referat blount

CHAPTER I INTRODUCTION 1.1 Background Blount disease is a developmental condition characterized by disordered endochondral ossification of the medial part of the proximal tibial physis resulting in multiplanar deformities of the lower limb. The first detailed description was provided by Blount in 19371, and this was followed by another extensive study by Langenskiold in 19522. Although Blount coined the term tibia vara, implying a solely frontal plane deformity, subsequent authors noted that multiplanar deformities are commonly seenwith this condition. Secondary to the asymmetrical growth with relative inhibition of the posteromedial portion of the proximal tibial growth plate, a three-dimensional deformity of the tibia with varus, procurvatum (apex anterior), and internal rotation develops, along with possible limb shortening in unilateral cases. This entity can lead to a progressive deformity with gait deviations, limb-length discrepancy, and premature arthritis of the knee.

1.2 Anatomical structure of bone The tissue bone is considered from two entirely different points of view. 1. individual bones are anatomical structures and 2. bone of entire skeleton is a physiological organ that it metabolically active Since the nonliving intercellular matrix of bone is calcified, or stonelike, it is one of the hard tissue. Indeed, its hardness provides the strength to individual bones as structures and enables them to serve three functions : 1. To provide the rigid framework for the trunk and extremities to withstand mechanical loads 2. To serve as lever for the locomotor function of skeletal muscles

1

3. To afford protection for vulnerable viscera, for example skull for the brain, the

spine for the spinal cord, and the thoracic cage for heart and lung. Bone of the entire skeleton as an organ severs two additional functions4. It contains haemopoetic tissue of the myeloid type for the the production of

erythrocytes, granular leukocytes and platelets 5. It is the organ of storage or reservoir for calcium, phospors, magnesium and sodium. Helping to maintain ilieu intereur of ionized mineral homeostasis by storing or releasing these substances. Thus in addition to being bone formity cells, osteoblast also govern metabolism in response to a wide variety of stimulating biochemical, mechanical, electrical and magnetic via spesific cellular receptors.

Bones from the viewpoint of their gross structure and classified as 1. Long bones, or tubular bones ( e.g femur ) 2. Short bones or cuboidal bones ( e.g carpal bones ) 3. Flat bones ( e.g scapula )

2

Furthermore, each bone consists of dense cortical bone ( spongiosa ) on the inside and a sponge like arrangement of trabecular bone ( spongiosa ) on the inside. In children, the covering periosteum is thick and loosely attached to the cortex and it produces new bone readily. In adults, by contasts, the periosteum becomes progresively thinner and more adherent to e cortex, and it produces new bone less readily. Thus fundamental difference explains, in part, why fractures heal more rapidly in young children than in adults.

Blood supply to long bones Thee distinct vascular systems exist in long bones : 1. An afferent vascular system comprising nutrient and metaphyseal arteries that together supply the inner two thirs of the cortex and periosteal arteries that supply the outer one third 2. An efferent vascular system that conveys venous blood 3. An intermediete vascular system of capillaries within he cortex The direction of blood flow through a long bone is normally centrifugal, that is from the medullary cavity the periosteal surface. The epiphysis and their epiphyseal plates ( physes ) comprise a captivating component of the skeletal system during the growing years of childhood. Because they are unique structural and functions units, it is not suprising that under abnormal circumstances,3

they react differentially from the rest of the skeleton. Consequently, a variey of unique disorders peculiar to epiphysis and ephyseal growth may be seen in children.

Nutrition of the epiphysis and its epiphyseal plate Knowledge of the unique blood supply to epiphysis and their epiphyseal plate ( physis ) is pivotal to an understanding of their disorders. Most pressure epiphyses are covered assentially by articular cartilage and receive blood vessels only through their bare bone areas . Others, such as the femoral head, being completely covered by articular cartilage, receive their blood vessels that must penetrate the cartilage clothing . In addition to supplying the epiphysis, the epiphyseal blood vessels are also responsible for the nutrition of the growing cells of the epiphyseal plate, therefore, ischemia of the epiphysis is associated with ischemia of the epiphyseal plate and subsequent disturbance of longitudinal growth of the bone. Whereas the shaft of a long bone grows in length from the epiphyseal plate ( physis ), the length from the epiphyseal itself grows in three dimensions from the deep zone of the articular cartilage. Types of epiphysis., a pressure epiphysis, situated at the end of a long bone, is subjected to pressure transmitted to the joint into which it enters. In this sense it may be considered an articular epiphysis. Furthermore, its epiphyseal plate ( physis ) provides longitudinal growth of the bone. A traction epiphysis, by contrast, is the site of attachment of tendons muscles, consequently, it is subjected to traction rather than to

4

pressure. Because it does not enter into the formation of a joint, it is nonarticular and does not contribute to the longitudinal growth of the bone. 1.3 Physiology of bone growth and remodeling Bone growth and remodeling Bones grow in length by one process ( involving endochondral ossification ) where as they grow in width by another process ( involving intramembranous ossification ) 1. Growth in length Since interstitial growth within bone is not possible, bone length can increase only by the process of interstitial growth within cartilage followed by endochondral ossification. Thus, there are two possible sites for cartilaginous growth in a long bone : 1. Articular cartilage 2. Epiphyseal plate cartilage

Epiphyseal plate cartilage The epiphyseal plate provides growth in the length of the metaphysis and diaphysis of a long bone. In this site of growth, a constant balance is maintained between two saparate processes : 1. Interstitial growth of the cartilage cells of the plate, making it thicker and thereby moving the epiphysis farther away from the metaphysis. 2. Calcification, death and replacement of cartilage on themetaphyseal surface by bone through endocondral ossification

Four zones of the epiphyseal plate can be distinguished :

5

1. The zone of resting cartilage anchors the epiphyseal plate to the epiphysis and

contains immature chondrocytes, a well as delicate blood vessels that penetrate it from the epiphysis and bring nourishment to the entire plate 2. Teh zone of young proliferating cartilage is a site of most active growth of the cartilage cells, which are arranged in vertical columns.3. The zone of maturing cartilage is reveals a progresive enlargement and maturation

of the cartilage cells as they approach the metaphysis. Those chondrocytes accumulate glycogen in their cytoplasm and produce phospatase which may be involved in the calcification of theirsurrounding matrix.4. The zone of calcifying cartilage is thin and its chondrocytes have died as a result of

calcification of the matrix. Thus structurally the weakest zone of the epiphyseal plate. Bone deposition is active on the metaphyseal side of this zone and as a new bone is added to the calcified cores of cartilage matrix, the metapysis becomes corresponding longer. Hormonal control of longitudinal bone growth Troughout the world, and especially in the developing countries, malnutrition remains the most common cause of retardation of longitudinal bone growth. Such malnutrition is also accompanied by disturbances of endocrine function.Human growth hormone, which is synthesized in the anterior pituitary gland, its growth promoting effect throughthe production of insulin like growth hormone in the liver. Thyroxine is also essential for normal longitudinal growth. Sex hormone are involved in the characteristic postpubertal growth spurt in adolscent boys and girls. Glucocorticoroids (cortisons) have an inhibitory effect on growth as seen in cushing syndrome. , whether naturally occuring secondary to prolonged thurapetic to children. Growth in width Bones increase in width by means of appositional growth from the osteoblast in the deep, or inner ( cambium ), layer of the periosteum, the process being one of intramembranous ossification. Simultaneously, the medullary cavity becomes larger through osteoclastic resorption of bone on the inner surface of the cortecs, which is lined by endosteum.6

Remodeling of bone During longitudinal growth, the flared metaphyseal regions of bone must be continually remodeled as the epiphysis moves progresively farther away from the shaft. This is accomplished by simultaneous osteoblastic deposition of bone on one surface and osteoclastic resorption on the opposite surface. However, remodeling of bone constinous throughout life, since some haversian system, or osteons, continually erode trough cell death as well as though factors that demand removal of calcium from bone, therefore deposition of bone must also continue to maintain bone balance. During the growing years, bone deposition exceeds bone resorption, and the child is in a state of positive bone balance. By contrast, in old age, bone deposition cannot keep pace with bone resorbtion and the elderly person is in a state of negative bone balance. Remodeling of bone also occurs in response to physical stresses or to the lack of them in that bone is deposted in sites subjected to stress and is resorbed from sites where there is a little stress. This phenomenon is generally referred to as wolffs law and is exemplified by marked cortical thickening on the concave side of a curved bone. As well as by the allignment of trabecular systems along the lines of weightbearing stress in the internal architecture of the upper end of the femur. It is likely the phenomenon of wolffs law is mediated by induced electrical potentials. For example, in a bowed tubular bone- or a curved trabecula cancellous bone a negative electrical charge or potential exists on the concave side ( compression force ) and a positive charge on the convex side ( tension force ). Furtermore, it would seem that a negative charge induces bone deposition, where as a positive charge induces bone resorption.

7

CHAPTER II BLOUNT DISEASE 2.1 Definition Blount disease is a developmental condition characterized by disordered endochondral ossification of the medial part of the proximal tibia physis resulting in multiplanar deformities of the lower limb. The medial portion of the upper tibial epiphyseal plate may become the site of localized epiphyseal growth disturbance known as tibia vara ( blounts disease, osteochdrosis deformans ), which is characterized by a progressive bow leg ( varus ) deformity. This is a progressive bow-leg deformity associated with abnormal growth of the posteromedial part of the proximal tibia. Physiologic Genu Varum In most children under 2 years old, bowing of the legs is simply a normal variation in leg appearance. Doctors refer to this type of bowing as physiologic genu varum. In children with physiologic genu varum, the bowing begins to slowly improve at approximately 18 months of age and continues as the child grows. By ages 3 to 4, the bowing has corrected and the legs typically have a normal appearance. 2.2 Epidemiology This disorder is more common in girls than boys. It usually becomes manifest at the age of about 2 years in the infantile type and after the age of 8 years in the adolescent type. The growth disturbance may involve only one tibia or both. Tibia vara is relatively uncommon in most areas of the world but is inexplicably common in two completely different types of country, namely finland and Jamaica. The estimated prevalence of infantile Blount disease in the population of young children with significant bowlegs in8

the United States is 0.007, or less than 1%; the prevalence of adolescent Blount disease may reach 2.5% in the population at greatest risk (see image below). The exact frequency in persons of all ethnicities is unknown and most likely is less than 1%. In addition to race and body weight, the frequency is increased if other family members have been diagnosed as having Blount disease. 2.3 Etiology The cause of Blount disease remains controversial, but it is most likely secondary to a combination of hereditary and developmental factors. Biomechanical overload of the proximal tibial physis due to static varus alignment and excessive body weight have been implicated in the etiology of infantile tibia vara. The compressive forces at the medial aspect of the knee appear to cause growth suppression. Although similar processes may be implicated in the development of adolescent tibia vara, static varus alignment is not a prerequisite. Dynamic gait variation secondary to increased thigh girth has been suggested to be implicated in the development of adolescent Blount disease. A number of authors have noted a positive family history of Blount disease in some affected individuals. Data supporting inheritance are limited but worthy of mention. Sevastikoglou and Eriksson based this contention on the finding of 4 persons with tibia vara in the same family, of whom 2 were identical twins. Schoenecker et al also found a positive family history in 14 of 33 patients. However, no direct proof of a genetic relationship has been discovered. 2.4 Classification Classification Lagenskiold and Riska System

Radiographically, the changes are similar to those of physiologic bowing but are more severe, and the tibia, rather than the knee, is in varus position with the shaft adducted without intrinsic curvature. Six radiographic stages have been recognized: I, a progressive increase in degree of varus deformity associated with irregularity of the entire growth plate; II, a lateromedial depression of the ossification line of the medial portion of the metaphysis and presence of a wedge-shaped medial end of the epiphysis develop;9

-

III, the cartilage-filled depression in the metaphyseal beak deepens and calcific foci may appear; IV, the cartilaginous growth plate becomes reduced to a narrow plate with definite irregularity of the epiphysis; V, the bony epiphysis and corresponding articular surface become greatly deformed, with separation of the bony epiphysis into two portions by a clear band; VI, the branches of the medially located double growth plate ossify, whereas growth continues in the normal lateral part.

Thompson and carter further classified : Infantile type Onset at the age less than three years. Bilateral involvement is common, particularly with an early-onset presentation. Juvenile type Onset at the age of four to ten years. Adolescent type Onset after the age of ten years.

10

2.5 Pathophysiology Blount disease most likely is caused by a combination of excessive compressive forces on the proximal medial metaphysis of the tibia and altered endochondral bone formation. It is unclear whether the deformity is caused by an intrinsic alteration of bone formation that is exacerbated by compressive forces or by compressive forces that cause a disruption in normal endochondral bone formation. Weight bearing must be necessary, since the disease does not occur in nonambulatory patients. Cook et al correlated epidemiologic and histologic findings in a model that provided evidence for the role of biomechanical overload in the pathogenesis of infantile tibia vara. They analyzed static single-limb stance in children and determined that 10 and 20 varus deformities, in children aged 2 years and 5 years, respectively, could generate compressive forces adequate to retard growth of the medial tibial physis. The combination of mechanical and biologic factors in tibia vara most likely impacts the disease to varying extents. Furthermore, excessive physiologic bowing often is found in individuals with the infantile form of the disease. It is known that epiphyseal compression inhibits physeal growth (the Heuter-Volkmann law) and distraction stimulates growth. Delpech demonstrated this stimulation by showing that release of abnormal pressure from a physis causes increased vertical growth. Such compressive forces cause a relative inhibition of growth of the medial portion of the proximal tibial physis, as compared with the lateral portion.

11

It is also known that damaged cartilage ossifies more slowly. Histologic sections of cartilage in the infantile form show damaged cartilage. If the cartilage on the medial aspect of the plateau is damaged, ossification is delayed on the medial side of the tibia compared with the lateral side. The result is a progressive varus angulation below the knee and an increase in the compressive forces on the physis, which changes the direction of the weightbearing forces on the upper tibial epiphysis from perpendicular to oblique. The obliquity of this force tends to displace the tibial epiphysis laterally. The trabecular pattern of the metaphyseal region in the tibia curves medially to align itself to the deviation of the stress. Many authors believe that disease progression is the result of this cycle of growth disturbance, varus deformity, and further growth disturbance. Distal femoral valgus or varus deformity and/or distal tibial varus or valgus deformities also can occur in conjunction with tibia vara. Whether these occur as compensatory mechanisms or are due to intrinsic factors of Blount disease is unknown. These deformities should be corrected at the same time the tibial vara deformity is corrected. Histologic specimens from the medial tibial condyle in the infantile form of the disease show changes principally in the zone of resting cartilage in the proximal tibial physis. These changes consist of (1) islands of densely packed cells that exhibit a greater degree of hypertrophy than would be expected from their topographical location, (2) islands of almost acellular fibrous cartilage, and (3) abnormal groups of capillary vessels. The pathogenesis of the adolescent form of the disease remains less clear than that of the infantile form. Some authors consider the 2 forms to have similar pathophysiology, while other authors consider them to be separate entities. Adolescent Blount disease does not appear to be as progressive or as common as the infantile form. Factors such as injury or infection of the physis have been suspected to play an etiologic role; however, most patients have no history of trauma or infection, leading many authors to discount them as the only possible causes. Once considered to be the result of a localized osteochondrosis of the medial portion of the upper tibial epiphysis, tibia vara is now thought to represent a localized form of epiphyseal dysplasia. The combination of diminished growth in the medial portion of the epiphyseal plate ( physis ) and continued normal growth in the lateral portion accounts for the progressive angulatory deformity12

of varus, that is, bow leg. After a number of years, the medial portion of the epiphyseal plate ( physis ) closes prematurely. 2.6 Clinical features The clinical presentation of the different types of tibia vara varies according to the age of onset. In infantile tibia vara, children generally start to walk early, usually when aged 9-10 months. At the onset of the disease, differentiating between early infantile Blount disease and marked physiologic bowlegs is difficult. Physiologic genu varum is a common torsional deformity that occurs secondary to normal in utero positioning. The tight posterior hip capsule causes an external rotation of the thigh at the hip. When combined with internal tibial torsion, the resulting appearance is a varus deformity. This physiologic deformity usually resolves spontaneously by the time the child is aged 2 years. In contrast to physiologic genu varum, infantile Blount disease can progress to severe deformity.

13

The infantile form is generally more prevalent in females, blacks, and those with marked obesity. It is associated with a prominent metaphyseal beak, internal tibial torsion, and leg-length discrepancy; involvement is bilateral in approximately 80% of cases. The metaphyseal prominence, or beak, may be palpable over the medial aspect of the proximal tibial condyle. Patients usually do not complain of pain. However, the deformity of the lower extremity can be quite pronounced. In contrast, patients with adolescent tibia vara usually complain of pain at the medial aspect of the knee. These patients are typically overweight or obese. In contrast to infantile tibia vara, involvement is unilateral in 80% of cases; the involved leg sometimes is shorter than the opposite leg by as much as 2-3 cm. The degree of varus deformity usually is not as severe as in individuals with the infantile form and usually does not exceed 20. In the early stages of tibia vara, there are no symptoms. Examination reveals a characteristic varus deformity of the knee, a deformity that is particularly striking when it is unilateral. Radiographically, there is defective ossification of the medial portion of

14

the upper tibial epiphysis, a beaked appearance of the underlaying metaphysic, and obvious retardation of longitudinal growth in the medial side of tibia. 2.7 Physical examination Visual analysis is the first step of the diagnostic, which is carried on by looking at the way the patient walks. The patients leg may indicate (varus deformity). The distance between both knees would then be measured. If the space between both knees exceed (1.25inches), further examination is required. 2.8 Imaging studies Plain Radiographs

The classic changes in the proximal part of the tibia in an established case of earlyonset blount disease include A sharp varus angulation of the metaphysis Widening and irregularity of the medial aspect of the growth plate Medial sloping and irregular ossification of the epiphysis Beaking of the medial part of the epiphysis

15

Radiographic indices used in the evaluation of lower-extremity bowing in infants and young children. The mechanical tibiofemoral angle (A) is the angle between a line drawn from the center of the hip to the center of the knee and a line drawn from the center of the knee to the center of the ankle. The tibial metaphyseal-diaphyseal angle (B) is the angle between a line drawn through the most distal aspects of the medial and lateral beaks of the proximal tibial metaphysis and a line perpendicular to a line drawn along the lateral aspect of the tibial diaphysis. The femoral metaphyseal-diaphyseal angle (C) is created by a line drawn perpendicular to the anatomic axis of the femur and a line drawn parallel to the distal femoral physis. The epiphyseal-metaphyseal angle (D) is created by a line drawn through the proximal tibial physis, parallel to the base of the epiphyseal ossification center, and a line connecting the midpoint of the base of the epiphyseal ossification center with the most distal point on the medial beak of the proximal tibial metaphysis. The percentage deformity of the tibia, % DT (E), is calculated as the degree of tibial varus (the medial angle between the mechanical axis of the tibia and a line drawn parallel to the distal femoral condyles) divided by the total amount of limb varus (femoral varus [FV] 1 tibial varus [TV]). Femoral varus is represented by the medial angle between the mechanical axis of the femur and a line parallel to the distal femoral condyles.

16

2.9 Management options Treatment is customized for each patient on the basis of a variety of factors, including the childs age, the magnitude ofthe deformity, the limb-length discrepancy, psychosocial factors, and the surgeons training and experience. On the basis of the results of the clinical examination and imaging studies, aIndications for operative treatment include increasing severity of symptoms or progression of deformity. list of current and anticipated deformities is created. Management options include observation with repeat clinical and radiographic examinations; use of long leg orthoses; and variou surgical options including relignment osteotomy, lateral hemiepiphyseodesis, and guided growth around the knee as well as gradual asymmetrical proximal tibial physeal distraction, resection of a physeal bar, and elevation of the medial tibial plateau. Treatment in the early stages of tibia vara in young children is aimed at preventing progression of the varus deformity. This can sometimes be accomplished by means of night splint of the type used for physiological bow legs. In older children, the varus deformity progresses despite splinting. It can be corrected only by osteotomy of the tibia, which may have to be repeated on one or more occasions during the remaining growth period.

Physiologic bowing is common in children who are less than 3 years old whereas Blount disease is reported to be less than 1% at this age. Corrective bracing is initiated for presumed early Blount disease only if the metaphyseal-diaphyseal angle is more than 16 degrees. If the angle is less than 9 degrees the patient is observed. Between 9

17

and 16 degrees, bracing is considered only if there is instability on walking. The patient is then evaluated on 4 month intervals.

Infantile Blounts = onset prior to 3y/o. Lanenskiold Classification(1-6). Metaphyseal diaphyseal angle (of Drennan) >13 degrees, Rx=KAFO stages I-IV, Stages V-VI(have metaphyseal bar) osteotomy over correcting to valgus. Xray=orthogram with patellas facing forward.--metaphyseal beaking.

Adolescent Blounts, usually overweight, black, RX=lateral hemiepiphysiodesis vs proximal tibial osteotomy Non operative Orthoses Several authors have reported encouraging results with the use of knee-ankle-foot orthoses with a medial upright and droplock hinges to unload the medial compartment of the knee in children younger than thirty-six months of age with early-stage (Langenskiold stage-I or II) Blount disease. The reported risk factors for failure of brace treatment include obesitywith aweight greater than the 90th percentile, varus thrust, an age older than three years at the initiation of the brace treatment, bilateral involvement, and Langenskiold stage-III or higher disease. However, the retrospective case series in which orthoses were used for patients with Blount diseas have included multiple variables, not included a control group, involved use of various designs of orthoses and various regimens, and provided limited details regarding the actual time that the brace was worn. Most of the time bowlegs or genu varum resolves on its own with time and growth. No specific treatment is needed unless the problem persists after age two. In the case of Blount's disease aggressive treatment is needed. Severe bowing before the age of three is braced with a hip-knee-ankle-foot orthosis (HKAFO) or knee-ankle-foot orthosis (KAFO). Bracing is used 23 hours a day. As the bone straightens out with bracing, the orthotic is changed every two months or so to correct the bowlegged position.

18

Operative treatment Surgical correction may be needed especially for the younger child with advanced stages of tibia varum or the older child who has not improved with orthotics. Surgery isn't usually done on children under the age of two because at this young age, it's still difficult to tell if the child has Blount's or just excessive tibial bowing. A tibial osteotomy is done before permanent damage occurs. Brace treatment for adolescent Blount's is not effective and requires surgery to correct the problem. In an osteotomy, a wedge-shaped piece of bone is removed from the medial side of the femur (thigh bone). It's then inserted into the tibia to replace the broken down inner edge of the bone. Hardware such as pins and screws may be used to hold everything in place. If the fixation is used inside the leg, it's called internal fixation osteotomy. External fixation osteotomy describes a special circular wire frame on the outside of the leg with pins to hold the device in place. Anatomy relevant For direct exposure for osteotomies on the medial aspect of the knee or pin fixations, surgeons must be aware of the location of the infrapatellar branch of the saphenous nerve. On the lateral side, it is the course of the peroneal nerve around the fibula that deserves attention. One must be aware that lengthening or shortening procedures can cause injury to the anterior tibial artery. Avoidance of injury to the neurovascular structures is paramount in obtaining a good result.19

Osteotomies in the epiphyseal or metaphyseal region of the proximal knee must necessarily avoid the epiphyseal plate in the growing child to prevent premature closure. It is important to remember that the epiphyseal plate is often "V" shaped, with the apex pointing inferiorly in the proximal tibia and superiorly in the tibia. Indications Operative treatment include increasing severity of symptoms or progression of deformity. In an osteotomy, a wedge-shaped piece of bone is removed from the medial side of the femur (thigh bone). It's then inserted into the tibia to replace the broken down inner edge of the bone. Hardware such as pins and screws may be used to hold everything in place. If the fixation is used inside the leg, it's called internal fixation osteotomy. External fixation osteotomy describes a special circular wire frame on the outside of the leg with pins to hold the device in place. Unfortunately, in some patients with adolescent Blount's disease, the bowed leg is shorter than the normal or unaffected side. A simple surgery to correct the angle of the deformity isn't always possible. In such cases an external fixation device is used to provide traction to lengthen the leg while gradually correcting the deformity. This operation is called a distraction osteogenesis. The frame gives the patient stability and allows for weight bearing right away.

20

Contraindications Surgical intervention is contraindicated in children who are younger than 2 years because it is difficult at this age to differentiate between Blount disease and excessive physiologic bowing that may resolve spontaneously. In patients with adolescent Blount disease, surgical intervention is recommended only when the patient complains of pain associated with the deformity. Rehabilitation Nonsurgical Rehabilitation A physical therapist will work with the family to teach them how to put on and take off the orthosis. Inspection and care of the skin is very important and will be included in the instruction. The child may need some help with gait training (learning how to walk properly). The therapist will help the child learn how to use any assistive devices (e.g., walker, crutches) that may be needed. Failure to correct the tibia vara deformity early often results in permanent damage to the growth plate and growing bone. Later, joint degeneration may occur.

21

After Surgery Osteotomy with internal fixation usually heals in six to eight weeks. The cast is removed five to six weeks after the operation if there's enough bone build-up to prevent change or loss of position. A second cast is applied that keeps the knee straight but the foot and ankle free to put weight through the leg. When the child has surgery with external fixators and distraction osteogenesis, gradual correction of the deformity takes place over the next three weeks. After the tibia is straightened, extra rods are used to stabilize the external frame. The frame is taken off about 12 weeks postoperatively. Parents or guardians should be advised that Blount's disease might not be cured with surgery. Results are usually good with infantile tibia vara. When treated at a young age and at an early stage, the problem usually doesn't come back. Older patients with advanced deformity have a much higher risk of recurrence of the deformity. Patients must be followed carefully throughout their growth and development. Unilateral bowing can result in that leg being shorter than the other leg. This is called a leg length discrepancy and may need additional treatment. 2.10. Complication The related complication for Blounts disease is pathological fracture, vascular disorder, wound infection and mal-allignment. 2.11 Prognosis During long-term follow up of blounts disease, Doyle et al found that the succesful rate of treatment depends on age and how severe is the deformity when being intervene. Fully known knowledge of blounts disease is important to the therapy itself. Prognosis on infantile blounts disease have to be diferrentiated with the adolescence. Infantile blounts disease will have a worst prognosis if being left untreated.

22

CHAPTER III CONCLUSION Blount disease is a developmental condition characterized by disordered endochondral ossification of the medial part of the proximal tibia physis resulting in multiplanar deformities of the lower limb. The cause of Blount disease remains controversial, but it is most likely secondary to a combination of hereditary and developmental factors. Biomechanical overload of the proximal tibial physis due to static varus alignment and excessive body weight have23

been implicated in the etiology of infantile tibia vara. The compressive forces at the medial aspect of the knee appear to cause growth suppression Visual observation is the first method of diagnosis. The family or doctor sees the problem when looking at the child or watching him or her walk. The distance between the knees is measured with the child standing with the feet together. If the space between the knees is more than five centimeters (1 1/4 inches) further testing is needed. Treatment depends on the age of the child and the stage of the disease. Between ages birth and two, careful observation or a trial of bracing (also called orthotics may be done. If the child doesn't receive treatment, Blount's disease will gradually get worse with more and more bowlegged deformity. Surgery may be needed to correct the problem. For the obese child, weight loss is helpful but often difficult

REFERENCES1. Salter, Robert B. Textbook of Disorders and Injuries of musculoskeletal system. Third

edition. Disorders of Epiphyses and Epiphyseal Growth, Blount Disease. Chapter 13.2. Solomon, louis. David j. Warwick. Apleys system of orthopaedics and fractures :

regional orthopaedics, the knee. Chapter 20, pge 449.3. A Patients Guide to Blounts Disease in Children and Adolescents. Anatomy.

Accessed at : http://www.concordortho.com on 12th May 201224

4. Kliegman R.M. et al. Nelson Text Book of Pediatrics. 18th ed. Blount disease. Saunders,

Elseviers. USA. 2007 ; 2788-27905. De Pablos J, Alfaro J, Barrios C. Treatment of adolescent Blount disease by asymmetric

physeal distraction. J Pediatr Orthop. Jan-Feb 1997;17(1):54-8.6. Bradway JK, Klassen RA, Peterson HA. Blount disease: a review of the English

literature. J Pediatr Orthop. Jul-Aug 1987;7(4):472-80. 7. Behrman, Richard E, et al. Ilmu Kesehatan Anak, edisi 15. Jakarta : EGC. 20008. Doyle BS, Volk AG, Smith CF. Infantile Blount disease: long-term follow-up of

surgically

treated

patients at skeletal maturity. J Pediatr Orthop. Jul-Aug

1996;16(4):469-76.9. Canale ST. Osteochondrosis or epiphysitis and other miscellaneous affections. In:

Canale ST, Beatty JH, eds. Campbell's Operative Orthopaedics. 11th ed. Philadelphia, Pa: Mosby Elsevier; 2007:chap 29. Accessed at : http://www.umm.edu/ency/article/001584.htm Reviewed last on 12 May 2012.10. Tachdjian MO, ed. The foot and leg: tibia vara. In: Pediatric Orthopedics. Vol 4.

Philadelphia:. WB Saunders Co;1990:2835-50.

25