patella is always dislocated laterally in congenital patellar dislocations (Fig. 10.33).


  • A312070_1_En_10_Figf_HTML.gif Primary care treatment: none.


  • A312070_1_En_10_Figg_HTML.gif When to refer: if a flexion contraction of the knee is present 3 months after birth.


  • A312070_1_En_10_Figh_HTML.gif Secondary care treatment: congenital patellar dislocation. Galeazzi procedure: open repositioning of the patella. A tenodesis of the patella is performed so that it will no longer deviate laterally using the tendon of the semitendinous muscle. The lateral retinaculum is divided lengthwise. The insertion of the vastus medialis of the quadriceps femoris muscle is released and repositioned laterally and distally onto the patella, the medial capsule and the medial retinaculum are reefed (Fig. 10.34). Roux-Goldthwait procedure: the lateral half of the patellar ligament is also transposed medially (Fig. 10.35) if there is a Q-angle of more than 20°. Occasionally the quadriceps tendon and/or the hamstrings have to be lengthened.


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Fig. 10.34
(a) Galeazzi procedure for congenital patellar dislocation. A tenodesis of the patella is performed using the tendon of the semitendinous muscle. (b) Modification of this procedure: the lateral retinaculum is divided lengthwise. The insertion of the vastus medialis muscle is released, and fixed laterally and distally onto the patella. The medial capsule and the medial retinaculum are reefed and attached


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Fig. 10.35
(a) Q-angle. This is the angle between the upper leg and the patellar ligament. The patellar ligament normally deviates 15–20° laterally with respect to the quadriceps. (b, c) Roux-Goldthwait procedure. The lateral half of the patellar ligament is transposed medially


Congenital absent patella

Part of the hamstring insertion can be attached to the quadriceps muscle to benefit extension if there is weakness of the quadriceps femoris muscle accompanied by an active extension deficit of the knee.


Repeated Kneecap Subluxation/Dislocation






  • A312070_1_En_10_Figa_HTML.gif Complaint: symptoms vary widely. Sometimes the only symptom that the patient has is that the kneecap is regularly displaced laterally when flexing and veers back in extension. A repeated subluxation of the kneecap is usual in this case. In the case of a full dislocation the knee will be very painful and the patient will usually fall. The knee is held in flexion. The pain disappears after the knee is passively extended as the kneecap springs back into position.


  • A312070_1_En_10_Figb_HTML.gif Assessment: a dislocated patella is palpable on the lateral side of the knee. However, we usually have a situation in which the patella has returned to its normal position. To get an impression about the instability of the patellofemoral joint the knee is flexed slightly by the examiner and the patient is asked to relax the quadriceps muscle. The examiner can then cause abnormal lateralization by pressing the thumbs against the medial side of the patella.


  • A312070_1_En_10_Figc_HTML.gif Differential diagnosis:



    • recurrent patellar subluxation/dislocation



      • voluntary patellar subluxation/dislocation


      • habitual patellar subluxation/dislocation


      • recurrent posttraumatic patellar


      • subluxation/dislocation


  • A312070_1_En_10_Figd_HTML.gif Explanatory note: recurrent patellar subluxation/dislocation. There are two conditions in which non painful repeated dislocation of the patellar may occur: voluntary patellar subluxation/dislocation and habitual patellar subluxation/dislocation. Recurrent posttraumatic patella subluxation/dislocation occurs after an initial significant trauma and is painful.


Voluntary patellar subluxation/dislocation

This type is due to hypermobility disorders such as in Down7 and Ehlers-Danlos syndromes7.


Habitual patellar subluxation/dislocation

This a subluxation/dislocation in normal children with no associated ligamentous laxity. In general there are knee anomalies, especially a misalignment of the extensor apparatus. The first dislocation in a habitual patellar subluxation or dislocation is generally not caused by a trauma. The patella dislocates upon knee flexion. The dislocation is a consequence of a developmental disorder with the following possible manifestations: atrophy of the vastus medialis of the quadriceps femoris muscle; a more proximal insertion of the vastus medialis: external torsion, combined with a valgus position of the leg, causing a larger Q-angle (Fig. 10.35); a shallow femoral groove; a proximally localized patella; or combinations of the above listed developmental disorders. In a proximally localized patella (patella alta) the distance between the apex of the patella and the attachment to the tibial tuberosity is greater than the length of the patella. Normally, the distance between the apex of the patella and the tibial tuberosity is as great as the length of the patella. Variation of more than 20 % indicates an abnormal position.


Recurrent posttraumatic patellar subluxation/dislocation

A traumatic patellar dislocation affects 3–4 in 10,000 children between 10 and 17 years of age. In the first instance there has been an extensive valgus/flexion trauma, causing a laxity in the medial retinaculum that can lead to recurrent dislocations. Recurrences are seen in 30–50 % of cases after an initial traumatic patellar subluxation/dislocation,.





  • A312070_1_En_10_Fige_HTML.gif Supplementary assessment: anteroposterior and lateral X-rays of the knee and an axial X-ray of the patellofemoral joint. In a recurrent posttraumatic subluxation and dislocation there are often calcifications at the level of the medial retinaculum. Such calcifications are caused by a traumatic tear in the medial retinaculum. Sometimes there is an avulsion fracture on the medial part of the patella. There is an osteochondral fracture of the patellofemoral joint in 40 % of cases.


  • A312070_1_En_10_Figf_HTML.gif Primary care treatment: in the case of patellar subluxation/dislocation you should encourage the patient to extend the knee. The patella will tend to reduce spontaneously. If this is not the case, analgesics and muscle relaxants can be given. After which the patient can again be encouraged to extend the knee while the examiner pushes the patella from lateral to medial. A repetetive subluxation is best treated conservatively. Children with no surgical treatment after repetetive subluxations had less pain and osteoarthritis and fewer repetetive subluxations than did those who had proximal or distal realignment procedures. In patients treated conservatively the number of subluxations decreased dramatically as they approached 30 years of age.


  • A312070_1_En_10_Figg_HTML.gif When to refer: as a rule, after at least three subluxations/dislocations. A natural healing tendency is minimal after that. Dislocations of the patella will continue if no treatment is carried out.


  • A312070_1_En_10_Figh_HTML.gif Secondary care treatment: voluntary patellar subluxation/dislocation. In the first instance one should try quadriceps exercises and a patellar anti-dislocation orthosis. An operation should be avoided as much as possible. In problem cases in children a Galeazzi procedure can be performed. After the child stops growing heighten the lateral part the patellofemoral groove by means of an osteotomy.


Habitual patellar subluxation/dislocation

The growth plates will be damaged in a child if one carries out an operation on bone. For this reason, soft-tissue surgery should be chosen with a Galeazzi or modified Galeazzi operation for a proximal realignment (Fig. 10.34) possibly combined with a Roux-Goldthwait procedure for distal realignment (Fig. 10.35). However, despite these interventions patellar subluxations/dislocations may keep occurring. In that case, a bony operation can be considered after the child stops growing.

The tuberosity is displaced medially in the case of a Q-angle larger than 20°. Combining a medial with distal transposition (Hauser procedure) may only be carried out if there is a proximally localized position of the patella (patella alta) (Fig. 10.36). If this is not the case, distal transposition of the tibial tuberosity will cause premature degenerative changes in the patellofemoral joint. However, even when the tibial tuberosity is only displaced medially, it is in fact also displaced posteriorly, which can cause patellofemoral problems. An alternative is the Elmslie-Trillat procedure, in which a segment of the cortex of the tibial tuberosity is rotated medially. Early degenerative patellofemoral joints changes developed in those with distal realignment. Those with proximal realignment had fewer patellofemoral changes, but the recurrence was 25 %. A correction osteotomy proximal to the tibial tuberosity may be carried out if the excessive Q-angle is caused by a valgus position of the knee or by internal torsion of the lower leg. In the case of a shallow femoral groove, the lateral part of the groove can be raised anteriorly by means of an osteotomy.

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Fig. 10.36
Hauser procedure: medial and distal displacement of the tibial tuberosity. A combination of medial and distal displacement may only take place if the patella has a proximal position (patella alta). Only a medial displacement of the tibial tuberosity is performed if there is no elevated patella position (Redrawn from: Hauser EDW. Total tendon transplant for slipping patella. A new operation for recurrent dislocation of the patella. Surg Gynecol Obstet. 1938;199–214)


Recurrent posttraumatic patellar subluxation/dislocation

An arthroscopy after the first dislocation should first be considered if osteochondral fractures are suspected. Small fragments can be removed, and large fragments can possibly be reduced and fixed. The knee is immobilized for 5–10 days in a plaster of Paris cast or a patellar anti-dislocation orthosis if there is no osteochondral fracture. This is followed by prescribing quadriceps and hamstring exercises. A release of the lateral retinaculum can be carried out and the medial capsule can be reefed and sutured if recurrent subluxations/dislocations occur after this. This treatment is based on the situation after at least three dislocations.


Differential Diagnosis Knee Misalignment





































Bowleg
 

Bilateral
 

 Up to the age of 2 years.

Physiological genua vara

 After the age of 2 years without skeletal abnormalities (with a tibiofemoral varus >5°).

Idiopathic excessive genua vara

 Cranial thinning, broad wrists.

Rickets (infantile osteomalacia)

 Short body length.

Skeletal dysplasia

Bilateral or unilateral genu varum

Blount disease (tibia vara, osteochondrosis deformans tibiae)

 After the age of 2 years with skeletal abnormalities.

 Infantile type

 Metadiaphyseal angle >16°.
 

 After the age of 8 years with skeletal abnormalities.

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Jun 26, 2017 | Posted by in PEDIATRICS | Comments Off on Knee
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