Oxford Handbook of Clinical Surgery (4 edn)
Annotate
Cite
Developmental dysplasia of the hip (DDH) 458
Slipped upper femoral epiphysis (SUFE) 460
The limping child 462
The child with a fracture 464
Non-accidental injury (NAI) 466
Legg–Calvé–Perthes disease 468
Motor development 470
Club foot or congenital talipes equinovarus (CTEV) 471
Flat feet (pes planus) 472
The osteochondritides 474
Developmental dysplasia of the hip (DDH)
DDH covers a spectrum of abnormalities from a mildly underdeveloped stable hip to well-established dislocation and/or acetabular dysplasia in the older child. The incidence is 1–2 per 1000 newborns in the UK. It is bilateral in 20%. It was previously called congenital dysplasia of the hip (CDH), but as it may also be acquired after birth, the term was changed. Early detection is important.
Risk factors
Family history. First-degree relative.
Breech presentation at or after 36 weeks of gestation.
Foot abnormalities. Congenital talipes calcaneovalgus and metatarsus adductus.
Oligohydramnios.
Children with syndromes.
Torticollis.
Clinical features
Barlow test (dislocatable hip). It tests if a hip is unstable. Take the baby's leg between your thumb and index finger and place your other fingers onto the buttock. Flex and adduct the hip. Posterior-directed force is applied in line with the shaft of the femur. In case of instability, the femoral head then subluxes or dislocates which you can palpate in the buttock.
Ortolani Sign (dislocated hip). Now abduct the leg. If the hip is dislocated and reducible, you will feel the femoral head moving into the joint. This often does not produce a palpable clunk.
Irreducible hip.
Shortened leg.
Limited hip abduction.
Asymmetry of skin creases can be present; many children with normal hips have asymmetry of thigh and buttock skin creases.
Abnormal findings can prove easy to miss if the dislocations are bilateral.
Screening
All children with risk factors and an abnormal neonatal clinical hip examination have a hip ultrasound. The majority of hips are fully developed at full term plus 6 weeks. Therefore, the ultrasounds of those children with risk factors, but normal clinical findings, are done at that point. Those children with obvious clinical abnormalities on hip examination have the ultrasound done earlier.
Paton RW et al. reported in 2009 that there is no association between postural and fixed talipes equinovarus and DDH.1 Since it can be difficult for non-paediatric orthopaedic surgeons to differentiate the different foot abnormalities, it is continued to scan the hips of children with club feet. Evidence shows that there is no advantage of universal baby hip screening over selective at risk screening.
Radiology
Ultrasound is the investigation of choice. Baby hip ultrasound was pioneered by Dr Graf from Austria. It is more accurate than radiographs. It visualizes the cartilage and allows dynamic testing of the hip joint. A Graf alpha angle of ≥60° is classed as normal.
Radiographs are taken in children who present late, usually after the age of 6 months.
Treatment
0–6 months of age. A Pavlik harness is applied. This is a soft harness which flexes the hips and knees and directs the legs away from the body midline, thereby directing the femoral heads towards the hip joints. It allows limited hip movements. It is used until the hips normalize, which can take several months; it works 90% of times.
6–18 months. If the harness is unsuccessful or if a child is older than 6 months, they need a closed or open reduction of the hip joint and hip spica cast immobilization. Some children need a hip adductor tendon release in the groin and occasionally, a femoral osteotomy. A removable hip abduction brace is used after spica removal.
≥18 months. These children usually need an open reduction of the hip joint, a hip adductor release, and a femoral ± pelvic osteotomy and hip spica immobilization. A hip abduction brace is normally not necessary after hip spica removal because of the improved bone alignment.
Reference
Slipped upper femoral epiphysis (SUFE)
This is reported to have an incidence of 4–7 per 100 000 population. It is caused by the displacement of the femoral epiphysis (growth plate) in relation to the femoral neck. It is the commonest cause of a limp in a boy aged 12–14 or girl aged 11–13 (growth spurt at puberty). In this age group, it must be actively excluded in a limping child.
Risk factors
Obesity. Classic is the limping, obese, 13y-old boy with knee pain.
Rapid growth.
Hormone disturbances. Hypothyroidism, renal rickets, pituitary deficiency, growth hormone deficiency, and treatment with it).
Male—♂:♀, 3:1.
Side affected. Left > right.
Classification
This is usually classified by the ability to weight bear on presentation.
‘Unstable’ slips cannot walk due to pain and present like a fracture.
Diagnosis is easy.
‘Stable’ slips can weight bear, though usually with a limp.
Presentation is usually late, i.e. after 2–3 weeks of limping.
Fifty per cent will have no pain; pain is commonly referred to the knee.
Any child with knee pain must have there hip examined.
A summary of presentation and prognosis can be seen below.
Clinical features
There will be an obvious limp, usually in an overweight child, commonly male.
The affected limb will be shorter and lies in external rotation.
Abduction is limited; when the hip is flexed, it will rotate externally—this sign is almost diagnostic of the condition.
Radiology
Anteroposterior and lateral views of BOTH hips should be insisted on. The slip is often easier to see on the lateral view. The slip is in an inferior and posterior direction (down and backwards). Widening of the physis may be a sign of impending slip (i.e. ‘pre-slip’).
Klein's line giving Trethowan's sign. If you draw a line on the superior aspect of the femoral neck (called), it should cut through the femoral head; if it does not, it is diagnostic of a SUFE (see Fig. 13.1).
Normal (left) and Abnormal, i.e. SUFE (right) Klein's lines.
Management
The acute slip (i.e. <3 weeks history) can be managed by gentle manipulation and cannulated screw fixation in the reduced position. This is controversial, however, as any manipulation may damage the already damaged epiphysis and possibly cause avascular necrosis.
Standard treatment is stopping the slip from worsening and the slip is usually pinned in situ (where it is with no manipulation) with one cannulated screw percutaneously.
Deformed epiphysis can remodel by up to 60°. Residual deformity can be corrected via an osteotomy once the epiphysis has fused if there is a functional deficit.
The condition can be bilateral in some cases. This is much more likely if there is an underlying endocrine disorder. Some surgeons advocate prophylactic pinning of the unaffected side, but this is controversial.
Complications
Avascular necrosis of femoral head.
Chondrolysis. Rapid progressive loss of cartilage; joint space narrowing is seen on X-ray.
Subtrochanteric fracture. If pins entry point placed too low.
Late osteoarthritis. Estimated 10%.
Further reading
The limping child
The limping child is the acute abdomen of children's orthopaedics. It can be caused by many things, ranging from a stone in the shoe to leukaemia.
History
The most important initial question is, ‘Has the child always limped?’ If so, the most common causes are:
DDH (see 
p. 458).
Cerebral palsy.
Limb length discrepancy from congenital disorders.
Muscular dystrophy.
If there has been a normal gait and then the child starts to limp, then the possibilities are highly varied. The main points to glean are:
How long, what side, and what causes it? Is it constant or intermittent?
Are there any associated complaints?
Is there a history of trauma?
How is the child's general health?
What is the child's past medical and birth history?
Remember, what causes an older child to limp will cause a younger child to refuse to weight bear. This will be perceived as more serious by the parents and therefore, these patients will present much earlier.
Examination
Look at the child walking. Decide on whether there is a limp! This is often a symptom used by parents (and grandparents) to make sure that you take their complaint seriously and a limp may not be the problem at all.
What type of limp is it?
Short leg. Limb length discrepancy.
Antalgic. Less time on affected than unaffected limb due to pain.
Trendelenberg. Pelvis dips and trunk sways on affected side due to weak hip abductors.
Bizarre. Usually psychological, e.g. completely stiff leg.
Tailor examination to history. Inspect limbs from hips to toes. Skin discoloration may indicative of infection. Try to use distraction techniques to get the true picture.
Tenderness? Bony tenderness with swelling and bruising is a clinical fracture. Infected areas will be painful and usually red, hot, or swollen.
Joints. Concentrate joint examination as appropriate, but always examine hips if knee pain present. Put all joints through full passive range of motion.
Limb lengths? Assess individual leg lengths with patient lying on the couch with legs straight. Look for level of heels and malleoli. If one leg is short, assess if discrepancy is within femur or tibia by flexing both hips and knees together. Look at the legs from the side to see if the front of the lower legs is at different levels (if yes—femoral shortening) and/or if the front of the thighs are at different levels (if yes—lower leg shortening).
Lymphadenopathy? From generalized infection, local infection, or blood disorder.
Full systemic examination must also be performed.
Remember common things are common! The age of the patient is a very useful screen (see Table 13.1).
| Young (0–5y) | Child (5–10y) | Adolescent (10–15y) | All ages |
|---|---|---|---|
DDH | Perthes’ disease | SUFE | Septic arthritis |
Septic hip | Irritable hip | AVN of femoral head | Cellulitis |
Limb length discrepancy | Juvenile rheumatoid arthritis | Overuse syndromes | Stress fracture |
Occult fracture | Non-accidental injury (NAI) | ||
Neoplasia | |||
Neuromuscular disease |
| Young (0–5y) | Child (5–10y) | Adolescent (10–15y) | All ages |
|---|---|---|---|
DDH | Perthes’ disease | SUFE | Septic arthritis |
Septic hip | Irritable hip | AVN of femoral head | Cellulitis |
Limb length discrepancy | Juvenile rheumatoid arthritis | Overuse syndromes | Stress fracture |
Occult fracture | Non-accidental injury (NAI) | ||
Neoplasia | |||
Neuromuscular disease |
Investigations
X-ray. Always X-ray hips if no localizing signs. If one limb appears to be involved, especially in the younger patient, then X-ray the whole limb. Otherwise, X-ray bones/joints as appropriate from the clinical examination.
Blood tests. FBC, U&E, G, LFTs, CRP, ESR useful as full general screen.
Management
Dependent on diagnosis reached.
Further reading
http://www.aafp.org/afp/2009/0201/p215.htmlThe child with a fracture
Accidents are part of normal life! Some, usually the more severe, result in a fracture. In a city of 1 million inhabitants, there would be around 3000 children's fractures annually.
Most childhood fractures are minor, almost half affecting the forearm. They are weather-dependent, increasing in good weather when climbing (and falling) is common.
Clinical features
A clear history of trauma and a complaint of pain are present in all, but a small number of patients. In a young child, however, the pain may not be localized and instead of crying, they may present with pseudoparalysis of a limb, limp, or refusal to weight bear.
Look for external signs of injury. Bruising, due to a thick subcuticular fat layer is not a constant feature. Palpate for tenderness unless there is a clear deformity. Remember to examine the normal limb first and when examining the affected side, start away from the injury. This will gain the child's confidence. If you’re going to do something that hurts them, tell them rather than saying, ‘This won't hurt’. If you lie to them, you will lose their trust and make examination impossible.
Neurovascular status. Check the distal capillary refill and pulses as well as distal neurology in the form of power and sensation. Document all findings. It is good practice and also helps if there are any medicolegal issues about treatment.
Investigation. Though a fracture is a clinical diagnosis, this can sometimes be difficult in the child. A low threshold for X-rays should always be adopted. The joint above and below any injury must be visualized with two perpendicular views being standard practice.
Analgesia. Always splint an obvious fracture and give analgesia before X-rays. If a limb is clearly deformed (hence fractured), then a plaster should be applied before the X-ray. Radiographs of deformed limbs out of splintage are unacceptable. This is also the case for adults!
Unnecessary X-rays. Try to avoid ‘comparison’ views of the normal side if you are unsure about radiological features. With growing bones, ossification centres and epiphysis interpretation can be difficult. If you are unsure about a feature, show the X-ray to a senior.
Fractures. The classical fracture in a child is the greenstick injury. This is when there is a fracture of one cortex and a plastic deformation (i.e. a bend, not break) of the other at the same level. Even complete fractures tend to displace far less in children as the periosteum in children is highly structural, thick, and strong. It will hold the fracture in rough approximation. In adults, the periosteum is a very weak component of bone, hence the wider displacement.
Management
Fractures usually unite. If there is a minor greenstick fracture with little symptoms and no risk of displacement, then there is no need to apply a plaster cast. However, this is not normally acceptable to parents once they know their child has a broken limb.
In undisplaced, stable, greenstick fractures of the forearm, a fibreglass removable cast can be placed and the parents simply remove this in 4 weeks time with no need to be followed up in a clinic.
Normally the joint above and below the fracture needs to be immobilized. Often this is safer in children to ‘slow them down’ anyway. The fracture should be monitored in the fracture clinic. If a plaster is placed, then clear plaster instructions, in the form of a printed sheet, should be given to the parents. An example is shown Box 13.1
If the fracture is displaced or angulated, then it may require manipulation or, less commonly, open reduction and fixation under GA.
Angulation, if close to the joint and in the plane of motion of the joint, is very well tolerated. Remodelling of the bone will occur; a 15° angulation in a child <6y old and 10° angulation in a child 6–10y old is acceptable orthopaedically, though is often not accepted by the parents! Rotational displacement will not remodel and needs correction.
Return to the Accident and Emergency Department or Plaster room if your child complains of any of the following:
Numbness or pins and needles in the affected limb.
Restricted movement or tight swelling of the fingers or toes.
If the fingers or toes go white or blue.
If there is local itching, pain, or burning in the plaster.
A string foul smell is coming from the plaster.
The plaster becomes soft or loose.
Also, if the plaster is rubbing or digging in, this will irritate the skin and cause blistering.
Do NOT place anything down the plaster if it is itching. This will cause skin damage or blisters and may cause an infection.
Do NOT get the plaster wet.
Non-accidental injury (NAI)
Definition
Physical violence towards a baby or child. It is one part of child abuse which may occur in isolation or in combination with other forms of child abuse, including neglect, emotional abuse and/or sexual abuse. It denotes an injury that cannot be explained by an accident and where responsible adults do not have a viable explanation of how the injury occurred.
Incidence
The National Society for the Prevention of Cruelty to Children (NSPCC) reported in 2011 that 46 700 children were at risk of abuse in the UK.
It is estimated that 4 million children a year are abused in some manner in the USA.
It happens in all socio-economic classes, but is more common in the deprived. Twins, preterm babies, and special needs children are also at increased risk.
The majority of NAI fractures occur under 2y of age (80% of children with NAI fractures are under 18 months of age). The majority of accidental injuries occur in children over 5y of age (85%).
Suspicious features
Inexplicable delay from time of injury to medical advice being sought.
No convincing explanation of mechanism of injury.
Patterns of soft tissue injury, e.g. bruising in the shape of fingers or objects (belt, buckles) or in unusual areas (back, away from bony prominences), bites, and burns.
Unusual fractures or fracture patterns, e.g. rib fractures, non-linear skull fractures, transverse fractures of long bones, scapula, lateral clavicle, and vertebral fractures.
Fractures of differing ages on a radiograph.
No fracture in isolation is pathognomonic of NAI.
Rib, humeral, femoral, and skull fractures have the highest probability for abuse. Rib fractures are present in 5–27% of children who are abused. Diaphyseal fractures are four times more common than metaphyseal fractures in NAI.
Metaphyseal corner and bucket handle fractures. They are only present in a minority of children who present with NAI (the reported rates vary widely, 11–50%). Many references refer to them as pathognomonic or specific for NAI. However, a similar appearance can occur with other conditions (e.g. severe osteogenesis imperfecta, rickets, scurvy).
Corner fracture. A small piece of bone is avulsed due to shearing forces on the growth plate.
Bucket handle fracture (same as corner fracture). The fragment is larger and seen face on as a disc or bucket handle.
Two or more fractures are present in 66–74% of abused children, but only in 16% of non-abused children.
Periosteal reactions are common features in NAI; a very strong grip may cause such a reaction.
Always keep NAI in mind when dealing with any child with trauma.
Examination
A thorough history (this should be witnessed) and total body inspection and examination from head to toes is mandatory. Enquire about a history of fractures and deafness and look for blue sclera (osteogenesis imperfecta). Examination of genitalia should only be done by experts.
Note how the child interacts with the carer/parent.
Good communication and contemporaneous medical note writing is essential since every case of child abuse will be submitted to court.
Management
Contact consultant in charge, departmental child protection lead, and/or hospital child protection team (paediatric consultant on call, child protection practitioner).
Hospital admission if NAI is suspected, even if the medical condition does not require it.
Skeletal survey (skull, chest, abdomen, upper and lower limbs). This will be organized by paediatric team if NAI is suspected.
Blood tests (FBC, clotting screen, bone profile, calcium, phosphate, alkaline phosphatase, copper, caeruloplasmin, magnesium, fasting 25-hydroxyvitamin D, and parathyroid hormone).
Every hospital has a policy dealing with safeguarding of children.
Differential diagnoses
Osteogenesis imperfecta.
Haemophilia.
Birth trauma.
Rickets.
Leukaemia.
Scurvy (mimics NAI).
Legg–Calvé–Perthes disease
Definition
Idiopathic avascular necrosis of the proximal femoral epiphysis, first described independently by Legg, Calvé, and Perthes. The cause is unknown. The epiphyseal changes can lead to permanent deformity and osteoarthritis in adult life. The diagnosis is made on X-rays.
Key facts
Age of onset most commonly between 4 and 10y of age. If both hips look to be at the same stage, consider multiple epiphyseal dysplasia.
♂:♀, 5:1.
10–12% bilateral; the disease is usually at different stages.
Females have poorer prognosis.
Early onset up to age of 7y; late onset from age of 8y. The overall prognosis is better in the early group.
Pathology/radiology
Waldenström described four radiographic stages—ischaemia, fragmentation, reossification, remodelling.
Ischaemia. Compromise of blood supply of the femoral head. The articular cartilage still grows as it is nourished by the joint fluid, resulting in increased joint space and apparent mild joint subluxation on X-ray (Waldenström's sign); the head ceases to enlarge.
Fragmentation/resorption. New bone is laid down on the dead trabeculae, causing increased bone density. Subchondral fractures may occur, causing a black subchondral line (crescent sign). The hyperaemia and revascularization causes bone lysis and rarefication, giving a fragmented appearance on the X-rays.
Reossification (healing phase). The head is plastic and if it is not concentrically contained within the acetabulum, it will become deformed.
Remodelling. The plasticity is lost and the femoral head shape will remain. The normal internal architecture will return, but inside an altered shape if this has occurred. Deformity will lead to arthritis.
With non-operative treatment, revascularization and reossification takes 2–3y to complete in most cases.
Herring's lateral pillar classification. Now generally used at presentation (Catterall in the past). Groups A, B, C; a B/C group added later.
Group A. The lateral column of the proximal femoral epiphysis is of normal height.
Group B. The height is reduced, but >50% of the height on the other side.
Group C. The height is reduced to <50% compared to the other side.
Group B/C. Lateral pillar is narrowed (2–3mm) or poorly ossified with approximately 50% height.
Stulberg classification. Describes the end stage of the disease at skeletal maturity.
I. Normal spherical femoral head.
II. Round femoral head and fitting within 2mm of a circle on both anteroposterior and lateral radiographs.
III. Out of round by >2mm on either radiograph.
IV. Flat head and matching flat acetabulum (aspherical congruency).
V. Flat head with non-matching acetabulum (aspherical incongruency).
Catterall classification (grades 1–4; 1, 25% head involvement; 2, 50%; 3, 75%; 4, >75%). Superseded by lateral pillar classification. He described five head-at-risk signs (Gage's sign—V-shaped lucency at lateral epiphysis, horizontal growth plate, lateral calcification, subluxation, metaphyseal cystic changes). Foster reported poor reliability for head-at-risk signs.
Clinical features
Painless limp is common.
There may be pain in groin, inner thigh, and/or or only in the knee.
Again, every child with knee pain must have their hip examined.
Reduced hip abduction and internal rotation might be examined.
Management
Overall very controversial.
Annamalai et al. (2007)1 showed a great deal of variability in the UK in the decision-making process and treatment.
Non-operative symptomatic relief for the majority of patients. Physiotherapy/exercises; observation and serial radiographs.
Largest multicentre centre conducted in America by Herring et al.2,3 comparing non-operative management with operative management (either femoral varus or pelvic osteotomy) for early and late onset groups.
Early onset group. No difference in outcome between non-operative management, femoral varus, or pelvic osteotomy.
Late onset group. Improved outcome for lateral pillar groups B and B/C with either femoral varus or pelvic osteotomy over non-operative group; no difference for groups A and C.
Containment surgery has been advocated by others when the femoral head extrudes from the acetabulum irrespective of age (the femoral head is maintained within the depth of the acetabulum with femoral osteotomy, pelvic osteotomy, or both combined).
Bracing is not used by the majority of paediatric orthopaedic surgeons as part of management of Legg–Calvé–Perthes disease.
References
Motor development
Most children develop at roughly the same pace. Development is easier to understand if you realize that it will spread from head to feet, i.e. cephalocaudal.
Maturation of the nervous system occurs so that a child is able to do things more distally, the older they become. Fig. 13.2 summarizes this with some common ‘milestones’ of development.
WHO Multicentre Growth Reference Study Group (2006). WHO motor development study: windows of achievement for six gross motor development milestones. Acta Paediatrica Supplement 450: 86–95.
Club foot or congenital talipes equinovarus (CTEV)
Club foot is a congenital condition that presents at birth and may be isolated or part of a more widespread congenital disorder. Its incidence is approximately 1 in 1000 live births in the UK with a ♂:♀ ratio of 2:1. The cause is unknown.
It occurs with other neuromuscular disorders such as:
Arthrogryphosis.
Myotonic muscular dystrophy.
Myelomeningocele and other spinal dysraphisms (spina bifida).
Cerebral palsy.
Always perform a thorough examination of the hip and back to rule out other disorders/syndromes that might be associated with a club foot.
Clinical features
The hindfoot is plantar flexed (equinus) and in varus. There is midfoot and forefoot cavus and forefoot adduction. The forefoot looks supinated, but is actually pronated in relation to the midfoot. Overall, the foot is turned and twisted inwards so that the sole is facing towards the midline and backwards. In the true clubfoot deformity, the deformity is fixed to a varying degree. In the positional clubfoot deformity, the deformity is passively correctable and usually does not require any treatment.
Management
The cornerstone of treatment is to create a supple foot that is plantigrade that will allow the child to function well.
Treatment has been revolutionalized by the use of the Ponseti method of casting which can be performed in the outpatients. This is often run by specialist nurses/physiotherapy practitioners who work closely with the paediatric orthopaedic team.
Serial casts are applied that stretch the contracted tissues back to normal in a defined order. First, you correct the adduction and cavus, which also corrects the hindfoot varus and finally, the equines. About 80% of clubfeet need a percutaneous Achilles tendon tenotomy to correct the equinus.
The initial casting period goes over about 6 weeks with weekly cast changes. At the end of this period, the Achilles tenotomy is performed if necessary, followed by a further 3 weeks in cast. Thereafter, the feet are immobilized 23h/day with boots on a bar for 3 months and then only during the night until the age of 4–5y. Some children require a tibialis anterior tendon transfer when they are about 4–5y old because of a dynamic supination deformity. Recurrences are usually the result of non-compliance or if the child has a syndromic clubfoot.
Flat feet (pes planus)
There are always one or two children in every orthopaedic paediatric new patient clinic with flat feet. The children rarely complain of symptoms and the appearance and referral is often sparked by the parents.
Clinical features
Like all paediatric consultations, take an accurate neonatal, birth, and family history to look for associated problems. The cornerstone is whether the foot deformity is flexible (vast majority) or rigid.
Flexible flat feet correct fully once the big toe is extended and the arch reforms and when the child stands on tip toes.
Ensure you examine the ankle and Achilles tendon as this often causes a ‘compensatory’ flat foot due to the stiffness and is easily remedied by physiotherapy.
Natural history
The majority of children form normal foot arches by the age of about 3y. In some, the arches never form and they remain flatfooted.
Management
Flexible flat feet generally need simple reassurance and the patient can be discharged. Some children with more severe flat feet benefit at times from the use of insoles since insoles improve the mechanical leg alignment. This applies, for example, to children who present with knee pain and moderate to severe flat feet where the feet are in a pronated position when standing. Tight Achilles tendons need physiotherapy.
Rigid flat feet are associated with an underlying abnormality such as:
Congenital vertical talus (from birth).
Tarsal coalition. Fusing of some part of the tarsal bones via scar or bone (often adolescents).
Inflammatory joint disease.
Treatment is centred on the underlying disorder, i.e. tarsal coalition is often treated by offloading the area with orthotics and if this fails, attempts can be made to surgically resect the fibrous or bony coalition.
The osteochondritides
These conditions result in avascular necrosis of epiphyseal bone, similar to Legg–Calvé–Perthes disease, but less common. In general, they are troublesome rather than serious. Some are self-limiting.
Features
Most lead to aching and muscle spasm. Radiographic changes occur in the affected epiphysis, with varying degrees of density change and fragmentation.
Epiphyses commonly affected are:
Lateral condyle of the humerus (Panner's disease).
Carpal lunate (Kienbock).
Carpal scaphoid (Preiser).
Head of metatarsal (Freiberg).
Tarsal navicular (Kohler).
Patella (Larsen–Johanssen).
Vertebral epiphyseal plates (Scheuermann).
Vertebral body (Calvé).
Management
Usually symptomatic with limitation of activities and anti-inflammatory medication.
Traction apophysitis
An apophysis is a traction epiphysis which may undergo partial avulsion with avascular change followed by subsequent repair. These changes can be the result of trauma, overuse, or rapid growth. The commonest are:
Osgood–Schlatter's disease. Apophysitis of the tibial tubercle into which the patellar tendon inserts.
Sever's disease. Apophysitis of the apophysis at the posterior aspect of the calcaneum where the Achilles tendon inserts.
Clinical features
The patient is usually an adolescent who presents with aching, swelling, and/or pain.
Radiology
Radiographs show fragmentation of the tibial tuberosity/calcaneal apophysis.
Treatment
Explanation of the condition; limitation of activities; anti-inflammatory medication. Plaster immobilization for 4–6 weeks can be helpful in severe cases. Temporary use of a cushioned heel support for Sever's disease can be helpful.
Osteochondritis dissecans of the knee
Avascular necrosis of the subchondral bone, resulting in softening of the articular cartilage and bone that may become loose and separated from the rest of the femoral condyle. The cause is unknown, but it is thought that it might be the result of repetitive minor trauma.
Most lesions are located on the lateral side of the medial femoral condyle, but any joint can be affected.
Children between 5 and 15y of age are most commonly affected with the majority occurring in teenage boys.
Clinical features
Non-specific knee pain.
If the fragment has become loose, the patient will report crepitance, popping, giving way, and/or locking.
Natural history
In children and adolescents, spontaneous healing over about 18 months is the usual outcome. Patients with more advanced lesions have an increased risk to develop early osteoarthritis.
Investigations
Radiographs. The tunnel view will show the lesion the best.
MRI. The scan shows extent of the lesion and, if there is detachment, with fluid interposition between fragment and underlying bone.
Management
Activity restriction for the majority of cases.
Unstable lesions require arthroscopic stabilization.
