In general, fractures in children heal in 4 to 6 weeks; in adolescents in 6 to 8 weeks; and in adults in 10 to 18 weeks. This process from fracture to full restoration of the bone will take weeks to months, depending on the type of fracture, location, vascular supply, health, and age of the individual. Nonunion or delayed union is more likely to occur in adults and occurs in up to 10% of all fractures (affecting nearly 500,000 people each year in the United States).409
Older adults who have suffered a hip fracture have the highest rate of nonunion complications (15% to 30%). These individuals are almost four times more likely to die in the first year after fracture compared with those without fracture. Delay until surgery after hip fracture increases mortality significantly.319 Older women (more than 65 years) who survive the first year after a hip fracture may be at increased risk of death up to 5 years after the injury.207,300
Many people are at high risk for premature death or loss of independence following fracture; mortality after fracture is higher among men than among women.41,46 Less than 50% of older adults with a hip fracture will regain their prior level of function.457 The inability to stand up, sit down, or walk 2 weeks after surgery is the strongest predictor for mortality among older adults with surgically repaired hip fractures.187,490
A person’s condition before fracture (especially that of older adults with hip fractures) has important prognostic implications. Older adults who fall within 6 months following a hip fracture are more likely to demonstrate poorer balance, slower gait speed, and greater decline in ADL from the prefracture level than those who do not fall.457
Healthy functional status contributes to faster recovery time with fewer complications and reduced medical expenses.88 Negative predictors for healing include medications such as calcium channel blockers and NSAIDs, renal or vascular insufficiency, smoking, alcoholism, and diabetes mellitus. Treatment can also affect healing via inadequate reduction, poor stabilization and fixation, distraction damage to blood supply, and postoperative infection.
Associated complications such as nerve injury can occur, and it can take up to 12 to 18 months before reinnervation of the motor endplate is complete. Return of function is dependent upon this factor. If there are no signs of improvement by 7 months, spontaneous recovery is unlikely.540 Exploratory surgery may be indicated at that time.
A number of clinical disorders of ossification centers (epiphyses) in growing children share the common denominator of avascular necrosis and its sequelae. These disorders are grouped together and referred to as the osteochondroses430 with multiple synonyms (epiphysitis, osteochondritis, aseptic necrosis, ischemic epiphyseal necrosis). There are additional eponyms based on the name of the person or persons who described the disorder as well, such as Kohler’s disease (tarsal-navicular bone disease), Osgood-Schlatter disease, and Legg-Calvé-Perthes disease.
The underlying etiologic factors and pathogenesis are similar in all these entities, and the clinical manifestations are determined by the stresses and strains present. Most susceptible areas are the epiphyses, which are entirely covered by articular cartilage and therefore poorly vascularized.
Osteochondritis dissecans (OCD) is a disorder of one or more ossification sites with localized subchondral necrosis followed by recalcification. This condition affects the subchondral bone and the layer of articular cartilage just above. A piece of articular cartilage and fragment of bone separate and pull away from the underlying bone. These fragments can become loose bodies in the joint; the most common site of involvement is the medial femoral condyle.
OCD is caused by repetitive microtrauma resulting in ischemia and disruption of the subchondral growth. The articular cartilage softens, and fragment separation leads to cartilage injury that can progress to form a crater. Activity-related pain, swelling, and giving way are common symptoms. Pain is increased with passive knee extension and tibial internal rotation and relieved with tibial external rotation (Wilson’s sign).
X-rays and MRI help confirm the diagnosis. Management varies with the person’s age and the severity of the lesion and includes nonoperative management (activity modification, protected weight bearing, immobilization for 4 to 6 weeks) and operative treatment. Quadriceps strengthening and gradual return to activities follow immobilization. If conservative care is unsuccessful in bringing about healing, then surgery may be needed (e.g., microfracture, implant tissue to stimulate cartilage and bone growth).
The term osteonecrosis refers to the death of bone and bone marrow cellular components as a result of loss of blood supply in the absence of infection. Avascular necrosis and aseptic necrosis are synonyms for this condition.
The femoral head is the most common site of this disorder (sometimes called Chandler’s disease), but other sites can include the scaphoid, talus, proximal humerus, tibial plateau, and small bones of the wrist and foot. Avascular necrosis is the underlying cause for 10% of total hip replacement surgeries362 and overall affects approximately 20,000 people annually, often between the second and fifth decades of life.270
Osteocytic necrosis results from tissue ischemia brought on by the impairment of blood-conducting vessels. A minimum of 2 hours of complete ischemia and anoxia is necessary for permanent loss of bone tissue.224 The bony ischemia may be secondary to trauma disrupting the arterial supply or to thrombosis disrupting the microcirculation.
Bones or portions of bones that have limited collateral circulation and few vascular foramina are susceptible to avascular necrosis. Box 27-24 lists conditions associated with osteonecrosis. A number of these conditions are linked to osteonecrosis by the development of fat emboli (caused by altered fat metabolism) in the vascular tree of the involved bone.
The conditions associated with the development of fat emboli include alcoholism, obesity, pregnancy, pancreatitis, medications (e.g., oral contraceptives, corticosteroids), and unrelated fractures. Many cases of femoral head osteonecrosis are idiopathic (i.e., no known cause or risk factor can be identified).
Osteonecrosis has also been recognized as a complication in HIV-positive individuals; in fact, individuals who are HIV positive have a 100-fold greater risk of developing osteonecrosis than the general population.356 The exact mechanism for this remains unknown. It may be due to hyperlipidemia secondary to the use of protease inhibitors; however, avascular necrosis was reported before the era of highly active antiretroviral therapy (HAART).416 It does not appear to be related to the degree of immunodeficiency.
More recently, the use of bisphosphonates has been linked with osteonecrosis of the jaw (sometimes referred to as “dead jaw syndrome”), especially after trauma to the teeth or bones of the jaw such as occurs with dental surgery (e.g., tooth extraction). The reason this happens is not entirely clear. Scientists hypothesize that since the jaw has a high rate of bone renewal in response to stress via generation of an inflammatory response by the gums and teeth, bisphosphonates keep osteoclasts from reabsorbing damaged bone cells in the jaw. The damaged bone builds up and eventually results in osteonecrosis.
This phenomenon is most likely to occur in individuals treated for bone cancer with intravenous bisphosphonates. The dosage of intravenous bisphosphonates can be as much as 12 times more than the oral bisphosphonate dosage prescribed for osteoporosis. Individuals with cancer treated this way also undergo other bone-weakening treatments (e.g., chemotherapy, radiation therapy).
Certain bones are more vulnerable to osteonecrosis than others. These bones are covered extensively by cartilage, have few vascular foramina, and have limited collateral circulation. The femoral head is a prime example of a bone at risk. The superolateral two thirds of the femoral head receives its blood supply almost entirely from the lateral epiphyseal branches of the medial femoral circumflex artery (Fig. 27-26).

Figure 27-26 Blood supply to the femoral head in a child. (From Bullough PG: Orthopaedic pathology, ed 3, London, 1997, Mosby-Wolfe, p 263.)
The only other source of blood for the femoral head is the medial epiphyseal artery (contained within the ligamentum teres), which has limited anastomoses with the lateral epiphyseal vessels. Hip dislocation or fracture of the neck of the femur can compromise the precarious vascular supply to the head of the femur. The talus, scaphoid, and proximal humerus are also susceptible to osteonecrosis.
As the ischemia progresses, repair processes occur but are not capable of preventing necrosis and deformation of the bone, such as flattening and collapse of the femoral head. The articular cartilage and acetabulum are usually spared until late in the disease process, but the articular cartilage may be lifted off the underlying bone, resulting in irreparable damage to the joint.201 The entire process extends over many years, and unlike in osteochondrosis of immature bone (e.g., Legg-Calvé-Perthes disease), spontaneous healing never occurs.
Often no symptoms are observed during the initial development of osteonecrosis even though an ischemic condition of the bone exists.201 Hip pain is the usual initial presenting complaint, with a gradual onset, sometimes of many weeks’ duration, before diagnosis. The pain may be mild and intermittent initially but will progress to become severe, especially during weight-bearing activities.
If the femur is involved, the pain may be noted in the groin, thigh, or medial knee area. An antalgic gait is noted, and pain provocation occurs with weight-bearing activities and hip range-of-motion exercises, especially internal rotation and flexion and adduction. The affected individual will report a slowly progressive stiffening of the joint. When fracture occurs, it is usually at the junction between necrotic bone and reparative bone, possibly extending down through the reparative interface to the healthy inferior cortex of the femoral neck.340
Eventually degenerative joint changes and osteoarthrosis occur at the involved hip joint; the pathologic process is often relentless, with collapse of the femoral head imminent in spite of medical intervention.201
Osteonecrosis of the jaw is characterized by exposed bone in the mouth, numbness or heaviness in the jaw, pain, swelling, infection, and loose teeth. Delayed or poor wound healing after dental surgery may be the first indication of a problem. Crepitus as the jaw opens and closes may be present and is often described as like the sound of someone walking on ice.
Plain films may be normal initially. Bone scan, MRI, and CT scans are much more sensitive procedures and detect subtle bony changes.
The choice between conservative and surgical intervention depends on the size of the lesion, how early the diagnosis is made, and whether bony collapse has occurred. If surgery is not indicated, protected weight bearing is essential to prevent collapse of the lesion.
Surgical intervention may consist of core decompression for small lesions without evidence of structural collapse (most common procedure in early diagnosis) to relieve pain and delay or prevent structural collapse, hemiarthroplasty, or total joint replacement.292 Core decompression removes a core of bone from the femoral head and neck in an attempt to relieve intermedullary pressure, thereby promoting revascularization. This may be accompanied by bone grafting.475
Joint replacement may be required if femoral head collapse occurs or in order to prevent this complication. However, this procedure is limited by young age and high activity level as well as the limited life expectancy of the prosthesis.
New techniques for bone stimulation may be used, such as replacing the dead bone with living bone from the individual’s fibula to give added strength to the damaged area and possibly prevent or postpone joint arthroplasty in young individuals; see also the section on Fracture: Treatment in this chapter.
An osteotomy may be performed to shift the site to where maximal weight bearing occurs on a particular joint surface. Analgesics and NSAIDs are used for symptomatic relief of pain.
The prognosis depends on the extent of damage that has occurred before diagnosis in the case of nontraumatic disease. Unfortunately, many cases are diagnosed in an advanced stage of disease, when minimally invasive surgical procedures are no longer helpful.270 Early intervention (both surgical and nonsurgical) has definitely improved the outcome, but many people with femoral head osteonecrosis experience irreversible damage to the joint and will need total arthroplasty.
Legg-Calvé-Perthes disease, also known as coxa plana (flat hip) and osteochondritis deformans juvenilis, is epiphyseal aseptic necrosis (or avascular necrosis) of the proximal end of the femur. It is a self-limiting disorder characterized by avascular necrosis of the capital femoral epiphysis (the center of ossification of the femoral head). Complete revascularization of the avascular epiphysis occurs over a period of time without any treatment.
This condition occurs in approximately 1 in 1200 children, primarily boys (5: 1 ratio of boys to girls) between the ages of 3 and 12 years, making it the most common of the osteochondroses. Legg-Calvé-Perthes disease occurs 10 times more often in whites than in blacks.
Deformation of the epiphysis with changes in the shape of the femoral head and the acetabulum occur during the process of revascularization in a significant portion of affected individuals. This may lead to degenerative arthritis in young adult life.232 Changes in the shape of the acetabulum can be classified as type I (normal, concave acetabular margin), type II (flat, horizontal lateral acetabular margin), or type III (convex, sloping acetabular margin).161
The direct cause is a reduction in blood flow to the joint, though what causes this is unknown. It may be that the artery of the ligamentum teres femoris closes too early, not allowing time for the circumflex femoral artery to take over. Genetic coagulopathy has been suggested,476 possibly triggered by exposure to cigarette smoke in utero and during childhood.149
Delay in bone age relative to the child’s chronologic age suggests a possible general disorder of skeletal growth with focal expression in the hip. Mechanisms proposed to explain the delay in bone maturation include genetic, endocrine, nutritional, and socioeconomic factors.274
The disease process consists of four stages lasting from 2 to 5 years (Table 27-3 and Fig. 27-27). Because the growth plate of the femoral head lies above the insertion of the capsule of the hip joint in children and because the epiphyseal plate acts as a firm barrier to blood flow between the metaphysis and epiphysis, the femoral head depends on vessels that track along the surface of the neck of the femur to enter the epiphysis above the growth plate.

Figure 27-27 Radiograph of lower pelvis in Legg-Calvé-Perthes disease after revascularization of the necrotic femoral head shows enlargement of the head, with the original necrotic ossification center seen as a “head within a head.” (From Bullough PG: Orthopaedic pathology, ed 3, London, 1997, Mosby-Wolfe, p 263.)
Injection studies have demonstrated that the most important vessels supplying the epiphysis are the lateral epiphyseal vessels. These vessels are vulnerable to interruption of blood flow by trauma or by increased intraarticular pressure. It is possible that in Legg-Calvé-Perthes disease the ischemic events are episodic in nature and result from increased intraarticular pressure.60
Delays in bone maturation observed with this disease are correlated with the stage of the disease. The decrease in bone age delay in the later stages of the disease indicates that as the disease progresses, bone maturation accelerates and tries to catch up with the chronologic age. This phenomenon is referred to as bone maturation acceleration. This process occurs earlier in the epiphyses of the lower ends of the radius and ulna and short bones of the hands compared to the carpal bones.274
The Legg-Calvé-Perthes condition is characterized by insidious onset, initially presenting as the intermittent appearance of a limp on the involved side with hip pain described as soreness or aching with accompanying stiffness. The pain may be present in the groin and along the entire length of the thigh following the path of the obturator nerve or referred pain just in the area of the knee. There is usually pinpoint tenderness over the hip capsule.
Painful symptoms are aggravated by activity and fatigue and relieved somewhat by rest. Mild Legg-Calvé-Perthes disease is characterized by partial femoral head collapse, retention of a full range of hip abduction and rotation, and lack of subluxation on radiographic examination.
Delay in bone maturation is a common feature of this condition. Skeletal development is unevenly timed in the growing bones, with the maximum delay occurring in the distal limb segments. As the condition progresses, there are decreases in active and passive range of motion, as well as limited physiologic (accessory) motion affecting walking and running.
Severe Legg-Calvé-Perthes disease begins later and involves collapse of the whole femoral head, stiffness, and subluxation. Atrophy of the thigh musculature and restriction of hip abduction and rotation may develop. Short stature may develop as a result of epiphyseal dysplasia, and in those individuals who are left untreated, a flat femoral head will develop that is prone to degenerative joint disease.413
Late complications in adults with a childhood history of Legg-Calvé-Perthes include early OA of the hip and acetabular labral tears. Hip, groin, or back pain may be the first symptom in affected adults. Postural asymmetry, leg length discrepancy, decreased range of motion, and decreased strength may be accompanied by an abnormal gait pattern.37
Physical examination, clinical history, and radiographic examination (Fig. 27-28) confirm the diagnosis. MRI is widely accepted as the imaging method of choice, allowing early diagnosis and providing staging information necessary for adequate management.

Figure 27-28 Legg-Calvé-Perthes disease. A, Anterior view of the pelvis demonstrates fragmentation and sclerosis of the right femoral epiphysis (arrow) in a 6-year-old male. B, Follow-up film obtained 8 years later shows continuing deformity resulting from osteonecrosis. C, The child developed significant degenerative arthritis by age 12. (From Mettler FA: Primary care radiology, Philadelphia, 2000, Saunders.)
There are several different classifications used to determine severity of disease and prognosis. The Catterall classification specifies four different groups defined by radiographic appearance during the period of greatest bone loss.
The Salter-Thomson classification simplifies the Catterall classification by reducing it down to two groups: group A (Catterall I, II), in which less than 50% of the ball is involved, and group B (Catterall III, IV), in which more than 50% of the ball is involved. Both classifications share the view that if less than 50% of the ball is involved, the prognosis is good, while more than 50% involvement indicates a potentially poor prognosis.
The Herring classification studies the integrity of the lateral pillar of the ball. In lateral pillar group A, there is no loss of height in the lateral one third of the head and little density change. In lateral pillar group B there is a lucency and loss of height of less than 50% of the lateral height. Sometimes the ball is beginning to extrude the socket. In lateral pillar group C there is more than 50% loss of lateral height.410a
Many doctors utilize these classifications as they provide an accurate method of determining prognosis and help in determining the appropriate form of treatment.
The goal of treatment is to limit deformity and preserve the integrity of the femoral head. Mild disease may not require intervention, but careful follow-up with radiographic examination every 3 months is needed to observe for deterioration and progression of the disease.327
Current methods of treatment attempt to prevent deformation of the femoral head and restore the spherical and congruent femoral head contour of the acetabulum. This is done by ensuring that the vulnerable anterolateral part of the avascular capital femoral epiphysis is contained within the acetabulum, a process called containment. The femoral head can be molded to a normal shape as it heals. The idea is to accomplish this while the bone is biologically plastic and before it is irreparably deformed.232
The closer to normal the femoral head is when growth stops, the better the hip will function in later life. The way that surgeons achieve this goal is through containment. In the past, weight bearing was minimized, but more recently, therapy allows the child to continue weight bearing with the femur in an abducted and internally rotated position. Keeping the head of the femur well seated in the acetabulum decreases focal areas of increased load and minimizes distortion, thereby maintaining range of motion and preventing deformity.
The femoral head must be held in the joint socket (acetabulum) as much as possible. It is better if the hip is allowed to move and is not held completely still in the joint socket. Joint motion is necessary for nutrition of the cartilage and for healthy growth of the joint. All treatment options for Legg-Calvé-Perthes disease try to position and hold the hip in the acetabulum as much as possible. This healing process can take several years.
Conservative care is usually continued for 2 to 4 years. A variety of splints, braces, and positional devices may be used to maintain the proper position. When lack of motion has become a problem, the child may be admitted to the hospital and placed in traction. Traction is used to quiet the inflammation. Antiinflammatory medications may be prescribed. Physical therapy is used to restore the hip motion as the inflammation comes under control. This process usually takes about a week. Home traction may also be an option.
In some cases, surgery will be required to obtain adequate containment. Sometimes, adequate motion cannot be regained with traction and physical therapy alone. If the condition is longstanding, the muscles may have contracted or shrunk and cannot be stretched back out.
To help restore motion, the surgeon may recommend a tenotomy of the contracted muscles. When a tenotomy is performed, the tendon of the muscle that is overly tight is cut and lengthened. This is a simple procedure that requires only a small incision. The tendon eventually scars down in the lengthened position, and no functional loss is noticeable.
Surgical treatment for containment may be best in older children who are not compliant with brace treatment or where the psychologic effects of wearing braces may outweigh the benefits. Surgical containment does not require long-term use of braces or casts. Once the procedure has been performed and the bones have healed, the child can pursue normal activities as tolerated.
Surgical treatment for containment usually consists of procedures that realign either the femur (thighbone), the acetabulum (hip socket), or both. Realignment of the femur is called a femoral osteotomy. This procedure changes the angle of the femoral neck so that the femoral head points more toward the socket.
To perform this procedure, an incision is made in the side of the thigh. The bone of the femur is cut and realigned in a new position. A large metal plate and screws are then inserted to hold the bones in the new position until the bone has healed. The plate and screws may need to be removed once the bone has healed.
Realignment of the acetabulum is called a pelvic osteotomy. This procedure changes the angle of the acetabulum (socket) so that it covers or contains more of the femoral head. To perform this procedure, an incision is made in the side of the buttock. The bone of the pelvis is cut and realigned in a new position. Large metal pins or screws are then inserted to hold the bones in the new position until the bone has healed. The pins usually must be removed once the bone has healed.
If there is a serious structural change in the anatomy of the hip, there may need to be further surgery to restore the alignment closer to normal. This is usually not considered until growth stops. As a child grows, there will be some remodeling that occurs in the hip joint. This may improve the situation such that further surgery is unnecessary.
In severe cases, both femoral osteotomy and pelvic osteotomy may be combined to obtain even more containment.
Legg-Calvé-Perthes disease may vary in severity from a mild self-healing problem with no sequelae to a condition that will destroy the hip unless serious action is taken. Early on, it may be difficult to determine which course the disease will follow.
Even though the disease is self-limiting, the prognosis varies according to the age of onset (better prognosis in children whose onset is before age 5 years). Children over the age of 8 years at the time of onset have a better outcome with surgical treatment than with nonoperative care.191 There is some evidence to suggest that early delay in bone age (stage I of the disease) is linked with more severe disease.274
Older age, complete involvement of the femoral head, and noncompliance with treatment contribute to a poorer prognosis. Although girls are less likely to develop Legg-Calvé-Perthes disease compared to boys, they often have a poorer prognosis. The reason for this difference is unknown.
A delay in bone age maturation of more than 2 years in stage I of the disease has been linked with greater severity of the disease. However, children with Legg-Calvé-Perthes disease have a normal onset of puberty, and by the time they are 12 to 15 years old, their stature and bone age are the same as those of their peers.262
Osgood-Schlatter disease (osteochondrosis) results from fibers of the patellar tendon pulling small bits of immature bone from the tibial tuberosity. In the past, Osgood-Schlatter was considered a form of osteochondritis (inflammation of bone and cartilage), but more recent thinking suggests that the process is one part of the spectrum of mechanical problems related to the extensor mechanism. Rather than being an actual degenerative “disease,” Osgood-Schlatter is considered a form of tendinitis of the patellar tendon.
It is most commonly seen in active adolescent boys ages 10 to 15 years but can also affect girls ages 8 to 13 years. The ratio of boys to girls affected by OsgoodSchlatter disease is 3: 1.
Osgood-Schlatter disease is probably the result of indirect trauma (force produced by the sudden, powerful contraction of the quadriceps muscle during an activity) or repetitive stress (repeated knee flexion against a tight quadriceps muscle) before complete fusion of the epiphysis to the main bone has occurred. It is further aggravated by the longitudinal traction associated with bone growth in adolescents and the presence of external tibial torsion. Other causes include local deficient blood supply and genetic factors.
Another possible cause of Osgood-Schlatter lesions is abnormal alignment in the legs. Children who are knock-kneed or flat-footed seem to be most prone to the condition. These postures put a sharper angle between the quadriceps muscle and the patellar tendon. This angle is called the Q angle. A large Q angle puts more tension on the bone growth plate of the tibial tuberosity, increasing the chances for an Osgood-Schlatter lesion to develop. A high-riding patella, called patella alta, is also thought to contribute to development of Osgood-Schlatter lesions.326
In young athletes, the tendon is attached to prebone, which is weaker than normal adult bone. With excessive stresses on the tendon from running and jumping, the structure becomes irritated and a tendinitis begins. Often fragments representing cartilage or bone formations are found on the surface of the patellar tendon and are a potential cause of pain. These patellar tendon fibers can actually pull fragments away from the tibial epiphysis (Fig. 27-29).

Figure 27-29 Clinical radiograph of the knee in a 12-year-old child shows fragmentation and avulsion of the tibial tubercle. Swelling below the knee and an enlarged tibial tuberosity may be observed clinically. This condition, known as Osgood-Schlatter disease, is probably posttraumatic. (From Bullough PG: Orthopaedic pathology, ed 3, London, 1997, Mosby-Wolfe, p 98.)
Clinically, clients report constant aching and pain at the site of the tibial tubercle (just below the kneecap), which is often enlarged on visual examination. Symptoms are aggravated by any activity that causes forceful contraction of the patellar tendon against the tubercle, such as active knee extension or resisted knee flexion (e.g., going up or down stairs, running, jumping, biking, hiking, kneeling, squatting).
Besides the obvious soft tissue swelling, there may be localized heat and tenderness, the latter elicited with direct pressure over the tibial tubercle. Many children with this condition also have significant tightness in the hamstrings, iliotibial band, triceps surae (bellies of the gastrocnemius and soleus), and quadriceps muscles. Tightness in these areas can potentially increase the flexion moment and subsequent stresses at the tibial tubercle.
On physical examination, the examiner forces the tibia into internal rotation while slowly extending the child’s knee from 90 degrees of flexion; at about 30 degrees of knee flexion pain is reproduced that can be relieved by externally rotating the tibia.
Clinical diagnosis may be confirmed by radiograph (or ultrasonography to avoid exposure to x-ray), since many conditions are very similar (e.g., patellar tendinitis, chondromalacia patella, synovial plica). Although the films may be normal, epiphyseal separation, soft tissue swelling, and bone fragmentation can be visualized in many cases.
Immobilization is no longer advocated with this condition, although rest from aggravating activities and/or activity modification is recommended until symptoms have subsided. This time frame ranges anywhere from 2 to 3 weeks in some individuals to 2 to 3 months or more in others. Enough time must be allowed for revascularization, healing, and ossification of the tibial tubercle before resumption of unrestricted athletic participation. NSAIDs and ice are used regularly.
Treatment should include exercises to address the mechanical inefficiencies of the extensor mechanism, stretching for any areas of inflexibility, and strengthening areas of weakness (e.g., ankle dorsiflexion, pain-free quadriceps strengthening).
Balance and coordination should be assessed and rehabilitation provided as appropriate. Support may be provided through the use of a knee sleeve, brace, or narrow strap around the leg placing pressure over the tibial tubercle. This latter device is used to reduce the pulling stresses of the patellar tendon on the tubercle and subsequently reduce pain.
About 90% of children with this condition respond well to nonoperative treatment. Complete recovery is expected with closure of the tibial growth plate.147 Conservative measures are usually sufficient to provide pain relief and resolution of local swelling. Some individuals experience mild discomfort in kneeling; activity restriction is imposed until the individual is symptom free.
When conservative care fails to resolve painful symptoms, full-extension immobilization of the leg through reinforced elastic knee support, cast, or splint may be prescribed for 6 to 8 weeks. In chronic, unresolved cases, surgery may be necessary to remove the epiphyseal ossicle that forms in the tendon. In extreme cases, the epiphysis may actually be removed or holes drilled into the tibial tubercle to facilitate revascularization of the area.
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